Mayo Clinic Electrophysiology Manual 2014

Mayo Clinic Electrophysiology Manual
Mayo Clinic Scientific Press

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Mayo Clinic
Electrophysiology
Manual
Editor-in-Chief
Samuel J. Asirvatham, MD
Consultant, Division of Cardiovascular Diseases
Mayo Clinic, Rochester, Minnesota
Professor of Medicine and of Pediatrics
College of Medicine, Mayo Clinic
Associate Editors
Yong-Mei Cha, MD
Professor of Medicine
Paul A. Friedman, MD
Professor of Medicine
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Mayo Clinic electrophysiology manual / editor-in-chief, Samuel J. Asirvatham.
p. ; cm. — (Mayo Clinic scientific press)
Electrophysiology manual
Includes bibliographical references and index.
ISBN 978–0–19–933041–6 (alk. paper) — ISBN 978–0–19–933042–3 (alk. paper) — ISBN 978–0–19–994119–3 (alk. paper)
I. Asirvatham, Samuel J. II. Title: Electrophysiology manual. III. Series: Mayo Clinic scientific press (Series)
[DNLM: 1. Electrophysiologic Techniques, Cardiac—Examination Questions. WG 18.2]
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This book is dedicated to . . .
Usha, the source of my inspiration and for being the ever-dependable platform that gives me the confidence
to undertake the kind of study that makes this book and any task possible and enjoyable.
Rohit, Roshini, and Hemanth, for giving me the confidence in the fact that every generation is better than the one before.
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Preface
Putting together a textbook for cardiac electrophysiology is question about a figure, tracing, or anatomic section. Several
challenging. When many of us did our own training, there answer choices are presented and these choices are then dis-
were no textbooks on invasive electrophysiology, mapping, cussed in detail. Whether right or wrong, each choice in turn
and ablation. Although several outstanding textbooks have gives rise to another question reflective of a specific attempt
become available more recently, the rapidly changing land- to present the 3-dimensional texture of cardiac electrophysi-
scape in invasive electrophysiology makes it difficult to ology manifest on the 3 axes of anatomy, physiology, and bio-
write something that will remain relevant for a significant physics of energy delivery.
period. Invasive electrophysiology training continues to be some-
The idea for this textbook came about a few years ago, when thing of an apprenticeship, and we hope that the discussion
one of our trainees began taking extensive notes during our of these cases and concepts will provide a framework for all
group’s weekly 6:45 am case-based electrophysiology confer- those who are privileged to enter this fascinating area of learn-
ence. He suggested assembling these notes into a manual for ing, caring for patients, and safely curing an ever-increasing
future trainees, practicing consultants, and allied staff. The number of arrhythmia syndromes.
lectures themselves were deliberately targeted at a level just None of these concepts could have been appreciated, and
above the most accomplished or sophisticated member in the thus this book could never have been completed, without the
audience on that particular day. At the same time, we aimed assistance, input, and mutual education provided by what I
to develop teaching points, exemplified by the extraordinary truly believe is the greatest set of allied health professionals
findings and pathology in the patients we had the privilege in the world and the way in which they magnify the value
of caring for at Mayo Clinic. We also attempted to present we provide for our patients, especially those in the Cardiac
something of educational value for everyone in the audience, Ablation Laboratory. We are indebted to the outstand-
regardless of their level of training or exposure. At about ing editorial assistance provided by the production team at
this time, we were privileged to collaborate with William D. Mayo Clinic Scientific Press: June Oshiro, PhD, and Jane C.
Edwards, MD, Division of Anatomic Pathology, Mayo Clinic. Wiggs (editors); Susan R. Miller (editorial assistant); Ann
Through his unparalleled collaborative spirit and sharing Ihrke (proofreader); Kenna Atherton (manager, Scientific
his outstanding insights, anatomic dissections, and a set of Publications) and Roberta J. Schwartz, who was there with
1,000 hearts that he permitted our group’s study, we added me at the beginning; to the assistance of Deborah Veerkamp
anatomy to all our electrophysiology discussions. This inter- (production designer, Media Support Services), to the untir-
dependence of anatomy with intracardiac electrophysiology ing and enthusiastic assistance from Jennifer Mears (medical
has been highlighted throughout this textbook and bears secretary), and to our patients.
testament to Dr. Edwards’ unique contribution to all cardiac If there is one regret I have in choosing a career in cardiac
electrophysiologists. electrophysiology, it is that I can never again experience the
The core of this textbook is a collection of cases somewhat unparalleled wonder and joy of discovering the nuances and
loosely based on a unifying aim. Introductory chapters are hidden treasures of learning electrophysiology for the first
included to help those relatively new to our wonderful spe- time.
cialty, and they will help familiarize learners with the rules
and strategies we use in caring for patients in the electro- Samuel J. Asirvatham, MD
physiology laboratory. Most cases and chapters begin with a Editor-in-Chief
vii
Contents
Section I: Understanding the Tools and Techniques of Section II: Case Studies: Testing the Principles
Electrophysiology
Glossary of Catheter Names 217
1. Introduction to the Electrophysiology Manual:
Case 1 219
Fluoroscopic Views, Electrograms, and Relevant
Anatomy 3 Case 2 245
Samuel J. Asirvatham, MD Case 3 287
2. Use of Intracardiac Echocardiography in Cardiac Case 4 309
Electrophysiology 65
Case 5 317
Paul A. Friedman, MD, and Samuel J. Asirvatham, MD
3. Electroanatomic Mapping for Catheter Ablation of Case 6 327
Cardiac Arrhythmias 75 Case 7 337
Amit Noheria, MBBS, Traci L. Buescher, RN, and Samuel J. Case 8 347
Asirvatham, MD
Case 9 361
4. Diagnostic Maneuvers Commonly Used in the
Electrophysiology Laboratory: Understanding the Case 10 377
Rationale, Techniques, and Interpretation 85 Case 11 391
Samuel J. Asirvatham, MD
Case 12 411
5. Reentry, Transient Entrainment, and Concealed
Case 13 423
Entrainment 129
Win-Kuang Shen, MD Case 14 449
6. Approach to Wide QRS Tachycardias 137 Case 15 467
Yong-Mei Cha, MD, and Samuel J. Asirvatham, MD Case 16 489
7. Basic Cardiac Electrophysiology 171
Case 17 523
Hon-Chi Lee, MD, PhD, and Arshad Jahangir, MD
Case 18 561
8. Antiarrhythmic Drug Therapy: Understanding
Options for the Ablationist 191 Case 19 591
Arshad Jahangir, MD Case 20 615
9. Catheter Ablation and Device Therapy in Congenital Index 681
Heart Disease 203
Chenni S. Sriram, MBBS, Malini Madhavan, MBBS,
Peter A. Brady, MB, ChB, MD, Bryan C. Cannon, MD,
Christopher J. McLeod, MB, ChB, PhD, and Samuel J.
Asirvatham, MD
ix
Contributors
Samuel J. Asirvatham, MD Dorothy J. Ladewig

Consultant, Division of Cardiovascular Diseases, Mayo Associate Project Manager, Research Administrative
Clinic, Rochester, Minnesota; Professor of Medicine and Services, Mayo Clinic, Rochester, Minnesota
of Pediatrics, College of Medicine, Mayo Clinic
Hon-Chi Lee, MD, PhD
Peter A. Brady, MB, ChB, MD Consultant, Division of Cardiovascular Diseases, Mayo
Consultant, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota; Professor of Medicine,
Clinic, Rochester, Minnesota; Associate Professor of College of Medicine, Mayo Clinic
Medicine, College of Medicine, Mayo Clinic
Malini Madhavan, MBBS
Traci L. Buescher, RN Fellow in Cardiovascular Diseases, Mayo School of Graduate
Division of Cardiovascular Diseases, Mayo Clinic, Medical Education, College of Medicine, Mayo Clinic,
Rochester, Minnesota Rochester, Minnesota; Assistant Professor of Medicine,
Bryan C. Cannon, MD
Senior Associate Consultant, Division of Pediatric Christopher J. McLeod, MB, ChB, PhD
Cardiology, Mayo Clinic, Rochester, Minnesota; Associate Senior Associate Consultant, Division of Cardiovascular
Professor of Pediatrics, College of Medicine, Mayo Clinic Diseases, Mayo Clinic, Rochester, Minnesota; Assistant
Professor of Medicine, College of Medicine, Mayo Clinic
Yong-Mei Cha, MD
Consultant, Division of Cardiovascular Diseases, Mayo Jennifer A. Mears
Clinic, Rochester, Minnesota; Professor of Medicine, Cardiac Laboratory Office, Division of Cardiovascular
College of Medicine, Mayo Clinic Diseases, Mayo Clinic, Rochester, Minnesota
William D. Edwards, MD Thomas M. Munger, MD
Consultant, Department of Laboratory Medicine and Consultant, Division of Cardiovascular Diseases, Mayo
Pathology, Mayo Clinic, Rochester, Minnesota; Professor Clinic, Rochester, Minnesota; Assistant Professor of
of Laboratory Medicine and Pathology, College of Medicine, College of Medicine, Mayo Clinic
Medicine, Mayo Clinic
Amit Noheria, MBBS
Paul A. Friedman, MD Research Collaborator, Division of Cardiovascular Diseases,
Consultant, Division of Cardiovascular Diseases, Mayo Mayo Clinic, Jacksonville, Florida
Clinic, Rochester, Minnesota; Professor of Medicine,
Douglas L. Packer, MD
Consultant, Division of Cardiovascular Diseases, Mayo
Apoor S. Gami, MD Clinic, Rochester, Minnesota; Professor of Medicine,
Research Collaborator, Division of Cardiovascular Diseases, College of Medicine, Mayo Clinic
Mayo Clinic, Rochester, Minnesota. Present address:
Win-Kuang Shen, MD
Midwest Heart Specialists, Downer’s Grove, Illinois
Chair, Division of Cardiovascular Diseases, Mayo Clinic,
Arshad Jahangir, MD Scottsdale, Arizona; Professor of Medicine, College of
Research Collaborator, Division of Cardiovascular Diseases, Medicine, Mayo Clinic
Mayo Clinic, Scottsdale, Arizona. Present address: Center
Chenni S. Sriram, MBBS
for Integrative Research on Cardiovascular Aging, Aurora
Fellow in Cardiovascular Diseases, Mayo School of Graduate
Health Care, Milwaukee, Wisconsin
Medical Education, College of Medicine, Mayo Clinic,
Rochester, Minnesota
xi
Section I
Understanding the Tools and
Techniques of Electrophysiology
1
Introduction to the Electrophysiology
Manual: Fluoroscopic Views, Electrograms,
and Relevant Anatomy
Samuel J. Asirvatham , MD
INTRODUCTION This fluoroscopic image is from the RAO projection (ver-

tebral column to the left). However, without a simultaneously
The purpose of this chapter is to familiarize the reader obtained LAO projection (orthogonal view), it is impossible
with the typical fluoroscopic views and electrograms used to distinguish whether the catheter is in the right side or the
throughout this book. First, the rationale for the particular left side of the heart. Thus, choices A, B, and C are all possible
views used (right anterior oblique [RAO] and left anterior locations for this catheter. The fossa ovalis region, however,
oblique [LAO] projections) and the standard electrogram is posterior to the coronary sinus and is not a likely location
display format are introduced. The discussion then contin- for the catheter shown, as explained later in this chapter. Th is
ues to the important fluoroscopic landmarks relevant to the typical fluoroscopic image is similar to several seen through-
arrhythmias encountered in the electrophysiology (EP) labo- out this book, and each catheter position is explored in more
ratory. These landmarks are discussed in the context of the detail.
electrograms obtained from mapping these sites and their Usually when fluoroscopy is required to evaluate an
importance from an anatomic and ablation standpoint. anatomic structure, the standard anteroposterior (AP) and
The first topics are the common fluoroscopic and ana- orthogonal lateral views are ideal because most parts of the
tomic principles relevant to the EP laboratory; then the spe- body are oriented naturally in these views. For example, if a
cific differences in catheter use and electrograms obtained radiographic image of the face is needed, an AP view depicts
from the standard fluoroscopic catheter position in supraven- which structures are on the right and which are on the left
tricular tachycardia, atrial flutter, atrial fibrillation, and ven- because the face itself is oriented in an AP direction. Thus,
tricular tachycardia; and finally some unusual positions and on an AP view of the face, the right maxillary sinus is not
congenital variants. mistaken for the left orbit. The orthogonal lateral view of
the face shows the profi le view, and the lateral view allows
FLUOROSCOPIC AND ANATOMIC PRINCIPLES quick recognition of structures that are anterior (closer to
the nose) and posterior (closer to the back of the head and
Figure 1.1 is a fluoroscopic image obtained from a patient
neck).
with paroxysmal narrow QRS tachycardia.
Figure 1.2 shows the position of the normal heart when
What is the location of the catheter indicated by the arrow the chest is opened. Unlike most other organs visualized by
in Figure 1.1? diagnostic radiography, the apex of the heart is displaced to
A. Cavotricuspid isthmus the left. Thus, if the heart were visualized in an AP view, mul-
B. Mitral annular location tiple cardiac chambers are superimposed at any given loca-
C. Middle cardiac vein tion being analyzed. For example, the arrow in Figure 1.2
D. Fossa ovalis region would normally indicate the right ventricular outflow tract
E. Any of the above portion of the left ventricular outflow tract and possibly the
F. Cannot be determined from the information given left atrium all superimposed at that site fluoroscopically. The
Answer: F—Cannot be determined from the information orthogonal lateral view distinguishes between anterior and
given. posterior structures. However, the exact demarcation between
right and left atria and ventricles cannot be easily determined
Abbreviations are expanded at the end of this chapter. even with the orthogonal view.
3
4 Section I. Understanding the Tools and Techniques of Electrophysiology
What does the electrophysiologist performing complex

procedures require from fluoroscopy?
1. To quickly determine whether a given catheter is in the
right- or left-sided circulation (right vs left ventricle,
right vs left atrium, right superior pulmonary veins
vs right atrium, etc).
2. To determine whether a catheter is atrial or ventricular
to the annulus (right atrium vs right ventricle, etc).
3. To acquire anatomic knowledge of which atrial struc-
tures cross the plane of the annulus and which ven-
tricular structures, when being mapped, may have a
catheter located more atrial to the annulus.
4. To acquire accurate knowledge of where the annulus
and septum are located so that these determinations can
be made with the typical catheters used for ablation.
Figure 1.4 shows the heart as it is normally positioned in
the chest. In an AP view of the skull, the nasal structures
define the midline, orienting the parts to the right and to
the left. If the heart did have intraventricular and intra-atrial
Figure 1.1 Fluoroscopic image of paroxysmal narrow QRS septa exactly at its midline, then similar determinations of
tachycardia. The arrow is explained in the text. right and left could be made using an AP view, and any cath-
eter placed on the septum would define the midline. Since the
intra–atrial and intraventricular septa are not at the midline
In Figure 1.3, the borders of the cardiac silhouette are but are rotated to the left, the LAO projection is the equiva-
shown on an AP view chest radiograph alongside a dissected lent of an AP view of the normally placed heart. Here, with
heart in the same anatomic orientation. The various portions the camera rotated to the left and positioned looking directly
of the silhouette show the right atrium and left ventricle as at the “face” of the heart (with the septum being the “nose”),
well as the vascular trunk, yet the main cardiac chamber ante- this view can readily distinguish between catheters placed
riorly is the right ventricle. In basic EP, when only EP studies in the right and left sides of the heart.
and relatively straightforward procedures were done, the AP The right panel in Figure 1.5 shows the LAO projection. The
and lateral views were sufficient because only an approximate arrow indicates to the inferiormost portion of the intraven-
knowledge of catheter position was needed to safely and effec- tricular septum. Comparison of this position with Figure 1.4
tively perform those procedures. As procedures have become shows that in the LAO projection the view is straight at the
more complex, integration of fluoroscopic anatomic knowl- heart. Any catheter placed to the right and crossing the mid-
edge with the information obtained from mapping systems line would be in the left-sided circulation. What is not known
and ultrasonography has required more “pure” fluoroscopic from this view, however, is whether the catheter is in the left
views. ventricle or left atrium or left pulmonary vein, etc, but only
that it is to the left.
Knowing right from left is the first prerequisite of a fluo-
roscopic view, but it is also necessary to define atrial from
ventricular structures. The RAO projection shown in the left
panel of Figure 1.5 is the orthogonal view and equivalent to
the lateral view obtained, for example, in a skull radiograph.
Left This shows the profi le of the heart. The vertebral column
lung would be expected to be seen to the extreme left on the screen
Right and the sternum close to the extreme right on the screen.
lung
Since the ventricles are anterior, that is, closer to the sternum
than the atria, which are closer to the vertebral column, this
Heart
view can help distinguish atrial from ventricular structures.
Thus, by combining the RAO and LAO projections, the
electrophysiologist can quickly determine where (in which
cardiac chamber) a given catheter is located.
Figure 1.6 shows the RAO and LAO projections on fluo-
Figure 1.2 Anterior view of normal heart in an open chest. roscopy. These should be compared with Figure 1.5 to orient
The arrow is explained in the text. those new to electrophysiologic fluoroscopy to the views most
1. Introduction to the Electrophysiology Manual 5
RA LV
Figure 1.3 Left , Chest radiograph showing the silhouette of a normal heart (indicated by arrows). Right, Dissected heart shown in the
same position as the visualized heart. LV indicates left ventricle; RA, right atrium.
commonly used (and used throughout this book). The posi- in the ventricle or atrium? In the LAO projection, it is clearly
tion of the vertebral column allows immediate recognition of on the right side. The LAO view could be interpreted as show-
which view is the RAO and which is the LAO. In the RAO ing the catheter in the right atrium or in the free wall of the
view, the vertebral column is seen to the extreme left, and in right ventricle. But on the RAO projection, the catheter is
the LAO view, the vertebral column is seen to the right. located posteriorly and in the atrium, and this is the right
By asking the following question, the chamber in which atrial catheter.
a catheter is positioned can be determined. In the LAO view Although a cursory glance at these 2 orthogonal views
(Figure 1.6, right panel), is the catheter to the right or left, (RAO and LAO) allows quick determination of where a cath-
and in the RAO view (Figure 1.6, left panel), is the catheter eter is located, a precise knowledge of the location of the sep-
tum and the annulus is required in less obvious situations (as
shown in Figure 1.1).
A fluoroscopic image in the LAO projection may not
show exactly where the septum is. Similarly, the RAO image
may not show where the annulus is, although there is often
a posterior fat pad that is translucent where the cardiac and
diaphragmatic silhouettes cross. In EP-related fluoroscopy,
certain commonly placed catheters with characteristic elec-
trograms can be used to define the septum and annulus.
Figure 1.7 shows the important landmarks relevant to EP
procedures in the RAO and LAO projections. The course of
the main body of the coronary sinus is almost exactly on the
annulus. Thus, in the RAO projection, if the exact view is
adjusted so that the coronary sinus catheter is en face, then
it becomes simple to know which structures are ventricular
(anterior to the coronary sinus catheter) or atrial (posterior to
the coronary sinus catheter).
The His bundle catheter is used to define the septum in the
LAO view. Notably, the His bundle is almost always located
in the septum at the level of the annulus anteriorly. Since the
His bundle electrogram is unique, if a catheter shows this
Figure 1.4 Anterior view of a normal heart showing its external characteristic electrographically, then it is located at the His
topography. LAA indicates left atrial apex; LV, left ventricle; bundle region, and the LAO view can be adjusted to make the
RA, right atrium; RV, right ventricle. The lower arrow indicates the His bundle catheter seem to look straight out at the examiner,
right ventricular apex along the intraventricular septum. thus defining the septum. Any catheter or structure noted on
Ao
Ao
RA RV
RV LV
Figure 1.5 Left panel, Right anterior oblique projection, the orthogonal view showing the profi le of the heart. Right panel, Left anterior
oblique projection. The arrow indicates the inferiormost portion of the intraventricular septum. Ao indicates aorta; LV, left ventricle;
RA, right atrium; RV, right ventricle.
the right when the examiner is looking at the LAO projection electrogram where the atrial and ventricular electrograms are
relative to the His bundle catheter must be in the left-sided equally balanced. Thus, by combining the fundamentally pure
circulation (left ventricle, left atrium, etc). fluoroscopic views of the RAO and LAO projections with the
The coronary sinus mapping catheter also shows, along electrograms obtained by a catheter that defines the annu-
with any other catheter placed on the annulus, a characteristic lus (coronary sinus catheter) and the septum (His bundle
Figure 1.6 Right anterior oblique (left panel) and left anterior oblique (right panel) fluoroscopic projections. The white arrows indicate the
vertebral column. The yellow arrows indicate the catheter tip.
RAO
His
LAO
RA His
Fossa
ovalis
Right
CS ostium Fossa Left
ovalis
Ventricle
CS ostium
Fat pad
Fat pad
Diaphragm
Figure 1.7 Coronary sinus landmarks. CS indicates coronary sinus; LAO, left anterior oblique; RA, right atrium; RAO, right anterior oblique.
catheter), the electrophysiologist can more accurately define clearly defines the level of the annulus. Any catheter super-
placement of any given catheter. Also in Figure 1.7, the fossa imposed on this catheter is at the annulus, and any catheter
ovalis is posterior to the plane of the annulus, as would be anterior to the coronary sinus catheter in the RAO view is
expected being an atrial structure, and the coronary sinus in the ventricle. If a His bundle electrogram is obtained by
ostium opens to the right atrium and is therefore slightly the catheter at the position indicated by the yellow arrow in
atrial to the main body of the coronary sinus located on the the right panel of Figure 1.8, then the catheter is certainly
annulus. The more distal course of the coronary sinus tilts located on the septum and thus defines the septum in the
toward the ventricle as the distal tributary is the anterior and LAO view. Thus, any catheter such as the distal portion of
anterolateral ventricular veins. the coronary sinus catheter (white arrow) on the right in the
Figure 1.8 again shows the RAO and LAO fluoroscopic LAO projection is somewhere in the left part of the heart, eg,
projections. In the RAO fields, the catheter is en face and the left portions of the annulus, left atrium, or left ventricle.
Figure 1.8 Right anterior oblique (left panel) and left anterior oblique (right panel) fluoroscopic projections. The white arrows indicate the
coronary sinus catheter. The yellow arrow in the left anterior oblique view (right panel) indicates the His bundle catheter.
By accurately defining the annulus and the septum, a quick Thus, the distal proximal electrodes of the His bundle cath-
look at the catheter position can help define the likely cham- eter all have similar gain settings.
ber in which any given catheter is located. In the coronary sinus recording catheter (CS 1,2–CS 19,20),
The reader is invited to try to deduce the exact anatomic the smaller-numbered electrodes represent the distal record-
location of the other catheters shown in Figure 1.8 and then ing pairs. Thus, CS 1,2 is left ward in the LAO projection and
go back to the question following Figure 1.1 and deduce which mapping the left anterolateral portions of the mitral annu-
type of EP abnormality results in the catheter’s placement in lus. The most proximal recording pair is CS 19,20, located
that location for successful ablation. in the region of the coronary sinus ostium. As shown in the
The next topic of discussion is the typical electrogram LAO projection in Figure 1.8, the His bundle catheter that
obtained from catheters placed for EP study and ablation as defines the septum is approximately in line with the proximal
well as the setup and nomenclature of catheters and electrodes recording electrodes on the coronary sinus catheter. Thus, the
used largely throughout this book. Figure 1.9 illustrates a typ- proximal electrodes are probably close to the true coronary
ical intracardiac electrogram obtained during a sinus beat. sinus ostium.
First, the catheter labeled “HIS” is in the His bundle region. The ablation catheter is labeled “ABL dis” and “ABL prox”
The characteristic His bundle recording is noted, and 4 bipo- for the distal and proximal recording pairs of electrodes. All
lar electrograms are displayed. In the displays used in this electrograms displayed in this book are bipolar electrograms
book, the distal electrode has the smaller number. Thus, HIS unless specifically mentioned. Hardly any atrial electrogram
1,2 represents the recording between the distal poles 1 and 2 is noted on the distal ablation catheter electrode, whereas a
of an octapolar His bundle recording catheter (see Figure 1.8), fairly large atrial electrogram with similar gain settings is
with HIS 3,4 being more proximal and HIS 7,8 being the most seen from the proximal pairs. This difference suggests that
proximal pair of recording electrodes. The atrial electrogram the tip of the ablation catheter is in a ventricular location with
is the largest on HIS 7,8 and smallest in the distal recording the proximal recording pair close to or at the annulus. Most
pairs (HIS 1,2), which is expected. In the RAO projection, the of the tracings in this book display the distally recorded elec-
proximal electrodes are expected to be located posterior to trogram below the proximally recorded electrogram.
the annulus and therefore largely in the atrium. In general, In Figure 1.9, the catheter labeled “HRA prox” is the proxi-
similar gain settings are used on any given recording catheter. mal high right atrial electrogram.
Figure 1.9 Typical intracardiac electrogram obtained during a sinus beat.

Why are 2 electrograms—one that times with the P wave Most tracings in this book show recordings from 3 or 4
and another with a QRS complex—obtained from the high standard electrocardiographic (ECG) leads above the trac-
right atrial catheter? ings to correlate with the intracardiac electrograms (eg, leads
A. The catheter must have slipped into the coronary sinus II, I, and V1 shown at the top of Figure 1.9). Exact leads cho-
B. The electrodes are placed deep in the atrial appendage sen vary by type of arrhythmia to best illustrate the electro-
C. The catheter may be placed on the medial wall of the gram in each case discussion. The right ventricular recording
superior vena cava catheter is labeled “RV prox” (proximal recording electrode
D. The catheter is located above the right atrial–superior pair). The actual site in which the right ventricular catheter
vena cava junction has been placed is important.
E. Any of the above The electrophysiologist must constantly correlate elec-
F. None of the above trograms and fluoroscopic positions to derive maximum
information from these electrograms during an EP study.
Answer E—Any of the above.
For example, in the electrogram shown in Figure 1.10, the
To accurately determine the reason a ventricular electro- fi rst recorded beat shows the atrial activation sequence
gram is recorded in a catheter placed in the high right atrium, during sinus rhythm. Both the proximal coronary sinus
the fluoroscopic views are correlated with the electrographic electrograms (CS 17,18) and the distal coronary sinus
views. The RAO view shown in the left panel of Figure 1.5 recording electrode pair (CS 1,2) show nearly simultaneous
shows the tip of the right atrial appendage crossing the plane of activation in the coronary sinus beat. Th is appears para-
the annulus and draping over a portion of the proximal aortic doxical. As in sinus rhythm, the expectation would be for
root and the right ventricular outflow tract. Similarly, in the the proximal coronary sinus to be activated much earlier
LAO view (Figure 1.5, right), the left atrial appendage is seen than the distal coronary sinus. However, viewing the fluo-
draping over the anterior mitral annulus and portions of the roscopic image at this time would show that the coronary
right ventricular outflow tract. A catheter placed deep into the sinus catheter (20–pole catheter) is large and placed all the
appendage not only records electrograms that are near-field way around the mitral annulus. Thus, the distal coronary
from the atrial tissue and contact but also records a fairly large sinus electrodes record anterior left atrial activations via
ventricular electrogram as well. Also, the superior vena cava in the Bachmann bundle, and the proximal coronary sinus
the RAO fields at the level of the venoatrial junction is very close electrodes reflect coronary sinus and left atrial activation
to the junction between the aortic root and the left ventricu- occurring via the ostium of the coronary vein. The second
lar outflow tract. Left ventricular electrograms can usually be and third beats shown in Figure 1.10 are the patient’s typi-
recorded by a catheter placed in this location in the high right cal tachycardia. The mid–coronary sinus electrodes are the
atrium as well. If the catheter falls out of place and is located earliest of the recorded coronary sinus atrial electrograms.
anywhere along the annulus, including within the coronary They occur considerably earlier than the surface P-wave,
sinus, it records both atrial and ventricular electrograms. and a near-field signal is obtained in the mid–coronary
Figure 1.10 Complex electrograms on the coronary sinus catheter (arrows).

sinus (CS 11,12). Th is fi nding strongly suggests that the ear-

liest site of activation is very near or at the mid–coronary
sinus recording electrodes. Thus, correlating fluoroscopic
anatomy with the electrogram narrows the differential
diagnosis to a coronary sinus muscle–related tachycardia,
an epicardially located accessory pathway in the left poste-
rior region with long conduction times, or an unusual vari-
ant of atrioventricular (AV) node reentry. Th is and other
similar cases are discussed in detail throughout the book
(see Chapter 4 and Cases 6, 11, and 20).
Having explained the principles of fluoroscopic anatomy
relevant to EP and also the typical display of electrograms
to be used in this book, the discussion now moves to issues
specific to certain arrhythmias.
FLUOROSCOPIC ANATOMY RELEVANT

TO MAPPING AND ABLATION OF
SUPRAVENTRICULAR TACHYCARDIA
Figure 1.11 Right anterior oblique view. The arrow indicates the
Detailed electrogram analysis and explanation of pacing position of the catheter on the annulus, about to deliver ablation
maneuvers relevant to supraventricular tachycardia diagnosis energy.
appear throughout this book (Chapter 4 and Cases 1, 2, 3, 7, 9,
and 11). This section highlights situations in which an exact or to the bundle of His (more ventricular and if using high
knowledge of fluoroscopic anatomy and the corresponding energy) may occur. If the ablation catheter is on the tricus-
electrograms plays a vital role in supraventricular tachycar- pid annulus and high–energy ablation is being performed, a
dia ablation. rare but possible untoward effect may be injury to the right
coronary artery.
A 29-year-old man presented with repeated paroxysms of
Figure 1.12, the LAO projection obtained simultaneously
palpitations resulting from a rapid narrow QRS complex
with Figure 1.11, clearly shows the ablation catheter on the
tachycardia. The arrhythmia has been mapped, and abla-
left side of the heart (white arrow). With the catheter on the
tion energy is about to be delivered via the catheter indi-
annulus in the RAO view, this LAO view shows the cath-
cated by the arrow in the RAO image shown in Figure 1.11.
eter located posterolaterally in the mitral annular region.
Which structure may be inadvertently injured when ablat-
The septum, as defined by the His catheter (yellow arrow in
ing at this site?
Figure 1.12), shows that the proximal coronary sinus electrodes
A. Compact AV node
are fairly deep into the coronary sinus. A rare complication of
B. Bundle of His
C. Right coronary artery
D. Left circumflex artery
E. Any of the above
F. None of the above
Answer: E—Any of the above.
Although it is stated in the question, the reader may also
deduce that the RAO projection is being shown because of
the position of the vertebral column shadow appearing on the
left and the foreshortened view of the coronary sinus catheter.
The ablation catheter is seen on the annulus, with the distal
electrode ventricular to the annulus as defined by the coro-
nary sinus catheter and the proximal electrodes atrial to the
annulus. In this RAO projection, the ablation catheter is nei-
ther very anterior nor posterior (inferior). However, this view
does not show whether the catheter is located on the left side
of the circulation (mitral annulus) or on the right side (tricus-
pid annulus) or whether the catheter is located on the septum
or the free wall of either annulus.
If the catheter is located close to the His bundle catheter, Figure 1.12 Left anterior oblique view. The yellow arrow indicates
then injury to the compact AV node (slightly atrial location) the His catheter. The white arrow indicates the ablation catheter.
the coronary veins or with high energy along the annulus

can damage the circumflex artery (indicated by the arrow in
Figure 1.13). This is more apt to occur with epicardial abla-
tion either via the pericardial space from within the coronary
venous system or when ablating on the left atrial tissue as
it “overhangs” the mitral annulus rather than on the mitral
annulus itself.
In Figure 1.14, where the RAO and LAO images are both
shown, an ideal ablation site on the mitral annulus is shown in
the RAO view where the ablation catheter bridges the annu-
lus. However, in the LAO view, the ablation catheter should
be “separated” from the mitral annulus by the valve and other
annular tissue. When it is seen crossing over this coronary
sinus catheter, as in this example, it is likely that either a pul-
monary vein has been entered (more laterally) or the catheter
is prolapsed external to the annulus on the overhanging rim
of left atrial tissue. In this situation, ablation energy can be
delivered close to the coronary artery.
Table 1.1 summarizes the optimal fluoroscopic catheter
position for left-sided accessory pathway ablation.
In Figure 1.15, the arrow in both the RAO (left panel) and
LAO (right panel) projections indicates a catheter posi-
tioned in a very important location related to supraven-
tricular tachycardia ablation. Where is this catheter likely
located?
Figure 1.13 Reconstructed computed tomographic scan image. A. Left atrium
The arrow indicates the left circumflex artery. B. Right lower pulmonary vein
C. Fast pathway region
D. Compact AV node region
ablation in the region of the mitral annulus, particularly with E. Slow pathway region
high-energy ablation, is injury to the left circumflex artery.
Answer: C—Fast pathway region.
A reconstructed computed tomographic scan image is
shown in Figure 1.13. The coronary venous system tends to be Of the choices given for this question, the most likely site
atrial and superficial to the arterial system. Ablation within for catheter location is in the region of the fast pathway. It is
Figure 1.14 The right anterior oblique (left panel) and left anterior oblique (right panel) images. The arrow in the left anterior oblique view
indicates the mapping-ablation catheter.
Table 1.1 region because the eustachian ridge and tendon of Todaro
Fluoroscopic Catheter Position for Left–Sided Accessory keep the His bundle catheter rightward.
Pathway Ablation This concept is illustrated in Figure 1.16. The site of fast
1. Desirable: In RAO view, catheter straddles the annulus pathway lesions is behind the tendon of Todaro, whereas slow
(distal electrode ventricular, proximal electrode atrial). pathway lesions are located in front of or ventricular to the
2. Desirable: In LAO view, the ablation catheter is separated from tendon of Todaro in the region of the coronary sinus ostium.
the neighboring coronary sinus electrode by about 4 to 6 mm Thus, not only is the fast pathway exit site superior to the
(on the annulus). inferoposteriorly located slow pathway region, it is also more
3. Desirable: Movement of the catheter consistently alongside and atrial, being behind the eustachian ridge.
parallel to the annulus in the RAO view. Th is motion allows
Figure 1.17 shows a dissected autopsied human heart dis-
cooling of the catheter while maintaining contact at the annular
playing the regional anatomy relevant to the fluoroscopic
site of the accessory pathway.
4. Undesirable: In LAO view, the catheter overlaps (perpendicular
view shown in Figure 1.15. The slow pathway is located at
and across) the mitral coronary sinus catheter (may be desirable the ostium of the coronary sinus and the compact AV node
if trying to ablate an epicardial pathway). between the tricuspid annulus and the eustachian ridge. The
5. Undesirable: In either view, the tip of the catheter pointed fast pathway is essentially equidistant from the superior rim
against and perpendicular to the free wall/annulus (if impedance of the fossa ovalis and the tendon of Todaro. Mapping of this
pop occurs, then perforation is likely). site is important in several situations:
6. Desirable: Axis of ablation catheter movement is the same as
the axis of coronary sinus catheter movement during cardiac 1. In typical AV node reentry, the true fast pathway site is
contraction. earlier than the slow pathway site and, in fact, is earlier
than the atrial electrograms along the annulus.
Abbreviations: LAO, left anterior oblique; RAO, right anterior oblique.
2. With anteroseptal accessory pathways, since they gen-
erally connect atrium to ventricle just across the annu-
lus, the proximal His bundle and atrial electrograms
sometimes incorrectly thought that the proximal His bundle
recorded mid His bundle precede activation of the true
region represents the site of earliest activation during retro-
fast pathway sites.
grade fast pathway conduction (typical atrioventricular nodal
3. In some patients with typical AV node reentry and
reentry tachycardia [AVNRT] or during ventricular pacing).
unusual intra-atrial conduction patterns, the distal or
The true earliest atrial site of activation with retrograde fast
mid coronary sinus electrode may show earlier activa-
pathway conduction is behind the tendon of Todaro where
tion than the proximal coronary sinus electrode, giving
the compact AV node and the His bundle are anterior to the
a mistaken impression of a coexisting left-sided acces-
tendon of Todaro and the His bundle itself is anterior (ven-
sory pathway. On careful mapping, however, the true
tricular) to the annulus. On fluoroscopy, the telltale sign that
fast pathway sites precede even the earliest site in the
a catheter is behind the tendon of Todaro and/or the eusta-
eccentrically activated coronary sinus.
chian ridge is that the catheter points left ward in the LAO
projection. Thus, the His bundle catheter, used to define the Figure 1.18 shows diagrammatically that the surrogate for
septum, cannot be as left ward as a catheter at the fast pathway the fast pathway (proximal His bundle) is activated before the
Figure 1.15 Catheter positioned in an important location related to supraventricular tachycardia ablation. The left panel shows the right
anterior oblique view, and the right panel shows the left anterior oblique view. The arrows indicate the His bundle catheter.
D. Atrial tachycardia
E. None of the above
Answer: C—Atypical AVNRT.
HB
The rationale behind this answer is explained in more
detail in Chapter 4 and in Case 20. Clearly, left atrial tachy-
FO TT FP lesion
cardia is possible with a long antegrade conduction time
through the AV node. The essential finding on this tracing is
distal–to–proximal activation in the coronary sinus catheter.
IVC CS SP lesion The coronary sinus catheter has been placed in good posi-
TA tion (as in Figure 1.15). Thus, the proximal coronary sinus
is being mapped by CS 19,20, and the anterolateral free wall
Figure 1.16 Atrial input to the atrioventricular node. CS indicates of the mitral annulus is being mapped by CS 1,2. The only
coronary sinus; FO, fossa ovalis; FP, fast pathway; HB, His diagnosis that can be excluded is atypical AVNRT because,
bundle; IVC, inferior vena cava; SP, slow pathway; TA, tricuspid by definition, atypical AVNRT has for its retrograde limb the
annulus; TT, tendon of Todaro. slow pathway. The slow pathway is located in the region of the
proximal coronary sinus. Thus, late activation at the proxi-
mal coronary sinus excludes atypical AVNRT just as it would
proximal coronary sinus. The relative activation between the exclude a posterior septal atrial tachycardia, for example.
anatomic fast pathway site (approximately same as proximal Should the eccentric activation sequence in the coronary
His) and the proximal coronary sinus activation are the only sinus exclude typical AVNRT? Figure 1.20 illustrates the
ways to distinguish between typical and atypical AVNRT. importance of knowing the fluoroscopic anatomy of the fast
The V-A interval is not exact in making this distinction, as pathway region (Figure 1.15). When a catheter was placed as
discussed in Chapter 4. shown in Figure 1.15, the atrial activation was significantly
Figure 1.19 shows the electrograms obtained in a patient ahead of the earliest recorded atrial electrogram seen on the
with paroxysmal narrow QRS tachycardia. Catheters have coronary sinus catheter. The reasons for this are discussed in
been inserted into their usual locations and displayed in the Chapter 6 and Cases 3 and 7 and are summarized in Figure
typical format explained above (smaller numbers reflecting 1.20. Some patients have conduction block across the eusta-
distal electrodes, etc). Which of the following diagnoses can chian ridge (and crista terminalis); thus, activation proceeds
be excluded if the coronary sinus catheter has been placed to the left atrium and activation of the coronary sinus occurs
in a position similar to that shown in Figure 1.15? only through the left atrium–coronary sinus connections.
A. Typical AVNRT In some patients, the only physiologic left atrium–coronary
B. Presence of an anteroseptal accessory pathway sinus connection is in the distal coronary sinus, and in that
C. Atypical AVNRT situation, eccentric activation is seen in the coronary sinus in
typical AVNRT, as is the case in this patient. Less commonly
appreciated and rare is an anteroseptal accessory pathway. If
it is not mapped exactly at the site of earliest activation and if
the anatomic idiosyncrasies referred to above occur, eccentric
activation in the coronary sinus can be seen as well.
If the catheters, particularly the coronary sinus and
His bundle catheters, are placed similarly to those shown
in Figure 1.15 and the intracardiac electrograms shown
FP in Figure 1.21 are obtained, retrograde AV nodal conduc-
tion during ventricular pacing can be excluded. Again, the
Fossa coronary sinus catheter is well seated within the sinus. The
earliest activation in the coronary sinus is close to its distal
electrode. Unlike the previous example, however, the proxi-
SP mal His bundle catheter, a surrogate for the fast pathway, is
CS very late and therefore cannot represent retrograde conduc-
tion via the AV node and fast pathway. The proximal coro-
nary sinus is also late and, as explained earlier in this chapter,
Figure 1.17 Dissected heart displaying the regional anatomy
(right atrium and right ventricle) relevant to the right anterior excludes retrograde conduction via the slow pathway. Thus,
oblique fluoroscopic view shown in Figure 1.15. The arrows an accessory pathway must be present. The importance of the
indicate the typical activation pattern from the atrioventricular unusual fractionated electrograms at the site of earliest atrial
node (oval) to the fast pathway exit site. CS indicates coronary activation on CS 5,6 is discussed further in the “Identifying
sinus; FP, fast pathway; SP, slow pathway. Pathway Potentials” section of Chapter 4 and in Case 1.
II
V1
V6
RV
A
CS d HRA
HRA His His p

H V
A
His d
A
CS p
A
CS m
A
CS d
Figure 1.18 The surrogate for the fast pathway (proximal His bundle [His p]) is activated before the proximal coronary sinus (CS p).
The arrows indicate the activation patterns. CS d indicates distal coronary sinus; CS m, medial coronary sinus (second dot from the right);
His d, distal His bundle; HRA, high right atrium; RV, right ventricle.
Figure 1.19 Electrograms obtained in a patient with paroxysmal narrow QRS tachycardia.
an alternate location is necessary occasionally. In fact, the

right ventricular apex is probably the least informative loca-
tion from which to pace the ventricle in patients being evalu-
ated for supraventricular tachycardia.
Figures 1.22 and 1.23 show the RAO and LAO projec-
tions, respectively, with catheters placed during ablation for
supraventricular tachycardia. The RAO view shows that both
catheters are located in the ventricle. Where are these cathe-
ters located and why have they been placed in this position for
ventricular pacing? The catheter indicated by the white arrow
is placed in the posteroseptal right ventricle fairly close to the
base. Examining either the RAO or LAO views (closer to the
diaphragm) confirms its posterior position. The LAO view
shows its relatively septal position, and its fairly basal orien-
tation can be seen by comparing the distance from the tip of
this catheter to the coronary sinus and the sternum (apex) in
the RAO view. Right ventricular pacing may be specifically
Figure 1.20 Mechanisms for potentially variable coronary performed, obtaining good information from this location
sinus activation sequences from fast pathway exit, illustrating in patients with a suspected posteroseptal or posterior acces-
the importance of knowing the fluoroscopic anatomy of the fast sory pathway. Pacing from the apex causes fusion between
pathway region. (Adapted from Asirvatham SJ. Cardiac anatomic
AV nodal conduction and pathway conduction, but pacing
considerations in pediatric electrophysiology. Indian Pacing
closer to the pathway elucidates mapping of the abnormal
Electrophysiol J. 2008 May 1;8[Suppl. 1]:S75–91. Used with permission
of Mayo Foundation for Medical Education and Research.)
conduction sequence.
In Figures 1.22 and 1.23, what is the position of the cath-
eter indicated by the yellow arrow? This pacing and ablation
During ventricular pacing (as shown in Figure 1.21), the catheter is placed in a para-Hisian location. In both the RAO
electrophysiologist should be cognizant of the exact fluoro- and LAO views, the catheter’s location on the anteroseptal
scopic location of the coronary sinus and His bundle mapping region of the heart is slightly above and more ventricular to
catheters. An accurate knowledge of where the ventricular the His bundle pacing catheter. Reasons for pacing from this
pacing catheter is located is also important. site include performing para-Hisian pacing (see Chapter 4) or
Although it is usual to perform ventricular pacing maneu- discerning the retrograde His bundle deflection more clearly
vers from the right ventricular apex, pacing the ventricle from than would be possible from ventricular pacing at the apex
Figure 1.21 Intracardiac electrograms excluding retrograde atrioventricular nodal conduction during ventricular pacing.
Ventricular pacing
at apex
VH A
V-A 90 ms
Ventricular pacing
at mid septum
HV A
V-A 70 ms
Figure 1.22 Right anterior oblique view with catheters placed

for supraventricular tachycardia. The arrows are explained in
Figure 1.24 Top panel, Ventricular pacing at apex. Bottom
the text.
panel, Ventricular pacing at mid septum. The arrows indicate the
activation pattern.
(see below). This concept of the ventricular pacing site affect-

ing the nature of the electrogram obtained on the His bundle because of a near simultaneous wave front (ventricular myo-
recording catheter is illustrated in Figures 1.24 and 1.25. cardial activation and retrograde conduction tissue activa-
In the top panel of Figure 1.24, pacing is from the usual location reaching the His bundle region). In the bottom panel of
tion of the ventricular apex. On the recorded electrograms on Figure 1.24, the pacing site has been moved back close to the
catheter position A near the His bundle, it is very difficult to exit site of the right bundle branch. Here, conduction via the
discern where the retrograde His bundle deflection is located right bundle with a His bundle retrograde occurs faster than
the ventricular myocardial wave front during pacing from
site B, and thus, the His bundle electrogram can be seen more
clearly than when pacing is done at the ventricular apex.
Figure 1.25 illustrates the best site for seeing the retro-
grade His bundle. Pacing from near the His bundle region
itself causes immediate activation of the ventricular myo-
cardium, and the ventricular electrogram is early on the His
bundle recording catheter. Because of the insulation around
Ventricular pacing
at base
V H A
V-A 110 ms
Figure 1.23 Left anterior oblique view with catheters placed Figure 1.25 The ideal pacing site for seeing the retrograde
for supraventricular tachycardia. The arrows are explained in His bundle is near the base. The arrows indicate the activation
the text. pattern.
the His bundle, to activate this structure, ventricular activa- side/mitral annulus from the LAO view). On careful exami-
tion must first proceed down to the right bundle and then nation of the LAO view (Figure 1.27, right panel), the catheter
travel retrograde up the right bundle, causing a relatively long in question (white arrow) is clearly left of the midline with
V-H interval. Thus, in any of the several situations described the His bundle catheter defining the septum. In the RAO
in Chapter 6 where it is important to recognize the retrograde view (Figure 1.27, left panel), the tip of the catheter (white
His bundle electrogram, the pacing can be performed prefer- arrow) is ventricular to the coronary sinus. Comparison
entially from the base in a para-Hisian location. of this catheter’s course with the course of the transsep-
Figure 1.26 shows another common situation where the tal catheter (yellow arrow) shows that it has not reached
V-H interval during pacing becomes long, and the retro- the left atrium via the fossa ovalis or transseptal puncture.
grade His bundle deflection is clearer to observe, that is, Therefore, the most likely way that this catheter (white
with ventricular pacing from an apical site (or elsewhere) arrow) has reached the left side and crossed the midline is
but with placement of extrastimuli. The ventricular extra- via the coronary sinus. The main possibility that would need
stimulus block retrograde in the right bundle branch delays to be considered is that the tip of the catheter is within the
activation to the His bundle via transseptal conduction and middle cardiac vein or a posterior or posterolateral vein. The
retrograde left bundle activation. Although the coronary main difficulty of defining a catheter’s position in the middle
sinus activation sequence is eccentric, when retrograde right cardiac vein is distinguishing it from other closely separated
bundle branch block occurs and the V-H interval lengthens, veins or from a position where the catheter is on the inter-
the V-A interval also lengthens by an equivalent amount ventricular septum parallel to the middle cardiac vein. The
and without a change in the activation sequence. As dis- distinction between middle cardiac vein position and right
cussed in Chapter 4, this pattern of activation is diagnostic interventricular septal position is particularly important
of retrograde AV nodal conduction, namely, fast pathway because inadvertent ablation within the middle cardiac vein
conduction. may occur during attempts to ablate the slow pathway or the
Thus, the fluoroscopic location of the ventricular pacing cavotricuspid isthmus.
catheter is important for the correct interpretation of the Just as important as analysis of the RAO and LAO views,
resulting electrograms. These findings are summarized in with particular attention to the His bundle and coronary
Table 1.2. sinus catheter to define a given catheter’s position, is attention
In the RAO and LAO images in Figure 1.27, the catheter to the fluoroscopic movement characteristics of the catheter
in question is labeled with a white arrow in both views. The and response to the catheter-tipped torque being placed more
catheter indicated by the yellow arrow has been determined proximally on that catheter. This latter concept is explained
to be on the mitral annulus (annulus from the RAO view, left in the next 2 figures.
Figure 1.26 Retrograde right bundle branch block. The arrow indicates the retrograde His bundle deflection.
Table 1.2
Importance of Ventricular Pacing Site
Ventricular Pacing Sitea Advantages Disadvantages Comments
RV apex pacing Stable catheter position Difficult to discern retrograde The most common location
Familiarity with location His bundle electrogram for ventricular pacing but
Possibly a higher risk of often the least informative
perforation when interpreting pacing
maneuvers during ablation
procedures
Posterobasal RV pacing Preferentially favors conduction Catheter instability Excellent pacing site when a
via posterior accessory Frequent ectopy may occur posteroseptal or posterior
pathways from irritation (right or left) accessory
More generally, a pacing site pathway is suspected,
closer to the base favors particularly when AV nodal
accessory pathway conduction conduction is present and
over AV nodal conduction robust as well
Para-Hisian pacing (anteroseptal High and low output may Catheter instability Important site particularly
RV close to the distal His differentially capture His Capture may be intermittent for performing para-Hisian
bundle/proximal right bundle) bundle and myocardium Inadvertent capture of the pacing and defining the
or myocardium alone atrial myocardium can exact nature of retrograde
(para-Hisian pacing) give rise to misleading ventricular atrial conduction
Favors conduction via information
anteroseptal or anterior
accessory pathways
LV pacing Favors retrograde conduction Risk of thrombosis (may Following ablation of a
via a left-sided accessory be performed from the left-sided pathway, when an
pathway over the AV node coronary venous system) ablation catheter has already
Requires specific access been placed, the mitral
annulus can be advanced
to the ventricle to perform
LV pacing to better exclude
persistent but poor accessory
pathway conduction
RV outflow tract pacing Produces a clockwise activation Catheter stability Varying the direction of the
around the mitral annulus Possible increased risk of wave front following local
useful in defining left-sided perforation myocardial capture can be
accessory pathway slant useful in difficult accessory
(see Chapter 4) pathway ablation to
precisely define the slant and
insertions of the accessory
pathway
Abbreviations: AV, atrioventricular; LV, left ventricular; RV, right ventricular.
a
Ventricular extrastimulus placement from any location may induce retrograde bundle branch block and allow better discernment of the retrograde His bundle
electrogram.
Figure 1.28 shows the RAO and LAO positions with the When counterclockwise torque is applied, a catheter with
catheter in position to be analyzed (white arrow) when its tip anterior (ventricular) to the coronary sinus responds in
counterclockwise torque is applied on the guiding sheath a characteristic manner. The tip of the catheter should point
(yellow arrow) and catheter. Which of the following is away from the septum (rightward in the LAO projection)
likely true? until the catheter tip points to the lateral tricuspid annulus,
A. The catheter is in the middle cardiac vein and further counterclockwise torque brings the catheter tip
B. The catheter is in the posteroseptal region of the right back into the atrium. Clockwise torque causes catheters in
ventricle the ventricle to have better contact against the interventricu-
C. The catheter is in a posterolateral vein lar septum, or if the catheter is very basal, with counterclock-
D. This maneuver cannot be interpreted when a guiding wise torque the catheter tip goes into the coronary sinus.
sheath is being used In Figure 1.28, the operator is applying counterclockwise
Answer: A—The catheter is in the middle cardiac vein. torque to both the sheath and the catheter, yet the tip of the
Figure 1.27 Left panel, Right anterior oblique position of the catheter. Right panel, Left anterior oblique position of the catheter.
The arrows are explained in the text.
catheter in the LAO projection (right panel, white arrow) is opposite its usual movement. With this extremely simple
still clearly to the left of the midline (as defined by the His maneuver, it is crucial to avoid inadvertent damage to the
bundle catheter position). The more proximal curve of the coronary arterial system by ablating in the middle cardiac
catheter (proximal to the proximal electrodes) has moved vein. Counterclockwise torque application can be done to
left ward in the LAO projection and ventricular in the RAO test catheter tip position with or without the use of a sheath.
projection. This movement occurs because the catheter tip If the catheter is on the interventricular septum and not in
is lodged in the middle cardiac vein and acts as a fulcrum, the vein, the tip no longer acts as a fulcrum, and the entire
causing the catheter to torque proximally in the direction catheter moves away from the septum (rightward in the LAO
Figure 1.28 Left panel, Right anterior oblique position of the catheter. Right panel, Left anterior oblique position of the catheter.
The arrows are explained in the text.
projection). The opposite maneuver, that is, application of Another important fluoroscopic consideration with abla-
clockwise torque by the operator, is more difficult to perform tion of supraventricular tachycardia, particularly when
and analyze when a sheath is present because most sheaths considering epicardial posterior accessory pathways, is
tend to keep the catheter on the septum. angiography of the proximal coronary sinus. In Figure 1.31,
Figure 1.29 shows an example of clockwise torque being angiography is being performed on the proximal portion of
applied to a catheter in the middle cardiac vein (without a the coronary sinus through an end-hole mapping catheter.
guiding sheath). The proximal curve moves in the oppo- There is a protrusion near the ostium of the expected portion
site direction; that is, in the RAO projection it is relatively of the middle cardiac vein (white arrows). Here, angiography
more atrial and in the LAO projection it is relatively more has delineated a coronary sinus– or middle cardiac vein–
rightward, yet with the catheter tip staying in a similar related diverticulum.
location (fulcrum). It is important for the operator to real- Figure 1.32 shows diagrammatically a diverticulum occur-
ize, however, that the application of clockwise torque is ring between the middle cardiac and posterior cardiac veins.
less useful than the application of counterclockwise torque Such diverticula may, however, actually involve one of these
because a similar response to clockwise torque is seen if the aforementioned veins as well (middle cardiac or posterior cor-
catheter tip is on the intraventricular septum (not in the onary vein). Shown also is the extension of myocardium occur-
middle cardiac vein). The main reason for applying clock- ring along the coronary sinus and around the diverticulum.
wise torque is to see, after it has been established that the The distal musculature (lower parts) around the diverticulum
catheter is not on the intraventricular septum, whether the inserts into the ventricular myocardium, and the proximal
catheter tip is lodged in the middle cardiac vein or is still in musculature related to the coronary sinus inserts into the
the main body of the coronary sinus pointing to the middle atrial musculature. Thus, multiple possibilities for accessory
cardiac vein. pathway conduction exist. The importance for fluoroscopic
If the catheter is simply within the coronary sinus, then delineation of these structures (with angiography) is 2-fold:
strong clockwise torque application causes the catheter tip
to move further left ward in the LAO projection, as shown in 1. To clearly define the ostium of the diverticulum and
Figure 1.30. This catheter is located close to or within a pos- target energy delivery at this site to electrically isolate
terolateral vein. Epicardial pathways may be related to any of the diverticulum at the ostial level.
the tributaries of the coronary sinus. However, in the middle 2. To perform coronary arteriography to exclude any
cardiac vein and posterior vein, associated diverticula are important arterial branches of the right or left coro-
most common. On the basis of the LAO projection only (as nary arterial system from being too close to the abla-
shown in Figure 1.30), one cannot be sure that the catheter tip tion site and thus at risk for damage and a myocardial
is not in a lateral atrial vein. infarction.
Figure 1.29 An example of clockwise torque being applied to a catheter in the middle cardiac vein without a guiding sheath. The arrows
indicate the coronary sinus ostium. Left panel, Right anterior oblique position of the catheter. Right panel, Left anterior oblique position of
the catheter.
Figure 1.32 A diverticulum occurring between the middle cardiac

and posterior cardiac veins. The myocardium extends along the
coronary sinus and around the diverticulum.
the EP laboratory for EP study and radiofrequency abla-

Figure 1.30 In this left anterior oblique projection, the catheter tion of the accessory pathway (approximately 18 years after
is now located close to or within a posterolateral vein. The arrow DC ablation). Why would a patient require ablation of an
indicates the pulmonary vein. accessory pathway even after the AV node has been ablated
successfully?
A. Recurrent orthodromic reciprocating tachycardia
Figure 1.33 shows the catheter positions (RAO and LAO B. Recurrent antidromic reciprocating tachycardia
views) in a 72–year-old man who had implantation of a per- C. Preexcited atrial fibrillation
manent dual-chamber pacemaker after AV nodal ablation. D. Recurrent pacemaker-mediated tachycardia
The patient has a history of recurrent orthodromic recipro- E. A and B
cating tachycardia. His ablation was performed in the era of F. C and D
DC ablation, and determinate tachycardia and his AV node
Answer: F—C and D.
were ablated. Since his pathway showed both antegrade and
retrograde conduction, the ECG still showed preexcitation With the AV node ablated, reciprocating tachycardia (either
during atrial pacing or sinus rhythm. He was referred to antidromic or orthodromic) is no longer possible. Of course, if
another accessory pathway is present, a pathway-to-pathway
tachycardia can still occur, but not reciprocating tachycardia
involving the AV node. As patients get older, the chance of
atrial fibrillation unrelated to the accessory pathway increases.
Since the accessory pathway still can conduct antegrade, pre-
excited atrial fibrillation, a potentially malignant arrhythmia,
is still possible after AV nodal ablation. Although this patient
did have atrial fibrillation with some preexcitation, the main
reason for his referral to the EP laboratory was recurrent
pacemaker syndrome. In pacemaker syndrome, retrograde
ventriculoatrial activation results in a sensed retrograde
atrial electrogram by the pacemaker lead in the atrium, trig-
gering a paced A-V interval and ventricular pacing. Th is ven-
tricular paced beat again gives rise to retrograde conduction,
and the process repeats itself. Usually this pattern of recip-
rocating activation occurs because of retrograde conduction
via the AV node, and programming a postventricular atrial
refractory period longer than the retrograde conduction time
prevents this arrhythmia from occurring. This patient had a
very long retrograde conduction time through a poorly con-
ducting retrograde pathway. Thus, the postventricular atrial
Figure 1.31 Right anterior oblique view of a diverticulum in the refractory period could not be prolonged enough to prevent
middle cardiac vein (arrows). recurrent, incessant pacemaker-mediated tachycardia.
Figure 1.33 Right anterior oblique (left panel) and left anterior oblique (right panel) views of the catheter positions in a 72-year-old man
who had implantation of a permanent dual-chamber pacemaker after atrioventricular nodal ablation. The arrows are explained in the text.
He was thus referred for radiofrequency ablation using a This can be a technically challenging maneuver because the
20–electrode multipolar catheter placed along the tricuspid tricuspid annulus is somewhat elliptical and more anterior
annulus (Figure 1.33, white arrows) and an ablation catheter at lateral locations relative to the mitral annulus, making it
used for mapping along the posterolateral tricuspid annular hard to know when the true annulus is still being mapped.
locations. Alternatives used to help in ablation of these difficult arrhyth-
mias include placing a multielectrode catheter on the annu-
Why would a multielectrode catheter, similar to that dis-
lus after obtaining a fairly stable annular position or using
cussed for the coronary sinus, be placed along the tricuspid
small flexible microelectrode catheters placed into the right
annulus?
coronary artery. The operator should not hesitate to use these
A. To help map and ablate typical atrial flutter
techniques to map the lateral annulus in patients with Ebstein
B. To help map and ablate a right-sided free wall accessory
anomaly or Mahaim fibers. Particularly when previous abla-
pathway
tion has failed, the information from these catheters can be
C. To help map and ablate an atypical or scar-related atrial
helpful. To judge annular location, one must look to see if
flutter
the ventricular and atrial electrograms are fairly balanced
D. To help map and ablate a right atrial automatic
(if a large A and small V, the catheter may be too atrial in
tachycardia
those locations). Such cases illustrate why it is important for
E. All of the above
an electrophysiologist to have a thorough understanding of
Answer: E—All of the above. fluoroscopic-anatomic-electrogram correlations.
The anatomic proximity of the coronary sinus to the mitral The intracardiac electrograms obtained during atrial pac-
annulus provides an excellent annular mapping position. ing in another patient with a right-sided accessory pathway
This relationship not only defines the anatomy of the annulus are shown in Figure 1.34. As is the convention explained ear-
but allows fairly balanced atrial and ventricular electrograms lier in this chapter, the multielectrode catheter on the free
to map retrograde and antegrade conduction and flutter cir- wall of the right atrium (as in Figure 1.33) is labeled “IS” (for
cuits related to the mitral annulus. There is no equivalent isthmus, since this catheter is frequently used during cavotri-
vein for the tricuspid annulus in which to place a catheter, cuspid isthmus ablation, as described later in this chapter).
and thus, imaging of annular tachycardia (eg, typical flut- The distal electrodes are more caudally placed (IS 1,2), and
ter, atypical flutter, lateral scar-related tachycardia, right the proximal electrodes (IS 19,20) are closer to the right atrial
atrial tachycardia) can be facilitated with a tricuspid annulus superior vena cava junction. The ablation catheter is posi-
catheter. To map this region, most commonly a single rov- tioned similar to what is shown in Figure 1.33, that is, on the
ing catheter is used to map sequentially along the annulus. annulus in a posterolateral location.
Figure 1.34 Intracardiac electrograms obtained during atrial pacing in a patient with a right-sided accessory pathway.
If radiofrequency energy is delivered at the position shown multielectrode catheters that record the earliest ventricular
in Figures 1.33 and 1.34 via the ablation catheter, what is activation. In the last beat of this tracing, where preexcitation
the likely result? during atrial pacing is lost, there is no effect on the near-field
electrogram seen on the ablation catheter. This observation
A. Loss of preexcitation
further shows that the near-field potential on the ablation
B. Loss of AV nodal conduction
C. No effect on AV node conduction or the accessory catheter, thought to be a pathway potential, is a bystander for
pathway this patient’s abnormal atrial ventricular conduction.
D. Ablation of both AV nodal and accessory pathway Could this be a pathway potential for a second accessory
conduction pathway? This is an unlikely possibility because the local ven-
tricular myocardium near the ablation catheter is activated
Answer: C—No effect on AV node conduction or the acces-
via a wave front that begins at the site of earliest activation
sory pathway.
recorded on the multielectrode catheter.
This case illustrates the importance of exact fluoroscopic Figure 1.35 shows diagrammatically a possible explana-
and electrogram correlation. If one looks at only the ablation tion for such bystander signals. During fetal development,
catheter’s recorded electrogram, the first few beats of the trac- AV node–like tissue is found throughout the tricuspid
ing shown in Figure 1.34 show what appears to be an excel- annulus. This tissue gradually regresses. Figure 1.35 shows
lent site for ablation. There is reasonable AV balance and a an example of such tissue that did not regress but does not
very sharp near-field potential recorded between the atrial constitute a true atrial ventricular bypass tract. When both
and ventricular electrograms. This sharp potential is highly atrial and ventricular connections exist with such tissue, an
suggestive of a pathway potential (see Chapter 4). However, accessory pathway, often with decremental properties, results
because of the recorded electrograms from the isthmus cath- (Mahaim fiber) (see Case 19). If such tissue persists into adult
eter (IS 1,2–IS 19,20), during the beats that show preexcitation life without an atrial connection but only a ventricular con-
with atrial pacing, there is a ventricular electrogram recorded nection, spontaneous ectopy from this remnant tissue may
that significantly precedes the “pathway potential.” These present as premature ventricular contractions. If only an
electrograms correlate with the fluoroscopic positions shown atrial connection persists, then no significant arrhythmia
in Figure 1.33 in the RAO and LAO projections, and there is results, but if EP mapping is undertaken (perhaps as part of
significant distance between the ablation electrode and the another procedure), then sharp His bundle–like potentials,
No connection with atrium
Conduction via rapidly

conducting tissue to point of exit
Figure 1.35 Atrioventricular node–like tissue that did not regress but does not constitute a true atrial ventricular bypass tract.
without evidence of direct conduction to the ventricle, result. to the diaphragmatic silhouette. All possible answers suggested
In an electrogram viewed in isolation (not correlated with a for this question are inferior structures. The LAO projection
fluoroscopic image), such bystander signals may be mistaken narrows the right-sided inferior structures (slow pathway, sub-
for a His bundle potential as well as a pathway potential as eustachian pouch vs the left-sided inferior structures, middle
discussed earlier in this chapter. cardiac vein, etc). However, the question reveals that a relatively
Thus, with reference to supraventricular tachycardia large atrial electrogram is being recorded. This would likely
ablation, key fluoroscopic locations of mapping or ablation exclude the possibility that the catheter slipped down into the
catheters and their correlated electrograms are important inferior vena cava. Although the RAO fluoroscopic projection
(Table 1.3), particularly in difficult cases, and are discussed in is consistent with catheter location in the inferior vena cava,
the case studies presented in this textbook. this vein, unlike the superior vena cava and pulmonary veins,
has not been found to have myocardial extensions. Thus, the
atrial electrograms are limited when the catheter is placed in
FLUOROSCOPY AND ELECTROGRAM
the inferior vena cava. The cavotricuspid isthmus is generally
CORRELATION RELEVANT TO ATRIAL
on the same plane as the floor of the coronary sinus. However,
FLUTTER ABLATION
in some patients, a recess or pouch is found and can measure 5
In Figure 1.36, the black arrow in this RAO projection to 10 mm below the plane of the floor of the coronary sinus.
indicates the ablation catheter. A large atrial electrogram Figure 1.37 is an anatomic dissection of a human heart
and far-field ventricular electrogram are recorded from the with a subeustachian pouch present. The heart is displayed in
distal electrode pair. Which is the least likely location for an LAO projection (compare with Figure 1.38). The subeusta-
the ablation catheter? chian pouch extends deeper than the floor of the coronary
A. Within the inferior vena cava sinus. Also well demonstrated in this figure are the boundar-
B. Slow pathway region ies of the subeustachian pouch formed by 3 valves or valvelike
C. In a subeustachian pouch structures, the tricuspid valve anteriorly, the thebesian valve
D. Within the middle cardiac vein (guarding the coronary sinus) medially, and the eustachian
E. All of the above valve end ridge posteriorly. A catheter located inside this
pouch records an atrial electrogram unlike a catheter in the
Answer: A—Within the inferior vena cava.
inferior vena cava (more posteriorly), as explained earlier in
As discussed above, the RAO projection does not show this chapter. The electrogram recorded from the pouch itself
whether the catheter is located on the right or left side of the may be relatively small in some patients, but in others, as in
heart, but given the location of the coronary sinus catheter (yel- this example, where a pectinate muscle runs just anterior to
low arrow), the ablation catheter is relatively inferior and close the pouch, the atrial electrogram may be very large.
Table 1.3
Summary of Fluoroscopy-Electrogram Correlations for Supraventricular Tachycardia Ablation
Site Anatomic Location Relevance
Fast pathway exit site • Behind and slightly caudal to the proximal His • Necessary to map the fast pathway specifically
bundle location when it is unclear whether the His bundle atrial
• Behind (atrial to) the tendon of Todaro and electrogram or proximal coronary sinus electrogram
eustachian ridge is earliest during tachycardia or ventricular pacing
• Left ward orientation of the catheter in comparison • Ablation should not be delivered at this early site but
with the His bundle catheter viewed in the LAO rather in the region of the coronary sinus ostium
projection (slow pathway)
Middle cardiac vein • In the RAO projection ventricular to the coronary • Epicardial accessory pathways often involve this vein
sinus catheter or the closely related posterior vein or an associated
• In the LAO projection posterior and left ward of the diverticulum
His bundle catheter • Ablation energy may be delivered inadvertently
• Counterclockwise torque shows that the tip does within this vein with the operator thinking that the
not move away from the septum to the right catheter is on the right posterior interventricular
septum
• Energy delivery in this vein may damage the
coronary arterial system
Coronary sinus • Ostium is just atrial to the mitral annulus • Important to try to determine the distal extent and
• Distal veins are ventricular location of the proximal coronary sinus (ostium)
• Can be difficult to define the exact coronary sinus • A catheter placed in this vein should be placed
ostium beyond the site of possible pathway conduction
• Various pacing maneuvers performed from this
catheter exploit the distinction between coronary
sinus muscle and left atrial musculature conduction
(see Chapter 4, Case 11)
Tricuspid annulus • Difficult to define because no clear venous structure • If an endocardial catheter is placed atrial and
is similar to the coronary sinus ventricular, electrograms must be nearly equal
• Multielectrode catheter can be placed on the • In Ebstein anomaly, ablationists frequently
annulus endocardially underestimate how “ventricular” the annulus
• Occasionally a multielectrode mapping catheter can actually is and thus ablate atrial to the exact site of
be placed in the right coronary artery the accessory pathway (which is on the annulus)
Ventricular pacing site • RV apex • Difficult to find retrograde His
• RV outflow tract • Useful in defining slant of left-sided pathways
• Anteroseptal distal to His • Para-Hisian pacing, defining the retrograde His
• Posteroseptal ventricular site • Defining retrograde posteroseptal accessory
• LV pacing pathway conduction
• Following ablation to test for recurrent poor
conduction across an “ablated” left-sided pathway
Abbreviations: LAO, left anterior oblique; LV, left ventricular; RAO, right anterior oblique; RV, right ventricular.
Figure 1.38 shows the simultaneously obtained LAO fluo- jugular vein may be located on the roof of the large coronary
roscopic view (the RAO view is shown in Figure 1.36). The sinus. Differentiating tricuspid annular locations from the
ablation catheter is not in the left side of the heart, as deduced middle cardiac vein is explained in detail earlier in this chap-
from the location of the His bundle catheter. As explained ter, but the reader should compare the present fluoroscopic
initially in this chapter, the His bundle catheter defines the images (Figures 1.36 and 1.38) with those shown with middle
atrial and ventricular septa in the LAO view. Thus, catheter cardiac vein placement in Figure 1.28.
location in the middle cardiac vein or other veins is excluded The key region to be mapped during typical atrial flutter
within the coronary sinus. The extent of inferior separation ablation is the atrial myocardium between the tricuspid valve
from the coronary sinus catheter would strongly suggest that and the inferior vena cava. More specifically, both mapping
the catheter is in fact in a subeustachian pouch. However, and ablation catheters need to be placed in the subeustachian
a slow pathway location cannot be excluded, particularly if region between the eustachian ridge and the tricuspid valve.
there is a persistent left superior vena cava giving rise to a The inset in Figure 1.39 shows placement of 2 multielectrode
very large coronary sinus. In this instance, the slow pathway catheters. The first is labeled “I 1, 2–I 19, 20.” This catheter is
mapping catheter may be on the floor of the large coronary placed along the subeustachian isthmus. In the electrograms,
sinus and the coronary sinus catheter placed via the internal the distal electrodes (in this case engaging the coronary sinus
Figure 1.36 The black arrow in this right anterior oblique Figure 1.38 The simultaneously obtained left anterior oblique
projection indicates the ablation catheter. The yellow arrow fluoroscopic view (the right anterior oblique view is shown in
indicates the location of the coronary sinus catheter. Figure 1.36). The ablation catheter (white arrow) is not in the left
side of the heart. This can be deduced from the location of the His
bundle catheter, indicated by the yellow arrow.
ostium) are numbered 1,2 and displayed as “AA 1,2,” and the
proximal electrodes on the lateral right atrial wall are labeled
“AB 19,20.” location of these catheters and correlating the electrograms, a
A second catheter labeled “T 1,2–T 19,20” in the inset figure quick glance at the activation pattern can define whether there
is placed on the lateral right atrial wall just anterior to the crista is clockwise, counterclockwise, or fused activation occurring
terminalis. The equivalent labels displayed on the intracar- in the atrial tissue just posterior to the tricuspid valve (cavotri-
diac electrograms are labeled “AA 1,2–AA 19,20”; the smaller cuspid isthmus and lateral right atrium).
numbers refer to the distal electrodes. One or both of these The preceding example illustrates the importance of
catheters are labeled in a similar manner in the cases related understanding the fluoroscopic views, as visualized in the 2
to atrial flutter ablation. By understanding the fluoroscopic standard orthogonal views (RAO and LAO), and integrating
the information from the electrograms recorded by the cath-
eters. In the case illustrated in Figures 1.36 and 1.38, the LAO
view helps exclude the need for a left-sided catheter position
for the ablation catheter. However, to do this, the interatrial
septum is defined, and the electrograms recorded from the
His bundle catheter are used to determine that this catheter
IVC LA is, in fact, at the His bundle region (septum). The RAO view
is used to understand the inferior and annular (by compar-
ing with the coronary sinus catheter) location of the abla-
tion catheter and further exclude certain locations, such as
Eustachian valve the inferior vena cava, again by integrating the electrogram
Pouch information obtained from the distal recording ablation elec-
trodes. This case reinforces the need to continuously attempt
CS to predict electrogram characteristics on the basis of fluoro-
scopic analysis and also to predict the fluoroscopic locations
of catheters by visualizing the electrograms obtained.
Thebesian valve
Figure 1.40 shows an LAO fluoroscopic view and a corre-
Figure 1.37 An anatomic dissection of a human heart with a sponding diagrammatic representation of catheter position-
subeustachian pouch present, displayed in a left anterior oblique ing during cavotricuspid isthmus ablation procedures. The
projection. CS indicates coronary sinus; IVC, inferior vena cava; isthmus catheter (I 1,2–I 19,20) straddles the region where
LA, left atrium. ablation between the tricuspid valve and inferior vena cava
T 19,20
A Fossa
ovalis
Crista
terminalis
T 1,2
I 1,2
T 19,20 B
Coronary
Isthmus sinus
catheter
Figure 1.39 The electrograms show baseline atrial flutter. The inset shows placement of 2 multielectrode catheters. Curved arrows A and B
show patterns of activation.
is performed. Thus, the distal electrodes are likely medial accurate determination of bidirectional conduction block
to the ablation line, whereas the proximal electrodes (larger across the cavotricuspid isthmus. The crista terminalis–
electrode numbers, per convention) are lateral to the ablation related catheter (T 1,2–T 19,20) can also be used for lateral
line. As is explained in the case discussions, knowledge of the scar–related flutter cases, crista terminalis tachycardia cases,
precise location of the catheter is critical to allow quick and and sinus node modification, as well as atrial flutter ablation.
T 19,20
A Fossa
ovalis
Crista
T 19,20 terminalis
T 1,2
I 1,2
I 19,20 B
T 1,2
Coronary
I 19,20 I 1,2 sinus
Isthmus
catheter
Isthmus catheter
Figure 1.40 Left anterior oblique fluoroscopic view and a corresponding diagram of catheter positioning during cavotricuspid isthmus
ablation procedures. Right panel, the yellow arrow A indicates the counterclockwise wave front, and B is the clockwise wave front, as
described in the text.
The distal electrodes on the isthmus catheter typically ventricular to the plane of the annulus, as defined by the cor-
are placed just within the coronary sinus or at the coronary onary sinus catheter. The right panel shows a more typical
sinus ostium. This positioning can be well visualized in the and desirable location for an annular mapping catheter, with
LAO projection. Equally important, however, is that all the most of the electrodes in the approximate plane of the coro-
electrodes of this multielectrode mapping catheter be located nary sinus electrodes. The electrograms obtained reflect these
on the true cavotricuspid isthmus, ie, anterior to (in front of) catheter positions. For example, in the left panel, proximal
the eustachian ridge and just behind the tricuspid valve. This electrodes show a large ventricular electrogram with little or
positioning cannot be ascertained using the LAO projection no atrial electrogram. The distal electrodes show a relatively
but rather the RAO view, referencing the coronary sinus cath- larger atrial electrogram or balanced atrial and ventricular
eter as marking the annular location (isthmus just behind the electrograms. If such predicted correlation does not exist,
annulus). Several instances of either false documentation of then an anatomic reason must underlie the correct explana-
conduction block (pseudoblock) or the false impression of tion for the finding. For example, if balanced atrial and ven-
continued conduction after ablation (pseudoconduction) can tricular electrograms are seen from the proximal electrodes,
be traced to incorrect positioning of the isthmus catheter, with the catheter position shown in the left panel of Figure
which could have been avoided by careful analysis of the fluo- 1.41, then the tricuspid annulus is greatly displaced toward
roscopic views along with the corresponding electrograms the ventricular apex compared with the mitral annulus. This
(see Cases 14 and 17 for details). would be seen in a patient with Ebstein anomaly.
When pacing from the coronary sinus prior to ablation, The left panel of Figure 1.42 shows the RAO fluoroscopic
the mapping catheters pick up 2 wave fronts: one proceed- view of the catheter position during an atypical atrial flut-
ing in a clockwise pattern around the annulus, activating the ter ablation procedure. In the right panel, the electrograms
isthmus catheter in a distal to proximal manner (Figure 1.40, recorded from these catheters show widely split double
arrow A), and the second, a counterclockwise wave front that potentials recorded on the distal electrodes of the multipolar
causes a fused activation sequence along with the clockwise isthmus mapping catheter.
wave front on the crista terminalis catheter (Figure 1.40,
arrow B). What is the likely explanation for the split potentials
Figure 1.41 demonstrates the importance of the RAO seen on the electrograms recorded in Figure 1.42 with
view in defining a true annular location of a multielectrode this fluoroscopic location of the multielectrode mapping
mapping catheter placed on either the isthmus or the lateral catheter?
right atrial wall. The left panel shows the proximal and mid A. With ablation, during atrial flutter, the local atrial elec-
electrodes of the right atrial mapping catheter prolapsed trograms are becoming fragmented
Figure 1.41 Right anterior oblique view. The left panel shows the proximal and mid electrodes of the right atrial mapping catheter (arrow)
prolapsed ventricular to the plane of the annulus as defined by the coronary sinus catheter. The right panel shows a more typical and
desirable location for an annular mapping catheter (arrow) with most of the electrodes in the approximate plane of the coronary sinus
electrodes.
Figure 1.42 The left panel shows the right anterior oblique view of the catheter position during an atypical atrial flutter ablation procedure.
The black arrow indicates the distal electrodes of a 20-pole mapping catheter. The right panel shows the electrograms recorded from these
catheters. The arrows indicate widely split double potentials recorded on the distal electrodes of the multipolar isthmus mapping catheter.
B. The multielectrode catheter tip is located on or behind activate the atrial tissue just posterior to the crista terminalis
the eustachian ridge or eustachian ridge).
C. The multielectrode catheter tip is located on the crista As previously stated, the catheter tip (distal electrodes) is
terminalis placed medially during cavotricuspid isthmus ablation pro-
D. Conduction block has occurred across the isth- cedures. Therefore, the distal electrodes that demonstrate the
mus; therefore, the continued flutter must be a double potentials in Figure 1.42 could not be related to the
non–isthmus-dependent flutter crista terminalis, a lateral structure.
Answer: B—The multielectrode catheter tip is located on or
behind the eustachian ridge.
The posterior orientation of the multielectrode mapping Fossa ovalis

catheter tip suggests that the distal electrodes are not in or
near the coronary sinus ostium, but rather more posteriorly
located either on or behind the eustachian ridge. The LAO
projection cannot determine the difference between the dis-
tal electrodes in the coronary sinus or behind the eustachian
ridge, which clearly reinforces the importance of analyzing
the RAO view. The reason for the double potentials is the
natural line of conduction delay or block found in relation to
this structure. Coronary
Figure 1.43 illustrates the reason that double potentials Crista sinus
are normally present at certain right atrial locations. Both the terminalis
crista terminalis and the eustachian ridge represent areas of
functional conduction block or marked conduction delay. An
Figure 1.43 Right atrial activation during atrial flutter. The
electrode placed exactly on either of these structures records
yellow curved arrows show patterns of activation. The short white
an electrogram resulting from activation anterior to the
lines indicate conduction block. (Adapted from Olgin JE, Kalman
structure and a second electrogram recorded from activation JM, Fitzpatrick AP, Lesh MD. Role of right atrial endocardial
posterior to the structure, whether crista terminalis or eusta- structures as barriers to conduction during human type I atrial
chian ridge. Which electrogram occurs first depends on the flutter: activation and entrainment mapping guided by intracardiac
origin of the atrial activation wave front (a posterior pacing echocardiography. Circulation. 1995 Oct 1;92[7]:1839–48. Used
site, for example, causes the first of the 2 double potentials to with permission.)
Figure 1.44 shows a sequence of RAO fluoroscopic projec- sites that are activated 218 ms after the reference electrode,
tions of the ablation catheter during cavotricuspid isthmus coded in purple.
ablation. The top left panel represents the start of the ablation The red area is located near the interatrial septum. In the
line, and the bottom panel is from a site close to fi nishing context of fluoroscopic anatomy and electrogram correla-
the ablation line. These images demonstrate the importance tion, if, instead of having the information from the mapping
of the RAO projection in determining appropriate starting system, the electrophysiologist adds multiple electrodes or a
and ending points for the ablation line. Since the coronary point-to-point map reconstructed in his or her mind, then
sinus defi nes the annular site in the RAO view, the top left multiple sites in the left atrium are about equally early rela-
panel shows that the ablation catheter is likely ventricular tive to a reference. Th is finding would make it highly unlikely
to the tricuspid annulus (an Ebstein anomaly is an excep- that the true early site of activation is in the left atrium on the
tion). Also at this site the ventricular electrogram is expected free wall roof or inferior portion.
to be large, with little or no atrial electrogram present. The
top right panel shows that the crest of the eustachian ridge Which of the following is the least likely diagnosis for the
has almost been reached. Here, large atrial electrograms rhythm shown in the electroanatomic map in Figure 1.45?
are expected, with the ventricular electrograms appearing A. Typical AV node reentry
smaller and far-field. In the right panel, the atrial electro- B. A macro-reentrant atrial flutter with exit near the inter-
gram amplitude has begun to decrease. The catheter is likely atrial septum
behind the eustachian ridge and close to “descending” down C. An automatic atrial tachycardia originating on the
to the inferior vena cava. When the inferior vena cava itself right side of the interatrial septum
is reached, no atrial electrograms are found, and the ablation D. A macro-reentrant atrial flutter with the slow zone
line is complete. located between the right and left superior pulmonary
The example shown in Figure 1.44 is an idealized repre- veins
sentation. In actual practice, the anatomy of the cavotricus- Answer: D—A macro-reentrant atrial flutter with the slow
pid isthmus is complex, and several hills and valleys must be zone located between the right and left superior pulmonary
negotiated, with the ablation catheter being pulled back from veins.
an anterior location to the tricuspid valve to the inferior vena
cava (see Cases 14 and 16 for details). As is emphasized in Chapter 3 and in several cases (par-
Subsequent chapters in this textbook discuss what can be ticularly Case 16), the mechanism of tachycardia cannot be
learned from these systems and the difficulties sometimes defined by the mapping sequence alone but requires entrain-
involved in interpreting the data obtained. Here, this example ment and other pacing maneuvers to accomplish this (see
illustrates the importance of combining knowledge of fluoro- Chapter 5). For example, the tachycardia shown in Figure 1.46
scopic anatomy and electrogram analysis with information may represent either an automatic atrial tachycardia or a mac-
obtained from a mapping system. ro-reentrant atrial flutter, but if this is a flutter, the slow zone
Figure 1.45 is an electroanatomic map of the atria and por- is unlikely to be on the left side of the heart because multiple
tions of the coronary sinus during an atypical atrial arrhyth- sites are equally early in this chamber.
mia (atypical flutter vs automatic atrial tachycardia). Mapping Why is the earliest site, with respect to a reference elec-
systems essentially catalog the electrograms obtained from trode, close to a very late site (red area near purple area in
each site mapped in 3 dimensions. The rendered colored maps Figure 1.45)? One possible explanation is that there is an area
display in one of several ways the activation pattern during of conduction block just to the right of the interatrial septum.
tachycardia. Just as it is important to use views on fluoros- Thus, an automatic tachycardia (or a fast pathway exit from
copy that can easily delineate disparate anatomic structures AV node reentry) cannot conduct to neighboring tissue in the
for the ablationist, it is also helpful to maintain similar ana- right atrium and instead forms a long and circuitous conduc-
tomic views when using a mapping system. tion route to the other side of the block. A second explanation
In this electroanatomic map, a small heart figure (arrow) is that this is a macro-reentrant circuit with no site that is early
displays the orientation of the heart in this view, ie, looking or late but rather a circuit of continuous activation that can be
straight at the face of the heart, easily discerning right from mapped through the colors of the spectrum. The reason that
left, that is, the LAO view. Another legend provided with an a particular site is early or late depends simply on the location
electroanatomic map is the cartoon face above the image that of the reference electrogram and the boundaries set by the
shows the view is from the left side of the patient, again illus- operator to define the timing equivalent of the different col-
trating that a true anatomic view of the heart is an angulated ors. Review of the simple fluoroscopic anatomy offers no good
view for the body because of the anatomic left-sided disposi- reason why conduction block would occur just to the right
tion of the heart in situ. of the interatrial septum (crista terminalis, eustachian ridge,
The colors represent activation times relative to some etc, not located at this site), and a macro-reentrant flutter is a
intracardiac or electrocardiographic reference (see Chapter 3). more likely diagnosis. If the information is also provided that
A small color legend indicates that sites activated 73 ms before the atrial cycle length of the patient’s tachycardia is 285 ms,
a reference are coded in red with sequential color changes to this almost exactly matches the cycle length (73 ms + 218 ms)
RAA
RV
TA
HB
IVC-CS ABL
ABL
ABL
Figure 1.44 A sequence of right anterior oblique fluoroscopic projections of the ablation catheter (arrow) during cavotricuspid isthmus
ablation. The top left panel represents the start of the ablation line, and the bottom panel is from a site close to fi nishing the ablation line.
The top right panel shows that the crest of the eustachian ridge has almost been reached. ABL indicates ablation; CS, coronary sinus; HB,
His bundle; IVC, inferior vena cava; RAA, right atrial appendage; RV, right ventricle; TA, tricuspid annulus.
on both sides of the septum) is needed to defi ne which

site is earlier. Delineating the true early site is important
because ablating on the right side, particularly closer to the
His bundle region, may result in damage to the fast pathway
or the compact AV node. Similarly, if entrainment map-
ping for the same arrhythmia shows that the slow zone of
the tachycardia is within the interatrial septum, perhaps
close to the Bachmann bundle region (a not uncommon
situation with atypical flutters following atrial fibrillation
ablation), then right-sided and left-sided mapping of the
interatrial septum must also be performed. The operator
may now switch approaches and place 2 catheters on either
side of the septum to fi nd either the earlier site or the better
entrainment site.
Figure 1.46 shows the RAO and LAO fluoroscopic views
of the catheter position mapping both sides of the inter-
atrial septum. A small far-field His bundle electrogram was
recorded from the catheter on the right side of the interatrial
septum. The RAO view shows clearly which of the 2 cath-
eters is relatively more ventricular (right-sided catheter),
Figure 1.45 An electroanatomic map of the atria and portions of and the LAO view defines which catheter is to the left of the
the coronary sinus during atrial flutter. A full description of the interatrial septum. On either view, both catheters are fairly
characteristics of this figure appears in the text. AFL indicates superior and likely close to the roof of the atria. Possible loca-
atrial flutter; L, left; LA, left atrium; LAT, left atrial activation time. tions for these catheters include the anterior portion of the
Bachmann bundle (parallel myocardial fibers that reverse
mapped from early to late sites during the tachycardia. Thus, along the roof of the atria from one appendage to the other),
a macro-reentrant tachycardia is very likely. Nevertheless, superior to the fast pathway region, or the septal portion of
mapping of any kind provides information on the activation both annuli. Again, careful fluoroscopic examination reveals
patterns but not definitive information on the mechanism of that the transseptal sheath and tip of the coronary sinus cath-
tachycardia. eter are more cranial (higher) than the mapping electrode in
If pacing maneuvers document an automatic tachycar- the right atrium. Thus, it is unlikely that the catheter is at the
dia, then close mapping of the interatrial septum (catheters Bachmann bundle site (would have been higher on the roof)
Figure 1.46 Right anterior oblique (left panel) and left anterior oblique (right panel) fluoroscopic views of catheter position mapping both sites
of the interatrial septum. The white arrow indicates the transseptal sheath, and the yellow arrow indicates the tip of the coronary sinus catheter.
and is likely ventricular to and between the fast pathway and The Bachmann bundle region itself sometimes needs to be
the Bachmann bundle region. To avoid ablation near the con- specifically mapped for certain automatic tachycardias and
duction system or other undesirable locations, careful fluo- macro-reentrant flutters (interatrial flutter, post–atrial
roscopic interpretation along with correlated electrograms fibrillation, and ablation flutters). All the following maneu-
must first be done, and then the catheter position where the vers allow mapping of Bachmann’s bundle except:
correlation is made is tagged as an aid to memory on the
A. Endocardial mapping with the catheter withdrawn
electroanatomic map. In other words, the mapping system
from the right atrial appendage and placed on the roof
itself does not define the precise anatomic location of a given
of the right atrium near the interatrial septum
catheter and its correlated electrogram, but the operator
B. Withdrawing a catheter from the roof of the left atrial
must rely on careful analysis of fluoroscopic (and additional
appendage to the roof of the left atrium near the septum
echocardiographic) anatomy.
C. Mapping the oblique sinus of the pericardium
Figure 1.47 shows the morphologic anatomy of both atria
D. Mapping the transverse sinus of the pericardium
from an LAO projection. Comparison of the fluoroscopic and
electroanatomic images shown in Figures 1.45 and 1.46 with Answer: C—Mapping the oblique sinus of the pericardium.
this anatomic dissection is useful. The crista terminalis and
the eustachian ridge are evident in the right atrium. The septal Endocardial mapping of the Bachmann bundle can be
insertion of the eustachian ridge is the approximate site of the undertaken by placing the catheters on the roof of the respec-
fast pathway to the AV node. To deduce the exact location of tive atria, often best achieved by placing the catheter in the
the right-sided mapping catheter in Figure 1.46, the tip of the appendage, near the roof, and then withdrawing the catheter
coronary sinus catheter and the superior-most extent of the more septally. The oblique pericardial sinus recess is poste-
transseptal sheath are used to define the roof. The right atrial rior to the left atrium and between the ostia of the pulmo-
catheter, therefore, is lower than the roof, probably located nary veins and is not related to the roof of the atrium and the
between the fast pathway site and the Bachmann bundle. The Bachmann bundle region.
precise catheter location is further clarified when the height Figure 1.48 shows the LAO and RAO projections with an
of the right atrial roof is compared with that of the left atrial ablation catheter placed in the transverse sinus of the pericar-
roof. The right atrial roof is slightly more cranial than that dium. The transverse sinus is a pericardial recess that is bor-
of the left atrium. This relationship is preserved in most nor- dered inferiorly by the roof of the left atrium (the Bachmann
mal hearts. Keeping these relationships in mind, ablation- bundle), superiorly by the branching of the pulmonary arter-
ists can be relatively more certain that the true Bachmann ies, anteriorly by the posterior wall of the main pulmonary
bundle position is not being mapped or ablated, but rather artery, and posteriorly by the descending aorta. After peri-
that ablation is occurring lower, closer to the region of the cardial access is obtained, the catheter has been manipulated
fast pathway. around the lateral wall of the left ventricle and left atrium and
By repeatedly considering mapping system–derived infor- then under the pulmonary arteries to reach the transverse
mation, electrograms, fluoroscopic views, and the underlying sinus by deflecting the catheter tip inferiorly. Contact with
anatomy, an electrophysiologist strengthens his or her ability the Bachmann bundle can be obtained and aid in both map-
to interpret EP maneuvers and define the ideal and safe sites ping and ablation if required.
for ablation. Figure 1.49 shows the external topography of a normal
heart when viewed from a superior perspective. From this
perspective, the roof of the atria that would be connecting
the roof of the 2 atrial appendages is hidden from view by the
arch of the aorta and the curve of the main pulmonary artery
and its splitting into the right and left pulmonary trunks.
Thus, with pericardial access the operator would have to
reach the lateral limit of the left atrial appendage and then the
catheter would have to go inferior to the pulmonary trunks,
which in turn are inferior to the arch of the aorta, to reach the
transverse sinus. This is the location of the catheter shown in
Figure 1.48. This maneuver reinforces the need for the elec-
trophysiologist to have a clear understanding of fluoroscopic
anatomy to map and precisely diagnose otherwise difficult to
define arrhythmias.
For the ablation of atrial fibrillation, just as for any other
arrhythmias, an accurate understanding of the standard fluo-
Figure 1.47 The morphologic anatomy of both atria seen from a roscopic studies used as well as correlating the images seen
left anterior oblique projection. The arrows indicate the right and with the underlying anatomy and expected electrograms is
left atrial roof structures. critical. In addition to atrial fibrillation, angiography of the
Figure 1.48 The right anterior oblique (left panel) and left anterior oblique (right panel) projections with an ablation catheter (arrow)
placed in the transverse sinus of the pericardium.
pulmonary veins and other venous structures may need mapping and navigation systems. Although some of these
interpretation. Atrial fibrillation ablation requires perhaps issues are addressed in Chapter 3, the utility of more advanced
the most accurate understanding of such fluoroscopic and mapping systems is based on an accurate interpretation of
anatomic correlation since even a minor misinterpretation, fluoroscopy and the basic electrograms described in this sec-
for example, of the location of the pulmonary vein ostium, tion. Additionally, nonpulmonary vein sites that frequently
may give rise to unnecessary complications (pulmonary vein require ablation, such as the superior vena cava and the vein
stenosis, etc). Further integration of the basic fluoroscopic of Marshall, require understanding of the basic anatomy and
views and electrograms has to be made with more advanced corresponding fluoroscopic views.
Figure 1.50 shows angiographic images obtained with ret-
rograde injection of contrast into the pulmonary veins. The
top panels show injections of different pulmonary veins.
The arrow indicates the coronary sinus catheter. Which
fluoroscopic view is represented in these 2 panels?
A. Top left panel, LAO; top right panel, RAO
B. Both RAO
C. Both LAO
D. Both lateral views
Answer: C—Both LAO.
LAA As discussed initially in this chapter, the LAO is similar
to the AP view of any midline body structure such as the
face and immediately allows recognition of right-sided from
RAA left-sided structures. The coronary sinus catheter is coursing
from right to left in these LAO projections. Even if this cath-
eter is not visualized, the presence of the spine on the right
side of these images identifies these as LAO projections. The
top left panel shows injection of the right superior pulmonary
veins, and the top right panel shows the left superior pulmo-
Figure 1.49 The external topography of a normal heart when nary veins. As expected, in the LAO views, the right-sided
viewed from a superior perspective. LAA indicates left atrial vein is shown on the left in these images, and the left superior
appendage; RAA, right atrial appendage.
Spine
Spine
Figure 1.50 Top left and right panels, Angiographic images obtained with retrograde injection of contrast into the pulmonary veins.
Bottom panel, The RAO projection obtained simultaneously with one of the other views. The arrows are explained in the text.
pulmonary veins to the right (left side of the patient’s body). It it courses toward the left atrium. Thus, the right atrium
is important to note the following features: (and superior vena cava) and the right superior pulmo-
nary veins are superimposed in the LAO projection.
1. The right superior pulmonary vein has a very wide, fun-
nellike opening into the left atrium, making it difficult
The bottom panel in Figure 1.50 is the RAO projection
to know exactly where the ostium of the vein is located.
obtained simultaneously with one of the above LAO views.
The left upper pulmonary vein is more cylindrical, with
In the bottom panel, which vein is being injected?
a distinct change in the geometry at the junction with
A. Right superior pulmonary vein
the left atrium (cardiac silhouette).
B. Left superior pulmonary vein
2. In the LAO projection, the His bundle catheter defines the
C. Both veins
septum, and all left-sided structures are seen to the right
D. Cannot say from this projection alone
of the septum. The right upper pulmonary veins break
this “rule,” as the vein lies posterior to the right atrium as Answer: B—Left superior pulmonary vein.
As the name suggests, the right superior pulmonary vein by the white arrow (Figure 1.51, left panel). Catheter place-
and left superior pulmonary vein are both superior veins ment in the pulmonary arteries was rarely performed in
draining the right and left upper lobes of the lungs, respec- the earlier days of atrial fibrillation ablation. Catheters were
tively. However, the left superior pulmonary vein is consis- placed in the pulmonary artery to help with internal cardio-
tently and significantly anterior to the course and ostium of version (which was frequently used after multiple inductions
the right superior pulmonary vein and could well have been of atrial fibrillation) and sometimes to help map the pulmo-
called the “anterior superior vein.” In the RAO projection in nary veins without a need for transseptal puncture. The left
Figure 1.50 (bottom panel), portions of the vein are super- pulmonary artery is near the left superior pulmonary vein.
imposed on the ventricle (anterior to the coronary sinus More commonly used as a mapping catheter for the pulmo-
catheter). Thus, the pulmonary veins break both the “golden nary veins is a multielectrode circumferential mapping cath-
rules” stated above: where the coronary sinus catheter divides eter (Lasso [Biosense Webster Inc, Diamond Bar, California]
the atrial and ventricular structures and where the septum in and others) (Figure 1.52). The use and interpretation of elec-
the LAO divides the left- and right-sided structures. The right trograms obtained from these catheters are introduced later
upper pulmonary vein, although draining to the left-sided in this chapter and discussed in detail in the case discussions.
circulation, is seen along with right-sided structures in the An important principle of using these catheters is that they
LAO projection, and the left upper pulmonary vein, although should be placed fairly close to the pulmonary vein ostium.
draining into the atrium, has its more distal portions super- The right panel of Figure 1.52 shows a left upper pulmonary
imposed with a ventricle (anterior to the coronary sinus cath- vein angiogram. Even experienced ablationists may be fooled
eter in the RAO projection). into thinking that the confluence of 2 subsidiary branches,
Figure 1.51 shows the RAO and LAO projections with a shown by the white arrow, is the pulmonary vein ostium,
20–electrode mapping catheter placed into the upper pulmo- whereas in fact, the ostium is much further proximal, as indi-
nary veins. As explained in the atrial flutter section, the elec- cated by the yellow arrow. At times, it can be very difficult
trodes are numbered with the smaller numbers representing to define the exact ostium, either with simple fluoroscopy
the distal electrodes (the system used throughout this book). or angiography. Adjunctive imaging with ultrasound com-
In the LAO projection, the right and left upper pulmonary bined with accurate interpretation of the electrograms and
veins are clearly distinguishable, and the reader should corre- the results of the pacing maneuver is required to make a final
late these images with the corresponding angiographic images determination.
in Figure 1.50. Here and in the RAO projection, the left supe- Figure 1.53 is an RAO view of a circumferential mapping
rior (anterior superior) and right superior (posterior superior) catheter placed in the right upper pulmonary vein. As noted
pulmonary veins are easily distinguished as well. Incidentally in the discussion of Figures 1.50 and 1.51, the right superior
noted is the catheter in the left pulmonary artery, as indicated vein is clearly posterior compared with the left superior vein.
Figure 1.51 The right anterior oblique (left panel) and left anterior oblique (right panel) projections with a 20-electrode mapping catheter
placed into the upper pulmonary veins. The yellow arrows indicate multielectrode catheters placed in the superior pulmonary veins, and
the white arrows indicate the catheter in the left pulmonary artery.
LSPV
LA
LIPV
Figure 1.52 Left panel, Ostial location of a circumferential multielectrode mapping catheter. Right panel, Left upper pulmonary
vein angiogram. The arrows are explained in the text. LA indicates left atrium; LIPV, left inferior pulmonary vein; LSPV, left superior
pulmonary vein.
What can be difficult to determine, however, is whether the stenosis as it is likely that the ablation catheter is also within
circumferential mapping catheter is deep within the vein or the vein.
close to the ostium. An ablation catheter placed through a
second transseptal puncture is placed at a location where In Figure 1.53, the second deflectable catheter is indicated
radiofrequency energy is about to be delivered. If the cir- by the white arrow. Where is this catheter located?
cumferential mapping catheter is deep within the vein, A. Ostium of right upper pulmonary vein
delivering energy at this site may result in pulmonary vein B. Right inferior pulmonary vein
C. Right atrium
D. Right middle pulmonary vein
E. Cannot be determined with this RAO fluoroscopic
view only
Answer: E—Cannot be determined with this RAO fluoro-
scopic view only.
Thus, although the location of the circumferential map-
ping catheter cannot be determined in this projection alone,
fundamental determinations of catheter location (right vs
left and depth within the veins) require complementary
information.
Figure 1.54 shows the LAO projection obtained simultane-
ously with the RAO view shown in Figure 1.53. The circum-
ferential mapping catheter is seen in this LAO view to the left
of the septum and thus cannot be deep into the right upper
pulmonary vein. In the RAO view shown in Figure 1.53, the
circumferential mapping catheter appears to be so far pos-
terior to the coronary sinus catheter that an ablationist may
mistakenly think that the mapping catheter is deep in the
vein. However, the left atrial enlargement in this patient is so
severe that even a catheter placed at the ostium of the vein
Figure 1.53 A right anterior oblique view showing a appears to be more posterior. The LAO view is useful because
circumferential mapping catheter in the right upper pulmonary if the operator is to the left of the midline (the operator’s right,
vein. The arrow is explained in the text. the patient’s left), he or she cannot be deep in the vein that
intracardiac ultrasound) (see Chapter 2) placed also in the

right atrium at about the level of the ostium of the right upper
pulmonary vein.
Figure 1.55 shows the LAO and RAO projections with 2
circumferential mapping catheters placed, one in the left
superior pulmonary vein and the second in the left inferior
pulmonary vein. As expected in the LAO view, both catheters
are located to the left of the patient’s body and can be seen to
be lateral to (left ward of) the coronary sinus catheter. In this
patient, distinction between the upper and lower left-sided
veins is fairly straightforward on the LAO view alone; how-
ever, in some cases, the veins may be very close to each other.
The RAO view shows that the left superior vein catheter is
anterior to the left lower vein catheter. As noted earlier in this
section, the left superior vein has its main tributaries draining
the anterior parts of the left lung and thus, breaks the plane
of the coronary sinus catheter more distally. Careful observa-
tion of the RAO view, however, shows that the ostium of the
vein (along the course of the left upper vein catheter’s shaft)
reveals that the vein itself drains posterior to the right infe-
Figure 1.54 The left anterior oblique projection obtained rior vein. This is an important fluoroscopic observation that
simultaneously with the right anterior oblique view shown in helps an ablationist know when he or she is too deep into the
Figure 1.53. The arrow indicates the catheter in the right atrium. left upper vein. In other words, the ostium of the left upper
vein is slightly posterior to or in the same plane as the left
lower pulmonary vein, but as one progresses deeper into the
courses behind the right atrium and empties into the left vein in the RAO projection, the catheter is visualized more
atrium just to the left of the septum. Also, the ablation cath- anteriorly. Also in the RAO view, the plane of the ostia of
eter is in an excellent position to ablate atrial myocardium at the left-sided pulmonary vein is posterior to the plane of the
a fair distance from the ostium of the right upper vein. coronary sinus. Thus, if a catheter is placed via a transseptal
The catheter referenced in the question above is in approach and visualized in the RAO view close to the coro-
the right atrium, which is not evident on the RAO view nary sinus catheter, clockwise torque must be applied to move
shown in Figure 1.53 alone. Also, next to this right atrial the catheter more posteriorly to attempt to engage the ostia
catheter is the ultrasound probe (linear phased-array of the left-sided pulmonary vein. Also, if a catheter is placed
LSPV
LIPV
Figure 1.55 The left anterior oblique (left panel) and right anterior oblique (right panel) projections with 2 circumferential mapping
catheters placed, one in the left superior pulmonary vein (LSPV) and the second in the left inferior pulmonary vein (LIPV).
in the left lower vein to engage the left upper vein, any down- or free in the left atrium or relatively deep into the vein. It
ward deflection placed on the catheter should be released as is tempting to use the cardiac silhouette in the LAO projec-
the catheter is withdrawn and clockwise torque is applied tion to know when one is deep into a vein (for example, the
because the ostium of the upper vein is slightly posterior left lower vein). However, the silhouette in the LAO projec-
to the lower vein. Then, once the left upper vein is engaged, tion is primarily determined by the left ventricle, and if the
counterclockwise torque allows safe navigation into the vein left ventricle is enlarged (or a pericardial eff usion is present),
if required. then one can be fairly deep in the vein and still be within the
confi nes of the lateral margin of the cardiac silhouette in the
The circumferential mapping catheter in Figure 1.55 is in LAO projection.
a pulmonary vein. The LAO projection clearly shows that The ablation catheter (8-mm tip distal electrode) seen in
the vein is a left-sided pulmonary vein. The circumferential Figure 1.56 is at an important location in the regional car-
mapping catheter is likely located at which site? diac anatomy. Intracardiac ultrasound and manipulation
A. Left upper pulmonary vein of the mapping catheter have determined that the circum-
B. Left lower pulmonary vein ferential catheter is in fact at the ostium of the left superior
C. The left atrium not engaging the pulmonary vein pulmonary vein. The ablation catheter is in a plane between
D. Cannot be determined the plane of the coronary sinus (annulus) and the left upper
Answer: D—Cannot be determined. pulmonary vein (circumferential mapping catheter) in the
RAO projection. This region of atrial myocardium between
At times, the upper and lower left-sided veins arise fairly the annulus and the pulmonary veins is the position of the left
close to each other. The fact that in the RAO projection atrial appendage, located more superiorly, and the so-called
the catheter is located fairly posterior compared with the mitral isthmus, located more inferiorly (between the annulus
coronary sinus catheter suggests that this is the left lower and the left lower pulmonary vein). Therefore, more superi-
vein. As explained earlier in this chapter, the left upper orly, the mitral annulus is the most anterior structure. Then,
vein courses anteriorly, eventually crossing the plane of the immediately posterior to the annulus is the left atrial append-
coronary sinus and overlapping the ventricle in part of its age, and even more posteriorly located is the left upper pulmo-
course. However, also as noted above, the ostium of the left nary vein. Whereas, more inferiorly, as the catheter is dragged
upper vein is posterior to the ostium of the left lower vein in or torqued from the annulus posteriorly (clockwise torque),
many instances. Thus, if the circumferential mapping cath- the mitral isthmus is evident and then, further posteriorly,
eter is in the left upper vein, it is close to or at the ostium, the left lower pulmonary vein. This region where the abla-
but it may well be located in the left lower pulmonary vein tion catheter is located is also important when mapping or
as well. It is also difficult to determine on the basis of these ablating arrhythmogenic tissue found in the vein of Marshall
images whether the catheter is actually engaging the vein (see below).
Figure 1.56 Ablation catheter (8-mm tip distal electrode). Left panel, Right anterior oblique projection. Right panel, Left anterior oblique
projection. The arrows indicate the circumferential mapping catheter.
The left panel of Figure 1.57 was obtained during end expi- pulmonary vein. This and other uses of intracardiac ultra-
ration and the right panel at end inspiration in a patient sound with electrophysiologic procedures are covered in
who had mechanical ventilation under general anesthesia more detail in Chapter 2.
for the ablation procedure. What comment can be made In addition to intracardiac ultrasound, a great deal of
about the catheter position of both the circumferential information on cardiac anatomy with regard to atrial fibrilla-
mapping catheter and the ablation catheter? tion ablation has been obtained by other imaging modalities,
A. With inspiration, the catheters move deeper into the vein including cardiac magnetic resonance imaging and com-
B. With expiration, the catheters move deeper into the vein puted tomographic scanning. Figure 1.59 shows the relative
C. The ablation catheter moves deep into the vein with anatomy of the left atrium, esophagus, pulmonary veins, and
inspiration, but the circumferential mapping catheter’s the pulmonary arteries.
position is unchanged Seen first is the close relationship of the esophagus to
D. There is no apparent change in the fluoroscopic cath- the posterior wall of the left atrium in this patient, relatively
eter position during respiration closer to the left lower pulmonary vein than to the right lower
pulmonary veins. The esophagus itself is a dynamic struc-
Answer: D—There is no apparent change in the fluoroscopic ture, and its position relative to these veins may vary from
catheter position during respiration. one moment to another. The importance of this relationship
Although any one of the answers presented in this ques- is explored in several other cases in this book, particularly
tion may be correct and the position of the catheter is difficult Case 2. The right inferior pulmonary vein is the most poste-
to determine with these fluoroscopic images, there is no obvi- rior pulmonary vein, that is, the most rightward if the right
ous change. If any, there appears to be a little straightening of upper pulmonary vein and the left inferior and left upper
the ablation catheter in the inspiratory fi lm (right panel). pulmonary veins are left ward. The right inferior pulmonary
Figure 1.58 shows the circumferential mapping catheter vein is relatively rightward but is almost directly posterior
(arrow) viewed with intracardiac ultrasound at the same to the left atrium. This posterior orientation is related to the
time that the fluoroscopic images were obtained. The left fact that the equivalent branch of the pulmonary artery (right
panel shows end expiration, and the right panel shows end lower lobe artery) traverses anterior to the right inferior pul-
inspiration. There is a clear movement into the vein of the monary vein, separating this vein from the posterior wall of
circumferential mapping catheter with inspiration. Even the right atrium. This posterior orientation of the right lower
electrophysiologists experienced with fluoroscopic anatomy vein contrasts with the right upper pulmonary vein, which is
have difficulty knowing whether the circumferential map- an immediate posterior neighbor of the posterior wall of the
ping catheter is at the ostium or deeper within the vein. Yet, right atrium, with the right pulmonary artery branch supply-
with intracardiac ultrasound, it is obvious to the novice that ing the upper lobe and traversing posterior or superior to the
in the right panel, the mapping catheter is deep within the right upper pulmonary vein.
Figure 1.57 Th is patient had mechanical ventilation under general anesthesia for the ablation procedure. Left panel, End expiration.
Right panel, End inspiration.
Figure 1.58 The circumferential mapping catheter (arrows) viewed with intracardiac ultrasound at the same time that the fluoroscopic
images are obtained. Th is image is from the same patient shown in Figure 1.57. Left panel, End expiration. Right panel, End inspiration.
Figure 1.60 shows retrograde pulmonary venography to the annulus, in the RAO view it is much anterior to the
of the right lower vein in 2 different patients. The left panel ostium and the course of the right lower pulmonary vein. In
is an RAO view, and the right panel is an LAO view. In the the right panel, the ostium of the right lower vein is relatively
RAO view, the right lower vein is directly posterior and is left ward compared to the angiogram of the right upper pul-
in a plane overlapping the spine. The complex branching of monary vein shown in the top left panel of Figure 1.50. The
this vein is seen in many patients. The yellow arrow in the relatively midline location of the right lower vein is an impor-
left panel indicates a catheter placed at the ostium of the left tant fact to remember when trying to cannulate the right
upper pulmonary vein. Although this catheter is posterior lower vein. Thus, if a catheter is being moved from the right
upper vein to the right lower vein, it is not enough to simply
deflect the catheter downward to move it to a more inferior
Ao Eso location. Some counterclockwise torque is also required as
the catheter is withdrawn from the right upper vein so that
the catheter moves relatively more left ward while it is being
pulled or bent down to engage the right lower vein. It may be
useful for the operator to create a mental picture of a diago-
LSPV
nal where the right upper corner of the diagonal is the right
upper vein, the lower corner of the diagonal is the left lower
RSPV vein, and the right lower vein is located in the middle of this
diagonal, often equidistant from the right upper and left
lower pulmonary veins.
Of interest in the right panel of Figure 1.60 is a superior
branch with considerable tortuosity draining into the right
LA lower vein. Although not appreciated by early cardiac anato-
RIPV mists, now it is not uncommon to see cross-drainage (a trib-
LIPV utary of a superior lobe draining into the inferior vein, etc)
between the upper and lower pulmonary veins of either side.
Rarely but also seen is cross-drainage between the 2 lungs.
These cross-draining tributaries may be important when pul-
monary vein stenosis of 1 of the veins develops.
In the correlative electrograms obtained from the circum-
Figure 1.59 The relative anatomy of the left atrium, esophagus,
ferential mapping catheter placed in the fluoroscopic loca-
pulmonary veins, and the pulmonary arteries. Ao indicates aorta; tion of the pulmonary vein (Figure 1.61), the numbering of
Eso, esophagus; LA, left atrium; LIPV, left inferior pulmonary the intracardiac electrodes (His bundle, right atrium, coro-
vein; LSPV, left superior pulmonary vein; RIPV, right inferior nary sinus) is the same as explained earlier in this chapter (the
pulmonary vein; RSPV, right superior pulmonary vein. smaller numbers refer to the distal electrodes, etc) and used
Figure 1.60 Retrograde pulmonary venography of the right lower vein in 2 different patients. Left panel, Right anterior oblique view. In the
right anterior oblique view, the right lower vein (white arrow) is directly posterior and is in a plane overlapping the spine. The yellow arrow
indicates a catheter placed at the ostium of the left upper pulmonary vein. Right panel, Left anterior oblique view.
throughout this book. The circumferential mapping catheter is A. Ablation between poles 10 and 1 at the exact location of
labeled “LASSO.” Unless stated otherwise, the circumferential the circumferential mapping catheter
mapping catheters used at Mayo Clinic have relatively widely B. Ablation between poles 10 and 1 in the atrial myocardial
spaced electrodes (so-called unipolar Lasso). The electrogram close to the circumferential mapping catheter
obtained between poles 1 and 2 is labeled “LASSO 1,2” and C. No clear target for ablation
between 9 and 10 is labeled “LASSO 9,10,” and so forth. D. No further need for ablation for this pulmonary vein as
it is not arrhythmogenic
On the intracardiac electrograms shown in Figure 1.61,
what site is an appropriate target for ablation? Answer: C—No clear target for ablation.
Figure 1.61 Correlative electrograms obtained from the circumferential mapping catheter placed in the pulmonary vein.
An underlying theme of the subsequent case discussions and naturally, the pulmonary vein potential recorded from
in this book involves the concept of validation and target- those electrodes is later in timing than the pulmonary vein
ing of pulmonary vein potential. The 2 potentials seen on the potentials recorded in electrodes that are more proximal in
circumferential mapping catheter (initial far-field followed the vein. Thus, nothing more than the presence of the pul-
by a later near-field potential) represent left atrial activation monary vein potential earlier, as expected, at the ostium and
followed by the pulmonary vein potential. Often, operators later deeper in the vein can be surmised from the intracardiac
target poles 10 and 1 because the earliest activation of the electrograms shown in Figure 1.61.
pulmonary vein (earliest of the near-field pulmonary vein If the operator adjusts the circumferential mapping cath-
potentials) is apparently located at this site. This is, however, eter so that all electrodes are at the ostium and perpendicular
an instructive error. First, even if ablation is targeted for this to the long axis of the vein (as shown in Figure 1.63), then the
site, radiofrequency energy should not be delivered at the relative activation time of the pulmonary vein potentials can
same location where the circumferential mapping catheter is be measured, and the operator can consider starting energy
placed because this placement is ablating within the pulmo- delivery in the left atrium near the site of earliest activation.
nary vein. Even more important, however, is the need to exer- Activation mapping of the pulmonary vein potentials can also
cise great caution in analyzing the pulmonary vein potentials’ be considered if the circumferential mapping catheter shows
activation sequence. To say that the pulmonary vein potential similar amplitude of the left atrial signal in all the catheter
is earliest at pole 10 or pole 1 assumes that the circumferential poles and a similar ratio of far-field to near-field amplitude
catheter is located perfectly perpendicular to the long axis of on each of the poles. This ratio of signals also signifies that
the vein close to the ostium. This, however, is almost never the circumferential mapping catheter is ideally positioned for
the case, as can be seen in Figure 1.62. mapping.
The intracardiac ultrasound image shown in Figure 1.62 Figure 1.64 is an intracardiac electrogram obtained from
was obtained simultaneously with the intracardiac electro- a patient who previously had wide-area circumferential abla-
grams shown in Figure 1.61. Often, the circumferential map- tion performed and now has recurrent atrial fibrillation.
ping catheter is tilted into the vein, with some electrodes being From the perspective of the far-field left atrial signal, the cir-
deeper in the vein than others that are closer to the ostium. cumferential mapping poles 8,9,10 appear to be deeper in the
Thus, although this catheter appears to be mapping the cir- vein as they are of smaller amplitude than the far-field elec-
cumference of the vein at the ostium or a uniform location trograms (earlier left atrial activation signal) shown on the
within the vein, it often serves as a linear mapping catheter other electrodes.
with some electrodes deeper and some more proximal in the The simultaneously obtained intracardiac ultrasound
vein. This fact could also have been deduced from the elec- image (Figure 1.63) shows that the circumferential mapping
trogram (another reminder of the importance of constantly catheter is perfectly positioned at the ostium of the left lower
correlating fluoroscopy in electrograms with the relevant pulmonary vein in contrast with the catheter position shown
anatomy). For example, the far-field left atrial electrogram in Figure 1.62. The difference in amplitudes of the far-field
is very small in poles 4,5 compared with the circumferen- signal is likely attributable to prior ablation, with more com-
tial mapping electrogram obtained from pole 10,1. The cir- plex and fragmented signals in some locations around the
cumferential mapping poles 4 and 5 are deeper in the vein, pulmonary vein. Once the operator has determined that
the circumferential mapping catheter is ideally positioned,
he or she can look back at the sequence of pulmonary vein
Figure 1.62 Intracardiac ultrasound image obtained

simultaneously with the intracardiac electrograms shown in
Figure 1.61. The arrows indicate the circumferential mapping Figure 1.63 Circumferential mapping catheter in the
catheter electrodes in the pulmonary vein. pulmonary vein.
Figure 1.64 Intracardiac electrogram obtained from a patient who had wide-area circumferential ablation and now has recurrent atrial
fibrillation. The arrows indicate the far-field left atrial signal.
activation shown in Figure 1.64 and consider beginning abla- 4. On the ablation catheter (ABL d), the earlier deflec-
tion near circumferential mapping electrodes 2 and 3 (the tion is near-field and large, and an electrogram coin-
earliest pulmonary vein activation site). cident with pulmonary vein potential activation is not
During ablation of the left atrium close to circumferential apparent. Th is fi nding signifies that the ablation cath-
mapping poles 2 and 3, the electrogram shown in Figure 1.65 eter is in the left atrium and not located within the
is obtained. The pulmonary vein conduction (loss of pulmo- pulmonary vein. Thus, the left atrial signal is near-field
nary vein potential) (arrow) is blocked after the second beat rather than far-field as with the circumferential map-
in this tracing. In many ways, Figure 1.65 demonstrates an ping catheter.
ideal result of ablation to block pulmonary vein conduction,
including the following: The yellow arrow in Figure 1.66 indicates an ablation
catheter. Th is fluoroscopic image is an RAO projection,
1. There is no decrease in the amplitude of the near-field and the coronary sinus catheter has been labeled. Which
pulmonary vein potential prior to entrance block. of the following is the least likely location of the ablation
A decrease in the amplitude of the pulmonary vein catheter?
potential indicates that ablation is inadvertently being A. Left superior pulmonary vein
performed within the pulmonary vein. In other words, B. Right superior pulmonary vein
gradual fragmentation and then disappearance of the C. Left atrial appendage
pulmonary vein potential are undesirable findings, and D. Right ventricular outflow tract
if they are being observed, then energy delivery should E. Right atrial appendage
be stopped and the catheter should be pulled back fur- Answer: B—Right superior pulmonary vein.
ther into the left atrium.
2. There is significant delay and then abrupt block in con- As explained earlier in this chapter, the RAO projection
duction, again signifying that ablation is occurring in does not show whether a catheter is located in the right or
the atrium, causing further delay of conduction into left side of the heart. What is known is that this catheter is
the vein and then block. anterior to the plane of the coronary sinus. Thus, it is located
3. The intracardiac ultrasound shows an ideal catheter either in the ventricle or in one of the few “atrial” structures
position for the circumferential mapping catheter. that overlap the ventricle fluoroscopically in this projection.
Figure 1.65 Electrogram obtained during ablation of the left atrium close to circumferential mapping poles 2 and 3. The arrows indicate
the likely venous potential and are explained in the text.
As shown in Figures 1.50 and 1.51, the right superior pul- With the added information that this catheter is placed and
monary vein is considerably posterior to the coronary sinus advanced in the left atrium following transseptal puncture
catheter and at no time does it overlap the ventricle. Thus, the in a patient undergoing ablation for atrial fibrillation,
right upper pulmonary vein can be excluded as a potential which of the following locations is most likely?
location for this catheter. A. Left atrial appendage
B. Left upper pulmonary vein
C. Either left atrial appendage or left upper pulmonary
vein
D. Neither left atrial appendage nor left upper pulmonary
vein
Answer: C—Either left atrial appendage or left upper pul-
monary vein.
Both the left atrial appendage and the left upper pulmo-
nary vein overlap the mitral annulus (in the case of the left
upper pulmonary vein, the ostium is clearly posterior to
the annulus, but the deeper course of the veins is anterior).
While correlating the fluoroscopic image with the electro-
gram, one can quickly determine whether the catheter is
CS catheter
in the ventricle (large near-field ventricular electrogram if
the catheter is in the left ventricle vs far-field left ventricular
electrogram and near-field atrial electrogram if the catheter
is in the left atrial appendage or the left upper pulmonary
vein).
Figure 1.67 is a lateral view from an autopsied heart show-
Figure 1.66 Th is fluoroscopic image is a right anterior oblique ing the parallel course of the distal left superior pulmonary
projection. The white arrow indicates the coronary sinus (CS) vein and the left atrial appendage both arching relatively
catheter, and the yellow arrow indicates an ablation catheter. anterior and overlapping the annulus and portions of the left
(perforation occurs if undue pressure is applied). The cath-

LSPV eter then likely turns into the large medial lobe of the left
atrial appendage, whereas a catheter advanced into the left
superior pulmonary vein continues to proceed distally into
the lung parenchyma.
LAA Figure 1.69 shows the LAO projection obtained simultane-
ously with the RAO view shown in Figure 1.66. The catheter
has not “left” the cardiac silhouette and is somewhat medial
compared with the usual locations of the catheter placed in the
left upper pulmonary vein (see Figures 1.50, 1.51, and 1.55).
Figure 1.70 shows the intracardiac electrograms obtained
LV in a patient who had complete isolation of 4 distinct pulmo-
nary veins. Entrance block is clearly identified in all 4 veins,
and in addition, exit block is also found in the right upper
vein, the right lower vein, and the left upper vein. The circum-
ferential mapping catheter is labeled “LASSO” with states
1,2–10,1. The spontaneous initiation of atrial fibrillation is
Figure 1.67 Lateral view from an autopsied heart showing the shown in Figure 1.70. The earliest activation is clearly noted
parallel course of the distal left superior pulmonary vein (LSPV) in circumferential mapping catheter poles 1,2.
and the left atrial appendage (LAA), both arching relatively
anterior and overlapping the annulus and portions of the left In which venous structure is the circumferential mapping
ventricle (LV). catheter most likely placed to record the site of origin of
recurrent atrial fibrillation?
A. Left lower pulmonary vein
ventricle. The left lower pulmonary vein is considerably pos- B. Superior vena cava
terior to the left upper pulmonary vein. C. Inferior vena cava
Figure 1.68 shows both atria cut at the level of the tri- D. Vein of Marshall
cuspid and mitral annuli. Posteriorly from the plane of the E. Azygos vein
mitral annulus, the anatomic structures encountered are
Answer: B—Superior vena cava.
the left atrial appendage and then a ridge that separates the
ostium of the left atrial appendage from the left-sided pulmo- Several nonpulmonary vein foci for atrial fibrillation have
nary vein. The fluoroscopic differences between the left atrial been described. The most common is the superior vena cava.
appendage and the left upper pulmonary vein are summa- Although the vein of Marshall may also represent the site of
rized in Table 1.4. Further posterior is the posterior wall of origin for recurrent atrial fibrillation (see below), it is rarely
the left atrium and even further posteriorly is the right-sided large enough to accommodate even the smallest circum-
pulmonary vein. If a catheter is advanced further into the ferential mapping catheter. The azygos vein is a fairly large
left atrial appendage, the catheter likely meets resistance vein that drains the posterior mediastinum and empties into
the superior vena cava. Atrial fibrillation can originate from
the azygos vein, although this is less likely than origination
of atrial fibrillation from the superior vena cava itself. The
fact that the entrance into the left lower pulmonary vein is
blocked makes it highly unlikely for this vein to represent a
LAA continued source of atrial fibrillation initiation. In general,
exit block may exist without entrance block, but the reverse
is rarely true.
Figure 1.71 shows the positions of the circumferential
mapping catheter and ablation catheter in an LAO projec-
tion obtained simultaneously with the electrograms shown
in Figure 1.70. The circumferential mapping and ablation
catheters are clearly to the right of the midline, as defined by
the His bundle catheter in this LAO projection. The ablation
catheter is close to the ostium of the azygos vein.
Figure 1.72 shows the position of an ablation catheter in
Figure 1.68 Both atria are cut at the level of the tricuspid and a 64-year-old woman with long-standing paroxysmal atrial
mitral annuli. A ridge separates the ostium of the left atrial fibrillation who has been referred to the EP laboratory for
appendage (LAA) from the left-sided pulmonary vein. The arrow radiofrequency ablation. Her episodes of arrhythmia tend to
indicates the endocardial ridge. occur with exercise but more recently have been frequent and
Table 1.4
Distinguishing the Fluoroscopic Position of the Left Atrial Appendage and Left Upper Pulmonary Vein
Modality Used for Left Atrial Appendage Left Superior Comments
Localization Pulmonary Vein
RAO view Anterior to the plane of the coronary Anterior to the plane of the The left upper pulmonary vein
sinus catheter coronary sinus ostium lies posterior to the
plane of the annulus (coronary
sinus catheter) and then
courses anterior and parallel
to the course of the left atrial
appendage
LAO view Catheters in the appendage appear Ostium is typically within the The 2 structures are rarely
distinctly more medial (closer to lateral order of the cardiac confused in the LAO view but
the septum and within the cardiac silhouette, but as a catheter can be difficult to distinguish in
silhouette) than the left upper advances further, it appears to the RAO view
pulmonary vein overlap the lung parenchyma
well outside the cardiac
silhouette
Electrograms Large near-field atrial signals Characteristic pulmonary vein As a catheter is advanced further,
potential with far-field left atrial the left atrial appendage
and near-field pulmonary vein signals increases in amplitude,
signal whereas atrial and pulmonary
vein signals are smaller as the
catheter is placed in the more
distal portions of the left upper
pulmonary vein
Catheter-related ectopy More likely when the catheter is Less likely as the catheter is Pulmonary vein musculature
advanced further advanced further rarely seen more than 2.5 cm
into the left upper pulmonary
vein
Abbreviations: LAO, left anterior oblique; RAO, right anterior oblique.
unpredictable. She has had 2 previous ablation procedures the plane of the septum. The course of the catheter is simi-
that involved wide-area circumferential ablation around the lar to the multielectrode coronary sinus mapping catheter.
pulmonary veins, and at the second procedure, she had repeat Similarly, in the RAO projection (Figure 1.72, left panel), for
ablation around the pulmonary veins, linear ablation in the the most part, the ablation catheter and coronary sinus cath-
left atrium, and ablation of the cavotricuspid isthmus. Despite eter are identical in their course. The tip (distal and proximal
this, she has frequent recurrent episodes of atrial fibrillation. electrodes) of the ablation catheter, however, is pointed atrial
In the EP laboratory, entrance block has been identified to be (posterior) to the coronary sinus catheter because the tip of
present in all 4 pulmonary veins, and isolation of the superior the catheter has engaged an atrial vein draining into the coro-
vena cava is performed. With use of isoproterenol, spontane- nary sinus. The primary atrial vein that drains just anterior to
ous atrial fibrillation is frequently seen, and the earliest site the plane of the ostia of the pulmonary vein is the remnant
of origin for the initiating beats for each episode has been of the left superior vena cava, that is, the vein of Marshall.
mapped and ablation energy is about to be delivered. Had the catheter been positioned in a posterolateral ventric-
ular vein, the appearance on the LAO projection would be
In Figure 1.72, the ablation catheter (white arrow) is situ-
similar, but in the RAO view, the tip of the catheter would be
ated at the site where ablation is to be performed. Which
pointed ventricular or anterior to the coronary sinus.
cardiac location is this?
The dissection of an autopsied heart shown in Figure 1.73
A. Ostium of left lower pulmonary vein
displays the anatomic relationship of the ligament/vein of
B. Mitral valve isthmus
Marshall and the left atrium and pulmonary veins. In fetal
C. Vein of Marshall
life, the left superior vena cava runs in the “groove” between
D. Posterolateral cardiac vein
the anterior surface of the left-sided pulmonary veins and the
posterior surface of the left atrial appendage. Th is embryo-
Answer: C—Vein of Marshall. logic fact gives rise to 2 consistent anatomic correlates:
The LAO projection (Figure 1.72, right panel) shows that 1. The remnant of the left superior vena cava (vein of
the catheter courses from the right to the left, clearly crossing Marshall) runs in this same groove as it drains into
2. On the endocardial surface at the same location

(between pulmonary veins and appendage), a ridge is
raised and is sometimes referred to as the endocardial
marker for the vein of Marshall. This ridge is well visu-
alized in Figure 1.68 (arrow). This endocardial ridge is
raised both by the thickness of the atrial myocardium
at this site and the fact that this tissue is “indented” by
the left superior vena cava in fetal life.
These anatomic correlates to fluoroscopy and electrogram
interpretation present the ablationist with several approaches
to treating atrial fibrillation originating at the vein of
Marshall.
1. As shown in Figure 1.72, the ablation catheter can be
used to cannulate and ablate within the vein of Marshall
at the site of earliest activation.
2. The vein of Marshall can be cannulated and the ostium
of this vein electrically isolated.
3. The endocardial marker for the vein of Marshall (ridge
between the appendage and left pulmonary veins) can
Figure 1.69 The left anterior oblique projection obtained simulta- also be targeted for transmural ablation of the vein of
neously with the right anterior oblique view shown in Figure 1.66. Marshall.
In Figure 1.72, in the RAO projection (left panel), the sec-
the coronary sinus. Thus, although several atrial veins ond ablation catheter is superimposed on the catheter in the
may be present, the specific vein referred to as the vein vein of Marshall. In the LAO view (right panel), however,
of Marshall, if patent, is cannulated in the RAO plane there is considerable separation between these 2 catheters
posteriorly and between the plane of the appendage (measured at about 1 cm). This second ablation catheter is
and that of the left-sided pulmonary vein. placed in contact with the endocardial ridge. Regardless of
Figure 1.70 These intracardiac electrograms were obtained in a patient who had complete isolation of 4 distinct pulmonary veins.
Entrance block is clearly identified in all 4 veins, and in addition, exit block is also found in the right upper vein, the right lower vein, and
the left upper vein. The arrow indicates the earliest activation noted in circumferential mapping catheter poles 1,2.
the circumflex coronary artery or one of its branches. The

coronary sinus and the atrial veins are consistently poste-
rior (closer to the atrium in the RAO view) to the coronary
arterial system. This relationship can be easily visualized in
the tomographic image shown in Figure 1.13. The important
fluoroscopic anatomy-electrogram correlates for ablation of
atrial fibrillation are summarized in Table 1.5.
FLUOROSCOPIC ANATOMY AND

ELECTROGRAM CORRELATIONS FOR
VENTRICULAR TACHYCARDIA ABLATION
The catheter positioning in the RAO and LAO views for a

patient with ischemic ventricular tachycardia is shown in
Figures 1.74 and 1.75, respectively. The 2 ablation catheters
in the RAO projection (Figure 1.74) appear to be placed in
the same location. In fact, both catheters are placed in the left
ventricle on its inferior wall. The LAO projection (Figure 1.75)
shows that 1 catheter is more lateral (left ward) and the other is
Figure 1.71 The positions of the circumferential mapping closer to the septum. In Figure 1.74, 1 catheter has been placed
and ablation catheters in a left anterior oblique projection via a transseptal approach crossing from the left atrium to the
were obtained simultaneously with the electrograms shown in ventricle across the mitral valve, whereas the other ablation
Figure 1.70. The circumferential mapping and ablation catheters catheter has been placed retrograde across the aortic valve
are clearly to the right of the midline as defined by the His bundle to the left ventricular inferior wall. The distinction between
catheter (arrow) in this projection.
these 2 catheters is clearly apparent in the LAO projection
(Figure 1.75), with the transseptal catheter going toward the
the method in which the vein of Marshall is to be ablated, lateral cardiac silhouette and then crossing downward toward
care must be taken that, in the RAO projection, the cathe- the left ventricle. Even in the RAO view (Figure 1.74), the
ter is always atrial (posterior) to the coronary sinus. If the course of the catheters more proximally allows one to easily
ablation catheter points anteriorly at one of the ventricu- make a distinction between the retrograde and transseptally
lar veins, there is the potential for inadvertent ablation of placed catheter.
Figure 1.72 The position of an ablation catheter in a 64-year-old woman with long-standing paroxysmal atrial fibrillation who has been
referred to the electrophysiology laboratory for radiofrequency ablation. Left panel, Right anterior oblique view. Right panel, Left anterior
oblique view. The ablation catheter indicated by the white arrow can be used to cannulate and ablate within the vein of Marshall at the site of
earliest activation. The yellow arrow indicates the position of the second ablation catheter. The arrows indicate the mapping catheter locations.
infarction and the mitral annulus (mitral isthmus ventricu-

Endocardial ridge
location Left pulmonary lar tachycardia). Epicardial ICD leads are visualized in these
veins images. A sequential set of ablation lesions (“drag”) con-
necting the inferior wall scar to the mitral annulus is being
Ligament vein performed.
LAA of Marshall
Assuming that transmural lesions are created with com-
plete electrogram reduction during radiofrequency energy
delivery at each point in the drag, judging from the right
panel of Figure 1.76, has the line been completed?
Probe A. The ablation catheter has reached the coronary sinus
catheter, and thus, the line has been completed
B. The ablation catheter has not been dragged in a straight
line, and thus, further ablation is likely
C. The information required cannot be obtained from this
fluoroscopic view (LAO)
Figure 1.73 Dissection of an autopsied heart displays the D. The ablation catheter has crossed the plane of the coro-
anatomic relationship of the ligament/vein of Marshall and the left nary sinus and has unnecessarily ablated atrial tissue
atrium and pulmonary veins. LAA indicates left atrial appendage.
Answer: C—The information required cannot be obtained
from this fluoroscopic view (LAO).
When ablation is performed from a relatively more apical
Most ischemic ventricular tachycardia ablations require
site toward the mitral annulus, the primary interest is know-
energy delivery to the left ventricle. A common example is
ing the anterior-to-posterior (sternum toward the coronary
mitral valve isthmus–dependent ventricular tachycardia.
sinus catheter) direction of movement of the ablation cath-
Here, ablation is done usually on the inferior wall of the left
eter. Thus, the RAO projection is the ideal view to determine
ventricle between the mitral valve and an inferior infarction.
whether the mitral annulus has been reached. In the LAO
The approaches available to ablate the left ventricles are 1) ret-
view, the catheter may simply have gone from a more lateral
rograde transaortic access, 2) transseptal access via the mitral
site to a more septal site (particularly in this rather shal-
annulus, 3) use of the coronary venous system to ablate the
low LAO view similar to an AP projection). Because of the
epicardial surface of the left ventricle, and 4) transpericardial
supraimposition of the ventricle, annulus, atrium, coronary
access typically via a subxiphoid approach.
sinus, etc, in the LAO projection, it is impossible to deter-
The ablationist must be very familiar with the fluoroscopic
mine whether an adequate ablation line has been created in
anatomy and the course of the catheter with each of these
the LAO view. An accurate determination of whether an abla-
approaches. The fundamental principles of fluoroscopic anat-
tion line connects a more ventricular site (inferior wall myo-
omy, as explained earlier in this chapter, are very important
cardial infarction) to a more posterior site (mitral annulus as
for ventricular tachycardia ablation as well. For example, in
marked by the coronary sinus catheter) is best made in the
Figure 1.74, it is impossible to discern whether the implant-
RAO projection.
able cardioverter-defibrillator (ICD) lead is located in the
right or left ventricle. What can be seen is that the lead is in The arrow in Figure 1.77 indicates the ablation cathe-
the ventricle as it is anterior to the plane of the multielectrode ter located at the site of successful ablation of a patient’s
coronary sinus mapping catheter. Further, in the LAO view arrhythmia. The RAO view is shown. Which is the most
(Figure 1.75), the ICD lead is in the right side of the heart. likely location for this ablation catheter (arrow)?
Knowing that this lead was placed on the septum and in the A. Right ventricular outflow tract
same plane as the His bundle recording catheter, a consider- B. Left ventricular outflow tract
able distance is evident between the ablation catheter placed C. Right atrial appendage
by the retrograde aortic approach and the ICD lead. This rela- D. Left superior pulmonary vein
tionship with the ICD lead tells the operator that, although E. Left atrial appendage
this catheter is septal to the transseptally placed ablation
Answer: A—Right ventricular outflow tract.
catheter, it is still likely a good distance away from the inter-
ventricular septum (2–3 cm). These principles of interpreting This catheter position was obtained from a patient with
the standard fluoroscopic views must constantly be kept in recurrent right ventricular outflow tract ventricular tachy-
mind when correlating with mapping system data as well (see cardia, which was successfully ablated with point-to-point
Chapter 3 for details). mapping to determine the site of earliest activation during
Figure 1.76 is a fluoroscopic image (LAO view) obtained tachycardia. All the possible answers to the question above
from a patient undergoing ablation for ventricular tachycardia are reasonable to consider. The catheter has come up from
that involved the tissue between an inferior wall myocardial the femoral route and entered the atrium (posterior to the
Table 1.5
Important Features of Fluoroscopic Anatomy–Electrogram Correlate for Atrial Fibrillation Ablation
Cardiac Structure Fluoroscopic Anatomy–Electrogram Feature Comments
RSPV Significantly posterior compared to the left superior Ultrasound or pacing maneuvers sometimes
pulmonary veins required to defi ne the true site of the ostium
Funnellike opening to the left atrium with true ostium
difficult to determine
RIPV Directly posterior vein sometimes as much to the right The RIPV is left ward and inferior to the ostium of
as it is to the left the RSPV
Separated from the right atrium by the lower branch of The RIPV is rightward and superior to the ostium of
the right pulmonary artery the LIPV
RMPV Sometimes may occur with a separate ostium to that Best isolated as part of a wide area lesion involving
of the RSPV and RIPV all right-sided veins or along with the RSPV
The RMPV ostium is directly inferior (not left ward) to
the ostium of the RSPV
LSPV The ostium of the LSPV just posterior and superior to In the RAO projection, the LSPV is the most
the LIPV anterior of the pulmonary veins and can be
Further course of the LSPV is anterior and parallel to confused with the left atrial appendage
the left atrial appendage
Separated from the left atrial appendage at the ostium
by an endocardial ridge
LIPV Ostium directly inferior and slightly anterior to the Ablation often performed between the mitral valve
LSPV and the LIPV across the mitral isthmus and
Separated from the mitral annulus by the endocardial transecting the endocardial marker for the vein of
ridge and the “mitral isthmus” Marshall
Circumferential mapping Careful analysis of the far-field left atrial electrogram Ablation should never be performed at the site of
catheter positioning amplitude uniformity required to determine proper lateral placement
orientation at the pulmonary vein ostium prior to Electrogram amplitude reduction of the left atrial
analyzing the pulmonary vein potential activation signal with delay of pulmonary vein potential and
sequence then block is the ideal response to ablation
Intracardiac ultrasound helpful to determine Electrogram amplitude reduction of the pulmonary
orientation in the pulmonary vein vein potential should not be seen during ablation
Superior vena cava Azygos vein ostium may need to be mapped separately Phrenic nerve may need to be separately mapped
Typically mapped with a circumferential mapping and correlated fluoroscopically with catheter
catheter similar to that used for the pulmonary vein position or a mapping system
Vein of Marshall Posterior to the coronary sinus in the RAO projection If the ablation catheter is not clearly atrial
Endocardial marker for this vein seen between (posterior) to this coronary sinus catheter,
the planes of the atrial appendage and the left injury to the coronary arteries may occur during
pulmonary vein ablation energy delivery
Abbreviations: LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RAO, right anterior oblique; RMPV,
right middle pulmonary vein; RSPV, right superior pulmonary vein.
coronary sinus in the RAO view shown). Either the catheter tract may be superiorly “cranially” located at the right ven-
is located in the ventricle or is in one of the “atrial” structures tricular outflow tract but is not as anterior. The right or left
that break the plane of the coronary sinus as explained ear- atrial appendage does not allow a catheter to progress this far
lier in this chapter, namely, the atrial appendages or the left anterior to the coronary sinus catheter, thus making these
superior pulmonary vein. The LAO view, if supplied, would non–right ventricular outflow tract locations unlikely for the
immediately allow exclusion of any of the left-sided possibili- ablation catheter.
ties. Even without this, however, there is no clear evidence of The regional and fluoroscopic anatomy of the outflow tract
transseptal puncture, and most importantly, the electrode is is complex, as can be surmised by viewing the LAO projec-
advanced to a very anterior site just below the shadow of the tion of catheter position with simultaneous left coronary
sternum. The most anterior location in the normal human arteriography in Figure 1.78. In this LAO view, catheters
heart is the anterior wall of the right ventricular outflow inserted via the coronary venous system (cardiac vein), retro-
tract. In fact, the anterior wall of the outflow tract is just grade left ventricular outflow tract, His bundle, and the right
behind the sternum and costochondral junction and prone ventricular outflow tract all reach a similar location in the
to mechanical trauma during chest wall injuries and the like. heart and all have an important potential relationship with
As described later in this chapter, the left ventricular outflow the left main coronary artery and left anterior descending
artery. This region of the heart may be considered a quadrilat-

eral, with the left ward margin being the multielectrode car-
diac vein catheter, the rightward and inferior margin being
the His bundle catheter, and the right ventricular outflow
tract being located superiorly to the left ventricular outflow
tract catheter. Enclosed in the quadrilateral are the important
parts of the left coronary arterial system.
The discussion now turns to an exploration of the impor-
tant relationship between anatomy and the fluoroscopic
images obtained during ablation for outflow tract ventricu-
lar tachycardia. Several of the cases presented in this book
explain the practical importance of understanding the fluo-
roscopic anatomy and correlated electrograms for this region.
Here the important principles are presented.
Figure 1.79 shows the normal heart viewed from an ante-
rior perspective. The first important principle in understand-
ing outflow tract anatomy is that the right and left ventricular
outflow tracts are in fact misnomers. It would be better to
consider the right ventricular outflow tract as the anterior
outflow tract and the left ventricular outflow tract as the pos-
Figure 1.74 Right anterior oblique view from a patient with terior outflow tract. The 2 outflow tracts cross each other, with
ischemic ventricular tachycardia. The 2 ablation catheters (white the right outflow tract crossing over the left outflow tract.
and yellow arrows) appear to be placed in the same location. In For a significant portion, the right ventricular outflow tract,
fact, both catheters are placed in the left ventricle on its inferior particularly the region close to the pulmonary artery, is to
wall. One catheter (white arrow) has been placed via a transseptal the left of the left ventricular outflow tract. This is an impor-
approach crossing from the left atrium to the ventricle across the tant fact when correlating electrograms with fluoroscopic
mitral valve, whereas the other ablation catheter (yellow arrow) has anatomy. For example, if point-to-point mapping in the right
been placed retrograde across the aortic valve to the left ventricular ventricular outflow tract shows that the earliest ventricular
inferior wall. electrogram during tachycardia is occurring as the catheter is
advanced to a more left ward location in the LAO projection,
the true earliest site may not be in the left ventricular outflow
tract. On the other hand, if the earliest site of activation in
the right ventricular outflow tract is far-field signals obtained
when mapping the right and posterior locations in the right
ventricular outflow tract, a left ventricular outflow tract ori-
gin should be considered. A second important observation
from Figure 1.79 is that the transition from the right ventric-
ular myocardium to the pulmonary artery (pulmonary valve)
is relatively cephalad to the aortic valve (aortic valve “lower”
than the pulmonic valve). A third important observation is
that the anterior intraventricular groove with a left anterior
descending artery has a more immediate relationship with
the right ventricular outflow tract than the left ventricular
outflow tract.
Figure 1.80 shows an important cross-section of dissec-
tion at the level of the AV and semilunar valves. The centrally
located aortic valve has an immediate anatomic relationship
with all the other valves. Notable specific features include the
following:
1. The pulmonic valve and right ventricular outflow tract

Figure 1.75 Left anterior oblique view for a patient with ischemic
are always anterior to the aortic valve (and left ventric-
ventricular tachycardia. One catheter is actually more lateral ular outflow tract).
(left ward) and the other is closer to the septum. The white arrow 2. Both AV valves have an anatomic relationship with the
indicates the implantable cardioverter-defibrillator lead in the right aortic valve, and they are always posterior to the aortic
side of the heart. valve.
Figure 1.76 A left anterior oblique image obtained from a patient undergoing ablation for ventricular tachycardia. Left panel, Ablation
catheter (ABL) position at the beginning of a “drag” lesion. Right panel, The ablation catheter position at the end of the drag lesion.
CS indicates the coronary sinus catheter.
3. The left coronary artery and left anterior descending 5. The distal ventricular tributaries to the coronary sinus
artery are immediate posterior and left ward neighbors have a close relationship with the left anterior descend-
of the right ventricular outflow tract at the level of the ing artery and, thus, the left ward and posterior por-
pulmonic valve. tions of the right ventricular outflow tract at the level of
4. The proximal right coronary artery is a rightward and the pulmonic valve.
posterior neighbor of the right ventricular outflow
tract about a centimeter below the usual location of the
pulmonic valve.
Cardiac
vein
His
LCX
LAD
LVOT retrograde
approach
Figure 1.78 In this left anterior oblique view, catheters inserted

via the coronary venous system (cardiac vein), retrograde left
ventricular outflow tract (LVOT), His bundle, and a catheter placed
Figure 1.77 In this right anterior oblique view, the arrow indicates in the right ventricular outflow tract all reach a similar location in
the ablation catheter located at the site of successful ablation of a the heart. LAD indicates left anterior descending artery; LCX, left
patient’s arrhythmia. circumflex coronary artery.
These important relationships should be kept in mind

when interpreting fluoroscopy and correlating electrograms
obtained during outflow tract tachycardia ablations.
Figure 1.81 shows the complex catheter positions in a
patient with outflow tract tachycardia ablation. The RAO view
allows the viewer to determine which catheters are positioned
in more anterior structures (closer to the sternum) than oth-
Ao ers, with the LAO view allowing distinction of left-sided from
PA right-sided catheters and those known to be on the left side
distinguishing between free wall and septal locations (see
above).
The catheter indicated by the red arrow has been placed
in the pericardial space to aid epicardial mapping via a sub-
xiphoid approach. The tip of this pericardial catheter is fur-
ther from the base or annulus than the other key catheters, a
fact that is appreciated easily on the RAO view but cannot be
anticipated from the LAO view.
The balloon-like catheter fi lled with contrast is a multi-
electrode array catheter used for noncontact mapping and
RV
has been placed in the right ventricular outflow tract. The use
of this mapping system is discussed in Chapter 3.
The catheter indicated by the white arrow is placed in the
LV right ventricular outflow tract close to the pulmonic valve
(documented with intracardiac ultrasound), whereas the
catheter indicated by the yellow arrow has been placed retro-
grade into the left ventricular outflow tract close to the aortic
valve orifice. The pulmonic valve can be far cephalad to the
aortic valve in some patients.
Figure 1.79 The direction of the great arteries in a normal heart In the RAO view (Figure 1.81, left panel), the tip of the mul-
viewed from an anterior perspective. The arrows indicate the tielectrode catheter placed in the coronary sinus is encroach-
relative orientation of the outflow tracts. Ao indicates aorta; LV, left ing on the outflow tract catheter, and in the cranial caudal
ventricle; PA, pulmonary artery; RV, right ventricle. axis the tip is seen between the right ventricular outflow tract
catheter (higher) and the left ventricular outflow tract cath-
eter (lower). In the LAO view (Figure 1.81, right panel), the
Conus catheter, throughout its entire course, and the aorta and left
LAD ventricular outflow tract are always posterior to the catheter
PV
in the right ventricular outflow tract and pulmonary artery.
RCA Figure 1.82 diagrams the concept that the right ventricu-
LCX lar outflow tract is anterior and overlaps the left ventricular
AV outflow tract and aortic valve. A significant portion of the
subpulmonary valve and the right ventricular outflow tract
musculature is anterior to the aortic valve and the ostia of the
coronary arteries.
MV TV The RAO and LAO projections of catheter placement
during outflow tract tachycardia ablation are shown in
Figure 1.83. The white arrow indicates a circumferential
mapping catheter used during this procedure. Where is
CS
this catheter (white arrow) located?
A. Right ventricular outflow tract/pulmonary artery
B. Left ventricular outflow tract/aorta
Figure 1.80 Cross-section at the level of the atrioventricular and C. Anterior interventricular vein
semilunar valves. The arrow indicates the interatrial septum. AV D. Right inferior pulmonary vein
indicates aortic valve; Conus, conus branch of right coronary
Answer: B—Left ventricular outflow tract/aorta.
artery; CS, coronary sinus; LAD, left anterior descending artery;
LCX, left circumflex artery; MV, mitral valve; PV, pulmonary In the LAO projection (Figure 1.83, right panel), it
valve; RCA, right coronary artery; TV, tricuspid valve. may be difficult to determine in which outflow tract the
Figure 1.81 Left panel, In the right anterior oblique view, the tip of the multielectrode catheter placed in the coronary sinus is seen
encroaching on the outflow tract catheter and in the cranial caudal axis the tip is seen between the right ventricular outflow tract catheter
(higher) and the left ventricular outflow tract catheter (lower). Right panel, In the left anterior oblique view, the catheter, throughout
its entire course, and the aorta and left ventricular outflow tract are posterior to the catheter in the right ventricular outflow tract and
pulmonary artery. The arrows are explained in the text.
circumferential mapping catheter has been placed. It has

been placed using a retrograde aortic approach by follow-
ing the shaft and course of the catheter. Importantly, in the
RAO view (Figure 1.83, left panel), the entire circumference
of this catheter is posterior to the balloon catheter placed in
the anterior (right) ventricular outflow tract. As stated in the
discussion of Figure 1.81, the retrograde ablation catheter is
at the level of the aortic valve, and thus, the circumferential
mapping catheter is actually located in the aorta above the
level of the aortic valve. Why map the aorta for outflow tract
tachycardia? As is discussed in several of the cases in this
book, myocardial sleeves extend above the aortic valve (and
the pulmonic valve) and may be the origin for automatic or
triggered ventricular tachycardias. To map the circumference
of the aortic root, this type of multielectrode circumferential
catheter may be used. This technique may help identify the
earliest site of activation or, in some situations, allow circum-
ferential isolation of the supravalvar arrhythmogenic tissue.
Figure 1.84 shows the electrograms obtained simultane-
ously with the catheters positioned as shown in Figure 1.83.
The rhythm shows ventricular bigeminy with outflow tract
morphology premature ventricular contractions (positive in
lead III, etc). The QRS is positive in lead V1, suggesting an ori-
gin in the left ventricular outflow tract. During the premature
ventricular beats, an early electrogram is noted on the distal
Figure 1.82 The right ventricular outflow tract is anterior
coronary sinus electrodes that times about the same as the
and overlaps the left ventricular outflow tract and aortic valve. far-field early signal on the circumferential mapping catheter
A significant portion of the subpulmonary valve and the right (LS 1,2–10,1). These far-field signals, however, coincide with
ventricular outflow tract musculature is anterior to the aortic valve the onset of the QRS and are not particularly early, suggesting
and the ostia of the coronary arteries. that the arrhythmia originates from this location. However,
Figure 1.83 The right anterior oblique (left panel) and left anterior oblique (right panel) projections of catheter placement during outflow
tract tachycardia ablation. The arrow indicates a circumferential mapping catheter used during this procedure.
the arrows point to near-field “spike”-like signals occurring for atrial fibrillation. The electrogram was obtained after
throughout the cardiac cycle, and when seen preceding a partial isolation of the aortic root, and eventually, ablation
premature ventricular contraction, these signals occur early was completed to isolate the arrhythmogenic triggers from
and with a fi xed interval before the onset of the QRS com- the ventricular myocardium, thus eliminating the premature
plex for the premature ventricular contractions. This finding ventricular contractions and ventricular tachycardia.
of near-field/far-field electrogram changes is analogous to Although the case discussed above reflects epicardial
that explained earlier in the text for pulmonary vein triggers access, it is rare that epicardial ablation is required for outflow
Figure 1.84 Electrograms recorded simultaneously with the projections shown in Figure 1.83. The arrows are explained in the text.
tract tachycardia because the right ventricular outflow tract and definition of the focus of circuit of the ventricular tachy-
generally does not have a very thick myocardium, and true cardia is made. Most often there is failed endocardial ablation
epicardial location for focus or foci of tachycardia is rare. For either at a previous procedure or with initial attempts at a
the left ventricular outflow tract, the myocardium is thick, present EP study and ablation. The decision to use transsep-
but the epicardial aspect of the left ventricular outflow tract tal access or retrograde aortic access for endocardial map-
anteriorly is excluded from pericardial access by the overlying ping and ablation generally has to be made prospectively. If
right ventricular outflow tract. a mechanical aortic valve or complex atheroma in an older
Figure 1.85 shows the electroanatomic map and LAO fluo- patient (often seen with ischemic ventricular tachycardia) has
roscopic image from a patient with multiple sites of right ven- been noted at echocardiography, transseptal access is pre-
tricular outflow tract tachycardia. This patient has a coronary ferred. With certain types of ventricular tachycardia, careful
arterial venous fistula related to an anomalous conus branch mapping and choice of left ventricular access are particularly
of the right coronary artery. The circulatory disturbances important to maximize the chance for a successful result at
related to the fistula likely caused multiple foci of tachycar- ablation.
dia, some of which are epicardial in the rightward free wall Figure 1.86 shows the intracardiac electrograms obtained
portion of the right ventricular outflow tract. The arrow in in a 21–year-old patient with exercise-related ventricular
the right panel indicates a catheter faced epicardially via tachycardia. The second beat in the tracing is a typical prema-
a subxiphoid approach. This epicardial catheter can be placed ture ventricular contraction that has an identical morphology
very close to the other ablation catheter in the endocardial with the clinical tachycardia. The numbering of the coronary
right ventricular outflow tract. Such proximity between an sinus electrodes is as described earlier in this chapter, with the
endocardial catheter and an epicardial catheter for the left smaller numbers (CS 1,2) representing the distal electrodes.
ventricular outflow tract is not possible because of its “cen- The electrogram on the ablation catheter is unusual. A very
tral” anatomy and the “central” location of the aortic valve, as sharp near-field signal perceives a more fragmented signal, and
shown in Figure 1.80 and explained above. The utility of elec- a larger amplitude signal is noted on the distal ablation catheter
troanatomic mapping for ventricular tachycardia is discussed (ABL d). Such an electrogram is typical of that obtained when
more fully in Chapter 3. This technique can be very useful in the mapping catheter is at or near the infra-Hisian conduction
exactly determining whether a focus or slow zone of a circuit system (His-Purkinje tissue). The very sharp near-field signal,
is epicardial or endocardial in location. The red dots in the when recognized near the sites of early activation, alerts the
left panel of Figure 1.85 represent the epicardial ablation sites operator to 2 important consequences:
delivered with a successful result in this patient.
The decision to proceed with pericardial access for ven- 1. The site of origin is likely very superficial in the
tricular tachycardia is typically made after initial mapping endocardial surface and can be easily mechanically
Figure 1.85 The electroanatomic map (left panel) and left anterior oblique fluoroscopic image (right panel) from a patient with multiple
sites of right ventricular outflow tract tachycardia. The arrow is explained in the text.
Figure 1.86 Intracardiac electrograms obtained in a 21-year-old patient with exercise-related ventricular tachycardia.
traumatized (bumped), resulting in noninducibility of the left ventricle than it is to prolapse the catheter retrograde
the tachycardia. across the aortic valve.
2. Multiple fascicular (Purkinje) potentials may be Additionally, for both right- and left-sided fascicle-related
recorded on the left ventricular septum, most of tachyarrhythmia, the actual ventricular exit site or sites for
which are bystander (not arrhythmogenic) potentials. the tachycardia may be at a considerable distance (through
To correctly identify the exact site of origin, careful the moderator band for right ventricular tachycardias and
point-to-point mapping with continuous fluoroscopic through false tendons, causing lateral exit, for left ventricular
electrogram correlation is required. tachycardias) (Figure 1.88). Here again, exact correlation of a
A typical site for a fascicular origin of tachycardia related
to the left posterior fascicle is shown diagrammatically in
Figure 1.87. Because of the propensity for mechanical trauma
to the superficial arrhythmogenic conduction tissue, a trans-
septal approach may be preferred for this type of tachycardia.
It is generally more difficult to control the catheter entry to
RV LV
Moderator
band
Figure 1.88 For both right- and left-sided fascicle-related

tachyarrhythmia, the actual ventricular exit site or sites for
the tachycardia may be at a considerable distance (through the
moderator band for right ventricular tachycardias and through
false tendons, causing lateral exit, for left ventricular tachycardias).
Figure 1.87 A typical site for a fascicular origin of tachycardia The arrows indicate the pattern of electrical activation.
related to the left posterior fascicle. LV indicates left ventricle; RV, right ventricle.
mapping system with the fluoroscopic views gives the opera- 7. Finally, what special features of the regional anatomy
tor the best chance of clarifying the exact site of tachycar- where the catheter may be located need consideration
dia origin and applying the appropriate pacing maneuver to (outflow tract, right upper pulmonary vein, vein of
define the true arrhythmogenic sites of tachycardia origin. Marshall, etc)?
Thus, for ventricular tachycardia ablation, multiple meth-
The following discussion applies these principles to a few
ods of catheter access and familiarity with a resulting fluo-
unusual situations encountered in the EP laboratory.
roscopic position are required. Particularly with the outflow
tract, exact correlation of the fluoroscopic anatomy and the Figure 1.89 shows the RAO and LAO views of complex
resulting electrograms is imperative. catheter positioning in a patient undergoing an EP study
and radiofrequency ablation. The yellow arrow shown in
the LAO view (right panel) indicates the His bundle cath-
CORRELATION OF FLUOROSCOPY AND
eter which, at this site, recorded a clear His bundle electro-
ANATOMY IN LESS COMMON SITUATIONS
gram. The white arrows in both views indicate the ablation
The final section of this chapter discusses a few examples of catheter. Where is the ablation catheter located?
unusual catheter positioning in less commonly encountered A. Right ventricle
situations. The purpose of this discussion is not to provide B. Left ventricle
an exhaustive account of anomalous situations but to dem- C. Cavotricuspid isthmus
onstrate that the careful application of the principles of D. Mitral isthmus
interpreting standard fluoroscopic views can help define flu- E. Azygos vein
oroscopic catheter positions even in unusual cases. Chapter 9 Answer: C—Cavotricuspid isthmus.
includes a more detailed discussion of common issues pre-
Following is a systematic examination of this catheter’s
sented to electrophysiologists with regard to congenital heart
position:
disease.
Regardless of how unusual a catheter position may seem 1. Judging from the route that this catheter takes prior to
fluoroscopically, the following questions should be consid- reaching its final position, it is likely being inserted by a
ered sequentially:
retrograde transaortic approach.
1. In the RAO view, where is the catheter in relation to 2. In the RAO view, there is a multielectrode catheter
the annulus, as defined by the coronary sinus? Is it placed close to the annulus, but there is no catheter
ventricular or atrial? (correlate with LAO view) in the usual position of the
2. In the LAO view, where is the catheter in relation to coronary sinus. This increases the difficulty of deter-
the septum (perhaps as defined by the His bundle cath- mining whether the mapping electrodes are in the
eter)? Is it left-sided or right-sided? ventricle or the atrium. However, judging from the
3. In the LAO view, once the chamber has been defined, is fluoroscopic translucency present between the dia-
the catheter closer to the septum or the free wall of that phragmatic shadow and the cardiac silhouette (pyram-
chamber? idal space fat pad) that usually defines the annulus, the
4. Is the presentation potentially an exception to the gen- catheter appears to be close to the annulus.
eral rules regarding the standard fluoroscopic views? 3. A second mapping/ablation catheter is inserted via
For example, remembering that a catheter in the left the femoral route and placed very close to the catheter
atrial appendage or left upper pulmonary vein overlaps being analyzed in both the RAO and LAO view.
the ventricle and “breaks the plane” of the coronary 4. The unusual course of this catheter seen in the LAO
sinus. view makes interpretation difficult. The catheter is
5. Do the electrograms obtained from the catheter the placed retrograde transaortically to be positioned in
position of which is being analyzed correlate with the the left side of the heart. Yet, the LAO view shows that
standard fluoroscopic views? For example, a catheter the catheter is in fact clearly located to the right of the
believed to be in the appendage, if advanced further, septum as defined by the His bundle catheter’s position
may be associated with a large-amplitude atrial elec- (yellow arrow) in the LAO view. Thus, there are 2 con-
trogram. If no electrogram is seen, then the catheter tradictory determinations. The access route leads to the
may be in the left upper pulmonary veins, or if a large conclusion that the catheter must be on the left side of
ventricular electrogram is seen, the catheter may have the heart, and the LAO fluoroscopic view shows the tip
prolapsed through the mitral valve. of the catheter on the right side of the heart. How to
6. What is the course of the catheter (proximal portion reconcile this? Possibilities that need to be considered
and shaft) in reaching its final destination? Has it been are whether this is this really an LAO view or if the His
inserted via a retrograde aortic approach, via the inter- bundle catheter is out of place. By observing the posi-
nal jugular vein, via the femoral vein, via a transseptal tion of the vertebral column in the LAO view, it cer-
approach, or via a subxiphoid pericardial approach? tainly seems that this is a reasonable LAO projection.
Figure 1.89 The right anterior oblique (left panel) and left anterior oblique (right panel) views of complex catheter positioning in a patient
undergoing an electrophysiology study and radiofrequency ablation. The arrows are explained in the text.
The principal point to be noted in Figure 1.89 is that a of the right atrium that includes the coronary sinus ostium
good His bundle electrogram is being recorded by the and the atrial tissue just posterior to the tricuspid valve (sub-
catheter in the His bundle location. eustachian isthmus) is excluded from the systemic blood
flow (Figure 1.90). Thus, to ablate the cavotricuspid isthmus,
One way to resolve these unexpected findings is to hypoth-
it is not possible to reach the tricuspid valve portion using
esize a connection between the left- and right-sided circula-
a catheter placed via a femoral vein or the internal jugular
tions (ventricular septal defect, atrial septal defect, etc). Thus,
vein. (This also explains why a coronary sinus catheter was
one possibility to consider is that a retrograde transaortic
not placed through the internal jugular vein.) This patient
approach has been used to place a catheter in the left ventricle,
has typical atrial flutter. Details of the diagnosis are presented
and from the left ventricle, the catheter has been positioned
to the right heart via a ventricular septal defect. Another pos-
sibility is that once the left ventricle was accessed via the ret-
rograde approach, the catheter was manipulated to the left
atrium and from the left atrium via an atrial septal defect or
patent foramen ovale into the right atrium. The RAO view
does not show clearly from the catheter positioning whether
an atrial septal defect or a very basal ventricular septal defect
Fontan LA Reverse
was used to cross into the right-sided circulation, and both
transseptal
possibilities remain considerations. Nevertheless, the even-
Original RA
tual position of the catheter is similar to that of the other map-
ping ablation catheter which, even without a coronary sinus
catheter in position, is determined to be in the region of the Via
femoral vein Mitral
cavotricuspid isthmus (annular on the RAO view, right-sided
in the LAO view).
Why would the operator choose to place a catheter in Tricuspid
the cavotricuspid isthmus through such a circuitous route?
The patient shown in Figure 1.89 has a history of congeni-
tal pulmonary atresia for which a Fontan procedure has been
performed. (The details of the types of Fontan procedures rel-
evant for electrophysiologists are discussed in Chapter 9.) In
this patient, the right atrium is connected to the main pulmo- Figure 1.90 Mapping the complete circuit in surgically corrected
nary artery via a conduit. In designing this conduit, a portion congenital heart disease. LA indicates left atrium; RA, right atrium.
Figure 1.91 Right anterior oblique (left panel) and left anterior oblique (right panel) views demonstrate ablation catheter access (arrows) to
the neo–left atrium using a reverse transseptal approach.
elsewhere in this book (Chapters 5 and 9). For the purpose of (neo–left atrium), and the other is in the systemic circula-
this section, once the diagnosis is established, a linear ablation side as in the normal heart. Thus, ablation is performed
tion is required from the tricuspid valve (or remnant of the first from the margin of the conduits to the inferior vena cava
valve in the case of patients with tricuspid atresia) to the infe- and then to access the neo–left atrium. A retrograde aortic
rior vena cava. However, this tricuspid isthmus is now in 2 approach is used to gain entry to the left ventricle, and in this
portions. One is continuous with the pulmonary venous flow patient, a “reverse transseptal” approach is used where the
Figure 1.92 The fluoroscopic image was obtained in a patient Figure 1.93 The orthogonal view from the same patient shown in
undergoing ablation for recurrent, drug-refractory paroxysmal Figure 1.92 is the right anterior oblique projection. The coronary
atrial fibrillation. The arrow indicates the coronary sinus sinus catheter appears to course from right to left as is typically
catheter from which the electrodes’ characteristic coronary sinus seen in the left anterior oblique view. This patient had a form of
electrograms are obtained. dextrocardia.
catheter is advanced from the left ventricle to the left atrium A. The RAO view since the coronary sinus catheter is seen
and via a residual atrial septal defect to the anterior portions end on
of the cavotricuspid isthmus. Completing the linear ablation B. The LAO view since the coronary sinus catheter is seen
using this approach terminates the flutter and achieves bidi- end on
rectional conduction block. C. The RAO view since the vertebral column is seen on the
In performing this linear ablation without the coronary right
sinus catheter in place to help defi ne the annulus, how does D. The LAO view since the vertebral column is seen on the
the operator know that the anterior portion of the line is right
complete; that is, that the tricuspid annulus/right ventricle Answer: D—The LAO view since the vertebral column is
has been reached? Here again, fluoroscopy must be corre- seen on the right.
lated with the electrograms obtained. In Figure 1.91, the
ablation catheter is gradually moved to a more ventricu- Earlier in this chapter is explained the importance of the
lar location (anterior in the RAO view) until atrial elec- coronary sinus catheter in defining the annulus and allowing
trograms were lost and only a ventricular signal is seen. separation of the ventricle from the atrium in the RAO view.
Th is would defi ne the anterior limit of the cavotricuspid In fact, the coronary sinus catheter position is typical for an
isthmus. Other cases in which such approaches to access RAO projection. Yet, in the RAO view (being the profi le view
excluded portions of the atrium (all ventricle) are presented of the heart), the vertebral column is seen on the left, defin-
in Chapters 5 and 9. ing the posterior or more atrial side of the annulus. In Figure
1.92, the vertebral column is clearly on the right, and thus,
The fluoroscopic image shown in Figure 1.92 was this view is an LAO view. Why then does the coronary sinus
obtained in a patient undergoing ablation for recurrent, catheter appear end on?
drug-refractory paroxysmal atrial fibrillation. The arrow The orthogonal view shown in Figure 1.93 is the RAO projec-
indicates the coronary sinus catheter from which the char- tion. The coronary sinus catheter here appears to course from
acteristic coronary sinus electrograms are obtained. Which right to left as is typically seen in the LAO view. The reason for
fluoroscopic view is being shown and why? this discrepancy is that the patient has a form of dextrocardia.
Ao
Ao
RV
RA
RV
LV
Figure 1.94 The position and orientation of the ventricular apex (arrow). Ao indicates aorta; LV, left ventricle; RA, right atrium; RV, right
ventricle.
Figure 1.95 Direction of the ventricular apex (arrows). Left panel, Right-sided direction of the ventricular apex, a form of dextrocardia.
Right panel, An example of mesocardia where the apex of the heart is in the midline.
Considering the heart in the standard orthogonal fluo-

roscopic views (LAO and RAO), one view is needed to look
straight at the heart and to clearly distinguish right from left.
Since the heart is shifted to the left normally, instead of the
AP view, the camera is moved to examine the heart from an
LAO projection, thereby allowing distinction of right- and
left-sided structures. The orthogonal view is the profi le view
or RAO view, allowing distinction of posterior (atrial) from
anterior (ventricular) structures relative to the annulus, as
defined by the coronary sinus catheter (Figure 1.94).
Figure 1.95 shows in the left panel a right-sided direction
of the ventricular apex, a form of dextrocardia. Thus, in this
situation, to look straight at the “face” of the heart, instead of
moving the camera angle to the left side of the body, the LAO
view, the camera is positioned on the right side, the RAO
view. The inverted positioning of the heart explains why the
RAO view, as shown in Figure 1.93, appears similar to the
LAO view in a normal heart. The right panel of Figure 1.95
shows an example of mesocardia where the apex of the heart
is in the midline. A standard AP view, as with visualization of
any other midline structure in the body, allows a quick deter- Figure 1.96 Right anterior oblique view of catheter positioning
mination of whether a catheter is placed to the right or left of during the ablation procedure for the same patient shown in
the septum. Since the RAO view is now the equivalent of the Figure 1.95. The arrows are explained in the text.
Figure 1.97 Angiographic images obtained during an ablation procedure. Left panel, Right anterior oblique view. Right panel, Left anterior
oblique view.
usual LAO view and helps decide whether a catheter is to the the atrial septum, it is clear that a venous structure is entered
right or left of the septum, the orthogonal view becomes the on the atrial septum, likely draining blood from portions of
LAO view, helping decide whether a catheter is atrial or ven- the left atrium directly to the right atrium. As explained in
tricular to the annulus, as defined by the coronary sinus cath- Case 20, remnants of the anterior cardinal system (retroatrial
eter. The difference, however, as can be seen in Figure 1.92, cardinal veins) sometimes persist in adult life and have their
is that since the vertebral column is to the right, structures ostium on the interatrial septum anteriorly. Figure 1.97 shows
to the right of the coronary sinus catheter are posterior and an example of one such vein with a highly unusual occurrence
structures to the left (closer to the sternum) are ventricular. of finding the His bundle near this vein.
Figure 1.96 shows catheter positioning during the ablation
procedure for the same patient shown in Figure 1.93. Even
though this is the RAO view, understanding that the patient CONCLUSION
has dextrocardia and the adjustments being made to inter-
Although there is no real limit to the unusual circumstances
pret catheter position enable quick identification of the abla-
that may occur and challenge the interventional electrophysi-
tion (shown by the white arrow), which is likely located in
ologist, the fundamental principles of analyzing the fluoro-
a left-sided pulmonary vein. The yellow arrow indicates the
scopic views, correlating electrograms, and correlating with
intracardiac ultrasound probe. Intracardiac ultrasound per-
the regional anatomy remain the same.
formed with the aid of this probe can be helpful in defining
This chapter reviews these fundamental principles, with
unusual anatomy and providing adjunctive information for
illustrations involving the common arrhythmias that pres-
the careful analysis of the fluoroscopic images.
ent for ablation in the EP laboratory and a few uncommon
Similar systematic analysis of fluoroscopic images can
situations. The method of labeling the fluoroscopic views and
be applied to angiographic images obtained during an abla-
catheter position as well as electrodes is explained and allow
tion procedure as well (Figure 1.97). In a young patient with
readers to appreciate the case presentations in this book.
recurrent narrow complex tachycardia, the His bundle elec-
trogram could be obtained only from an unusual fluoroscopic
location. The catheter is removed and a sheath placed at the ABBREVIATIONS
same location and contrast injected. An unusual angiogram
is obtained from which the simultaneous RAO and LAO AP, anteroposterior
images are shown. With reference to the coronary sinus cath- AV, atrioventricular
eter, the ostium of this vascular structure is atrial (posterior AVNRT, atrioventricular nodal reentry tachycardia
to the coronary sinus), and with retrograde injection, drain- ECG, electrocardiogram, electrocardiographic
age occurs from the left to the right. Branches of the coronary EP, electrophysiologic, electrophysiology
sinus, pulmonary vein, vena cava, etc, can quickly be dis- ICD, implantable cardioverter-defibrillator
counted from knowledge of fluoroscopic anatomy. Without LAO, left anterior oblique
further information or knowledge of the detailed anatomy of RAO, right anterior oblique
2
Use of Intracardiac Echocardiography
in Cardiac Electrophysiology
Paul A. Friedman , MD, and Samuel J. Asirvatham , MD
INTRODUCTION Most structures of interest are well visualized from the right
atrium or right ventricle; infrequently, the ultrasound trans-
Intracardiac echocardiography (ICE) is increasingly used ducer is advanced into the coronary sinus or pulmonary
during invasive electrophysiology procedures. Common artery for additional imaging of left-sided structures. A fre-
applications include guiding transseptal puncture, assess- quency setting of 7.5 MHz is a good starting point for most
ing potential complications (pericardial eff usion, pulmonary applications. For distinguishing thrombus from other struc-
vein stenosis), and identifying structures invisible under tures, scanning at multiple frequencies and at a higher fre-
fluoroscopy (pulmonary veins, surgical patches, aortic cusps, quency for finer resolution is helpful.
thrombi). It is important to distinguish intravascular ultra- For the purpose of orientation on insertion of the cath-
sound from intracardiac ultrasound. Intravascular ultra- eter, the tricuspid valve and right ventricle are easily identi-
sound uses high-frequency transducers (20–40 MHz) that fied. After the probe is advanced to the right atrium (under
provide excellent high-resolution images but have limited fluoroscopic guidance in less experienced hands), slow rota-
tissue penetration. Intracardiac imaging uses lower frequen- tion of the catheter at a setting of 7.5 MHz with a depth of
cies (5–10 MHz), increasing tissue penetration to 14 cm and 12 cm permits easy identification of the tricuspid valve, right
permitting “whole heart” imaging. ventricle, and right ventricular outflow tract, which are used
Several types of ICE devices are available. A 9F (9 MHz) as starting points of reference (Figure 2.2). This view is also
mechanical catheter (Boston Scientific Corp, San Jose, useful for global assessment of the presence of pericardial
California) uses a rotating element to create a radial 360° imag- eff usions. From this standard position, clockwise rotation of
ing plane perpendicular to the long axis of the catheter (Figure the transducer sequentially brings into view a portion of the
2.1, left panel). In our laboratory, we commonly use an 8F or left ventricular outflow tract and aortic cusps (Figure 2.3).
10F tip-mounted phased-array transducer with frequency With further rotation, the left atrium and pulmonary veins
agility (5.5–10 MHz) and full Doppler capability (Acuson are visualized. A slow clockwise scan from the position of
Corporation, Mountain View, California). The 64-element Figure 2.3 shows the mitral valve annulus, the left atrial
vector phased-array transducer configuration results in a 90° appendage, then the left superior and left inferior pulmonary
sector image (pie shaped) (Figure 2.1, right panel). veins (Figure 2.4), and subsequently the right inferior pul-
The purpose of this brief introduction is to provide practi- monary vein (Figure 2.5). The right superior pulmonary vein
cal points of reference for use of ICE and orientation to the is best imaged by further advancing the ICE probe toward
images that follow in the remainder of the book. Thus, only the superior vena cava in conjunction with modest addi-
images from the phased-array system are included. tional clockwise torque (Figures 2.6 and 2.7). When imaging
the right-sided pulmonary veins from the right atrium, the
depth setting is typically reduced to 60 to 80 mm or less to
GENERAL SETTINGS, VIEWS, AND enlarge the image. Imaging of the left-sided pulmonary vein
ORIENTATIONS is typically best done with a depth setting of 80 to 100 mm.
Additional clockwise rotation from the point of imaging the
In our laboratory, the imaging catheter is most commonly
right superior pulmonary vein permits visualization of the
advanced from the right femoral vein into the right atrium.
posterior right atrium, right atrial free wall, and pectinate
muscle, then the subsequent return to the tricuspid valve
Abbreviations are expanded at the end of this chapter. annulus and right ventricle.
65
RA
RA LA
LA
Figure 2.1 Imaging of the atrial septum with radial and vector phased-array intracardiac echocardiography. Left panel, A 9-MHz,
3.2-mm-diameter mechanical rotational ultrasound image of the right and left atria. The asterisk indicates the center of rotation; the
imaging plane is perpendicular to the long axis of the catheter. The imaging penetration depth is approximately 4 cm; however, because
of the radial image, the diameter of the image field is 8 cm. The yellow arrow indicates a catheter imaged in short axis. The white arrow
indicates the membranous fossa ovalis. For orientation, the patient is facing up (toward the top of the image) and the spine is located at the
bottom of the image. Right panel, Image of the atria acquired using a phased-array transducer imaging at 8 cm in 1 direction, with a sector
plane of view. The depth of penetration beyond the atrial septum is approximately 5 cm. The arrow indicates the membrane of the fossa
ovalis. At 7.5 MHz, spontaneous contrast within the left atrium is visible in this patient with ischemic cardiomyopathy. For orientation, the
patient’s head is to the right, feet to the left. LA indicates left atrium; RA, right atrium. (Adapted from Bruce CJ, Friedman PA. Intracardiac
echocardiography. Eur J Echocardiogr. 2001 Dec;2[4]:234–44. Used with permission.)
RVOT
RV
Figure 2.2 Imaging from the right atrium toward the right ventricle. Left panel, Illustration with perspective from within the right
atrium showing the phased-array ultrasound transducer with beam directed toward the tricuspid valve. Right panel, Image obtained with
transducer in the position shown in the left panel. At the very top of the image is the right atrium (not labeled). Below are the right ventricle
(RV) and right ventricular outflow tract (RVOT). The image is oriented with the transducer at top, and objects farther from the transducer
are lower on the image. For orientation, the patient’s head is to the right, feet to the left.
2. Use of Intracardiac Echocardiography in Cardiac Electrophysiology 67
RA
Ao
RVOT
RV
Figure 2.3 Clockwise rotation from the image shown in the right
panel of Figure 2.2 to image the aortic root. Ao indicates aorta; RA, Figure 2.5 The right inferior pulmonary vein, imaged from the right
right atrium; RV, right ventricle; RVOT, right ventricular outflow tract. atrium. Arrow indicates a lasso catheter, seen at the vein’s ostium.
RA
LA
LIPV LSPV
RSPV
RPA
Figure 2.4 Imaging of the left-sided pulmonary veins obtained

from the right atrium. Top panel, Illustration showing intracardiac
echocardiographic (ICE) probe in the right atrium, imaging
across the interatrial septum. The arrows indicate the left superior Figure 2.6 Top panel, The intracardiac echocardiographic (ICE)
pulmonary vein (top) and left inferior pulmonary vein (bottom). probe at the level used to image the fossa ovalis. Bottom panel, The
Bottom panel, Ultrasound image obtained with the probe in the ICE probe is advanced and rotated clockwise approximately 15° to
same position shown in the left panel. The septum is at the top. The image the right superior pulmonary vein. LA indicates left atrium;
veins are easily seen, enhanced with color Doppler, the red color LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary
indicating flow toward the transducer. The left superior vein is on vein; RA, right atrium; RPA, right pulmonary artery; RSPV, right
the right, the left inferior vein is on the left. superior pulmonary vein.
RSPV RSPV
LPA LPA
SVC Atrial
appendage
RAA
SVC
RSPV LIPV
RSPV
RSPV RA
Figure 2.7 Top left panel, Image of the right superior pulmonary vein (RSPV) and the left pulmonary artery shown in Figure 2.6. Top
right panel, With additional clockwise rotation, the RSPV is seen in full cross-section close to the probe. Bottom left panel, The RSPV
has a very close relationship with the superior vena cava (SVC). The intracardiac echocardiographic probe is advanced to the SVC-right
atrial junction or into the inferior aspect of the SVC to image the RSPV. Bottom right panel, An anatomic specimen showing the close
relationship between the SVC and the RSPV. In this image of the RSPV, there is no intervening left atrium, and a nearly cross-sectional
view of the vein is obtained. LIPV indicates left inferior pulmonary vein; LPA, left pulmonary artery; RA, right atrium; RAA, right atrial
appendage.
For closer examination of the pericardial structures for Transseptal Catheterization

the assessment of eff usion, the probe is bent into the right
ventricle and advanced. From this perspective, the right ven- The left atrium must be accessed for mapping and ablation
tricular apex and the right ventricle are well seen. Rotation of in many patients with Wolff-Parkinson-White syndrome,
the catheter permits subsequent visualization of the left ven- atrial tachycardias, and, most commonly, atrial fibrillation.
tricular structures (Figure 2.8). ICE is useful in guiding transseptal puncture. ICE provides
a clear view of the fossa ovalis (and its proximity to the aor-
tic root), facilitating proper localization and avoidance of
SPECIFIC ELECTROPHYSIOLOGY APPLICATIONS complications, particularly in the setting of complex unusual
anatomy.
Several practical uses of ICE have emerged and are discussed Prior to transseptal puncture, the ICE catheter is posi-
in detail in this section. tioned in the right atrium to image the membranous fossa
RV
ICE
His
CS
TV isthmus
RV
LV
Figure 2.8 Imaging of the ventricles. Top left panel, Right anterior oblique fluoroscopic view is shown with the intracardiac echocardio-
graphic (ICE) catheter advanced into the right ventricle. Top right panel, The corresponding ICE view. Bottom panel, With rotation of the
probe, the left ventricle is easily seen. Another example including an anatomic drawing of placing the ICE probe in the right ventricle to
image the left ventricle is shown in Figure 2.15. CS indicates coronary sinus; LV, left ventricle; RV, right ventricle; TV, tricuspid valve.
ovalis. This position is useful in 2 ways. First, as the transseptal catheter distend the fossa ovalis, further confirming correct
sheath and Brockenbrough needle are withdrawn toward the catheter position prior to puncture. The presence of bubbles
fossa ovalis, the position of the ICE catheter fluoroscopically within the left atrium immediately confirms appropriate
approximates the position of the fossa ovalis. More impor- catheter position. It is important to note that due to rever-
tantly, when the needle-containing sheath descends to the beration, ultrasound side-lobing, and imperfect alignment of
level of the fossa ovalis, it is clearly seen with ICE (Figure 2.9). the ICE planes and transseptal needle plane, ICE should not
The needle within the transseptal sheath is a refractile body be used alone to determine the depth of passage of the trans-
with prominent reverberations. The injection of saline facili- septal needle into the left atrium. Gentle puffs of fluoroscopic
tates localization of the tip by means of echocardiographic contrast as the needle is advanced show the left atrial wall (as
bubbles. Tenting is directly visualized when pressures on the the contrast sprays against it) as the needle approaches this
RA
Needle tip
Bubbles
LA
Esophagus
LA
Ao Eso
RA
Bubbles
LA
LSPV RSPV
LA
RIPV
LIPV
Figure 2.9 Transseptal puncture. Top panel, The needle tenting
against the fossa ovalis with bubbles in the right atrium as saline is
infused. Bottom panel, With puncture, the needle and bubbles are
seen to enter the left atrium. LA indicates left atrium; RA, right atrium.
Figure 2.11 Top panel, Intracardiac echocardiographic image

showing the left atrium, with the esophagus immediately posterior
to it. During ablation, if changes are seen in the esophageal wall,
energy delivery is discontinued immediately. Bottom panel,
3-dimensional computed tomographic reconstruction showing
the juxtaposition of the esophagus and the left atrium. Ao
indicates aorta; Eso, esophagus; LA, left atrium; LIPV, left inferior
pulmonary vein; LSPV, left superior pulmonary vein; RIPV, right
inferior pulmonary vein; RSPV, right superior pulmonary vein.
structure. In our laboratory, with routine use of ICE to guide

transseptal puncture, a pigtail catheter is not placed in the
aorta. Additionally, ICE can be used to detect a patent fora-
men ovale, if present, prior to transseptal puncture, as well
Figure 2.10 Pericardial eff usion. The intracardiac echocardio- as to permit localization of the site of puncture within the
graphic catheter is advanced into the right ventricle at the base of membranous fossa. Routine puncture of the muscular sep-
the outflow tract and is imaging across the septum. The left ventricle tum is avoided because of the greater technical difficulty and
is readily seen, and just beyond it is a sizable eff usion (arrow). subsequent limitation in catheter and sheath manipulation.
of transient hypotension, a pericardial scan quickly excludes

(or makes the diagnosis of) pericardial eff usion as the cause
(Figure 2.10). The development of regional wall motion abnor-
malities may also be detected intraoperatively, although this
requires greater operator experience and can be more techni-
cally challenging because of oblique views of many left ven-
tricular segments.
During ablation of atrial fibrillation, avoidance of ablation
at sites close to the esophagus may be important. ICE permits
delineation of the position of the esophagus in some patients
(Figure 2.11). However, use of this technique alone for assess-
ment of the esophagus has not been validated, and ICE should
be used in conjunction with other modalities.
More importantly, ICE is an effective tool for assessing
the development of intracardiac thrombus. Intracardiac
thrombus has been reported to develop on cardiac structures
or on ablation or mapping catheters in up to 10% of proce-
dures (Figure 2.12). Should thrombi develop, aspiration of
the thrombi through a long sheath, assessment of anticoagu-
lation status, and careful clinical evaluation of the patient’s
condition are warranted. Finally, ICE has also been used to
monitor pulmonary vein flow velocity as a screening tool for
pulmonary vein stenosis. However, discussion of Doppler
assessment of pulmonary veins is beyond the scope of this
introductory text.
Use of ICE to Guide Treatment

of Specific Arrhythmias
In several specific arrhythmias, ICE is particularly useful to

guide catheter ablation. In the ablation of atrial fibrillation,
ICE has been used to confirm the position of the pulmonary
vein ostia, which are not visualized fluoroscopically. When
making electroanatomic maps, we often use ICE to confirm
ostial position prior to labeling them. With the phased-ar-
Figure 2.12 Top panel, The intracardiac echocardiographic ray ICE catheter, the left-sided veins are generally well seen.
image shows a thrombus (arrow) that developed adjacent to the
However, following transseptal puncture, the catheters them-
left atrial appendage during the procedure. Bottom panel, A large
selves may cause shadowing or interference with the vein
fresh thrombus and several smaller thrombi were evacuated by
aspiration via the transseptal sheath. images. Several approaches can be adopted to improve image
quality. Manipulation of the ICE catheter and articulation of its
head by means of the controls on the shaft often permit iden-
tification of a position with an unimpeded ultrasonic window.
Assessment of Procedural Complications Alternatively, the catheter placed in the right ventricular out-
flow tract can provide unobstructed images of the left atrium
ICE allows early recognition of the development of a peri- and pulmonary veins by avoiding the transseptal catheters
cardial eff usion by enabling continuous monitoring of the (Figure 2.13). In our experience, however, this latter approach
pericardial space. This monitoring permits prompt detec- is not commonly needed.
tion and treatment of cardiac perforation with tamponade. ICE is also frequently useful in ablation of outflow tract
The pericardium is often well visualized by imaging the ventricular tachycardias. In these tachycardias, it may be
right ventricle from the right atrium just across the tricus- important to identify the position of the ablation catheter
pid valve. Counterclockwise rotation permits assessment of relative to the aortic valve, aortic cusp, and coronary artery
the region outside the right atrium; clockwise rotation shows ostium (Figure 2.14) or, in right-sided cases, relative to the
the left atrium and its surrounding pericardium. Placement pulmonic valve. ICE is particularly useful in patients with
further into the right ventricle provides close inspection of congenital anomalies and associated arrhythmias. While
the pericardium surrounding the ventricles and is essential a detailed review of the use of ICE in congenital lesions is
if the diagnosis is in doubt. Most commonly, in the setting beyond the scope of this chapter, Figure 2.15 depicts imaging
Catheter
Aortic
valve
LMO
Leaflets
Catheter tip
Aortic
valve
LMO Position of catheter tip
LA
LAA PV
Q-tip
LAD RCA
LSPV
LIPV LCX
Descending
aorta AV
ICE
MV TV
Fossa ovalis CS
RAA LAA
Figure 2.14 Use of intracardiac echocardiography (ICE) to

Q-tip
determine the position of an ablation catheter relative to the
ABL aortic valve (AV) and related structures. Top panel, An ICE image
obtained with the probe in the right atrium, adjacent to the AV.
A catheter is positioned via the retrograde approach into the left
LIPV coronary cusp with the tip at the hinge point of the left leaflet in
this patient with an aortic cusp ventricular tachycardia. Bottom
panel, The corresponding anatomic relationships. The atria have
Mitral annulus
been removed. ICE indicates the approximate position of the ICE
Tricuspid annulus
probe used to obtain the image in the left panel. The image plane
Figure 2.13 Top panel, Illustration of positioning of an is through the noncoronary cusp to the left coronary cusp. The
intracardiac echocardiographic (ICE) probe through the tricuspid text “LMO” on the top panel is positioned at the approximate
valve into the outflow tract to image the aorta, left atrium (LA), left location of the left main ostium (not shown in the frozen image in
atrial appendage (LAA), and left-sided veins. Middle panel, The the bottom panel). The distance from the catheter tip position to
corresponding ICE image. The Q-tip–shaped structure separates the LMO position is approximately 1 cm, indicating an acceptable
the LAA from the left-sided pulmonary veins. Bottom panel, A ablation location. Real-time continuous imaging of the catheter tip
specimen demonstrating the relationship between the LAA and assures that its relative position to the LMO is unchanged during
the left-sided veins, with the Q-tip structure in between. The Q-tip ablation. The upward-pointing arrow in the lower middle portion
structure contains the vein of Marshall prenatally, which often of the image indicates the position of the interatrial septum. CS
becomes atretic to form the ligament of Marshall postnatally. ABL indicates coronary sinus; LAD, left anterior descending artery;
indicates ablation catheter; LIPV, left inferior pulmonary vein; LCX, left circumflex coronary artery; MV, mitral valve; PV,
LSPV, left superior pulmonary vein; RAA, right atrial appendage. pulmonic valve; RCA, right carotid artery; TV, tricuspid valve.
PV
MV
MV
MV
LV
RV
Figure 2.15 Intracardiac echocardiography (ICE)–assisted ventricular tachycardia ablation. Left panel, Illustration of the ICE catheter
tip as it is positioned in the right ventricular outflow tract just inferior to the pulmonic valve, having been advanced from the right
ventricle. The oblique longitudinal axis ultrasound-imaging plane is shown, cutting through the mitral valve, the left ventricle, and the left
ventricular myocardium. Right panel, The corresponding ultrasound image. In this patient, an idiopathic aneurysm was noted in the left
ventricular wall. Standard electrophysiologic techniques were used to guide the ablation catheter to the critical arrhythmogenic substrate.
ICE was then performed, confirming that the catheter was in the aneurysm, linking the arrhythmia with the anatomic anomaly (white
arrow indicates the ablation catheter at the edge of the aneurysm). With energy delivery, the ventricular tachycardia terminated, and ICE
confirmed the presence of tissue changes (not shown). Additionally, a small localized pericardial eff usion (yellow arrow) was identified in
association with the region of myocardium ablated. LV indicates left ventricle; MV, mitral valve; PV, pulmonic valve; RV, right ventricle.
(Adapted from Bruce CJ, Friedman PA. Intracardiac echocardiography. Eur J Echocardiogr. 2001 Dec;2[4]:234–44. Used with permission.)
Inflow
Inflow
Figure 2.16 Use of intracardiac echocardiography to image a left ventricular assist device inflow cannula in a patient undergoing ventricular
tachycardia ablation. Left panel, Real-time imaging of the cannula can be helpful to identify the relative position of the ablation catheter (not
shown in this image) and the inflow catheter, as well to visualize potential suck down events in which the inflow cannula adheres to adjacent
myocardium impeding blood inflow. Right panel, Chest x-ray fi lm of the same patient demonstrates the position of the inflow cannula.
to confirm catheter position in an idiopathic aneurysm that ventricular assist devices to identify baffles, inflow cannulas
was found to be the cause of ventricular tachycardia. (Figure 2.16), and other structures as well as to identify con-
In summary, ICE can be particularly useful when the pre- genital anomalies that may be important in arrhythmogen-
cise position of the catheter relative to anatomic structures esis are shown in specific examples later in this book.
is important. It is also useful for real-time monitoring of the
potential development of complications, particularly eff u-
sions, and facilitating the management of complications. ABBREVIATION
Additional examples of the use of ICE in other conditions
such as congenital heart disease and the presence of left ICE, intracardiac echocardiography
3
Electroanatomic Mapping for Catheter
Ablation of Cardiac Arrhythmias
Amit Noheria , MBBS , Traci L. Buescher, RN, and Samuel J. Asirvatham , MD
INTRODUCTION Single-channel electrograms have been replaced by multi-

channel mapping that has the capability to study electrophys-
Throughout the detailed discussion of instructive arrhyth- iologic activity at multiple points of the cardiac chambers
mia cases that form the body of this book are found exam- simultaneously. With this expanded capability for mapping,
ples of the use of 3-dimensional mapping systems. Although it has become increasingly difficult for the electrophysiolo-
the systems provide a powerful tool to better treat complex gist to keep track of electrograms from different points, their
arrhythmia, the student of electrophysiology should be aware temporal association, and their context in relation to car-
of the various pitfalls that sometimes result in confusion and diac chamber anatomy during an electrophysiologic study
inaccuracy with interpretation. (J Cardiovasc Electrophysiol. 2004 Jul;15[7]:839–54). This has
Changes made in seemingly simple parameters such as led to development of electroanatomic mapping systems that
the mapping window component of the electrogram and use computer-based displays to graphically depict the electro-
choice of fiduciary point can completely change the map, physiologic inputs from an ever-increasing number of cardiac
especially for reentrant arrhythmias in structurally abnor- points in a 3-dimensional geometry portraying the cardiac
mal hearts. Further, the electrophysiologist has to be aware chamber anatomy. Computer algorithms further extrapo-
of the limitations in the technology being used. For exam- late the point-to-point information to generate the missing
ple, an ablation “point” being taken as circular ablation 3-dimensional space. Color coding of the 3-dimensional map
around a pulmonary vein being done may reflect neither is used to depict a number of electrophysiologic input char-
that particular spot (motion artifact) nor complete ablation acteristics such as activation time, voltage, and electrogram
at that site. fractionation. Display techniques, for example, the use of
To help the student appreciate the correct use of map- graded colors to depict the temporal relation of the inputs at
ping technology in electrophysiology, this chapter provides different sites, demonstrate the spread of the electrical wave
an overview of the technologies themselves. The examples in front across the cardiac geometry and provide information
this chapter give a basic appreciation of how the technology about surface activation. Contemporary computerized soft-
is used in arrhythmia management. The case discussions that ware allows real-time scrolling of the generated electroana-
follow include the specific utilities and pitfalls to avoid during tomic map in 3 dimensions. Moreover, the mapping systems
application of these technologies. are used concurrently with catheter-based endocardial or
epicardial ablation for arrhythmia treatment. The mapping
systems enable the simultaneous real-time depiction of the
BACKGROUND
position and orientation of the ablation catheter (usually the
same as the mapping catheter) along with the electroana-
The first human electrocardiogram was recorded in 1887
tomic map that has been generated to facilitate the accurate
and led the way to subsequent study and characterization of
positioning of the catheter for ablation. In addition, the abla-
cardiac arrhythmias. Intracardiac electrophysiologic study
tion points are logged in real time on the electroanatomic
began more than 4 decades ago with the recording of the
map itself to facilitate visualization of ablation sites and show
His bundle electrogram using a single catheter. Since that
how they interrupt the arrhythmia foci or circuits.
time, there have been notable technologic and procedural
Electroanatomic mapping systems have been used in
advancements.
clinical electrophysiology practice for the past 15 years and
Abbreviations are expanded at the end of this chapter. require considerable technologic skill for setup and additional
75
specialized training. While use of such technology may add the electroanatomic map with the detailed anatomic configu-
to the procedural time, it may reduce fluoroscopic exposure ration obtained from cardiac imaging with helical computed
and improve procedural success. Whether use of this tech- tomography (CT), magnetic resonance imaging (MRI), and
nology has actually led to improved success of conventional even intracardiac ultrasound has been developed and is com-
ablation procedures remains largely unknown. ing into clinical practice.
Electroanatomic mapping has allowed electrophysiolo- An electroanatomic mapping system comprises 6 com-
gists to tackle more complex and challenging cases in the ponents: 1) an arrangement for generation of magnetic
electrophysiology laboratory. Its curative possibilities have fields or feeble electric currents across the subject’s thorax;
extended the application of catheter ablation to almost 2) intracardiac catheters that are actively manipulated by the
all kinds of arrhythmias. As computer-generated electro- proceduralist and have electrodes picking up both the local
anatomic maps have become increasingly sophisticated, electrograms as well as the decay in the magnetic field or elec-
electrophysiologic interventions have become increasingly tric voltage; 3) an interfacing unit that collates multichannel
dependent on 3-dimensional characterization by these maps. inputs from the electrodes and feeds these to the process-
Developing simultaneously with the progress made in under- ing unit; 4) a signal processing unit that fi lters and amplifies
standing therapeutic targets for complex arrhythmias such as the signals; 5) a central processing unit (CPU) that analyzes
atrial fibrillation, ventricular tachycardia, and even ventricu- the inputs to synthesize spatially tagged electrophysiologic
lar fibrillation, electroanatomic mapping technologies have data; and 6) a user interface to interact with the CPU and
become almost indispensable for ablation of such arrhyth- manipulate the display (J Cardiovasc Electrophysiol. 2005
mias. Inappropriate data input without sound understanding Oct;16[10]:1110–6; Heart Rhythm. 2009 Aug;6[8]:1249–52).
of the physical mechanisms being applied by the computer
algorithms can easily lead to inaccurate maps, as well as mis-
interpretation of the maps generated, and extensive studies MAGNETIC ELECTROANATOMIC MAPPING
validating the accuracy of even properly generated electroan-
atomic maps are lacking (J Cardiovasc Electrophysiol. 2005 The magnetic field–based technique of mapping applies the
Oct;16[10]:1110–6). concept of measuring the strength of a magnetic field that
degrades as a function of square of the distance from a point
source for electrode localization. The first description of
BASIC PRINCIPLES its use in vivo was published by Ben-Haim et al (Nat Med.
1996 Dec;2[12]:1393–5). Three low-intensity magnetic fields
Electroanatomic mapping in general comprises 3 aspects: of slightly different frequencies are generated from 3 proxi-
1) the 3-dimensional localization of the intracardiac or epi- mate magnetic coils. A sensor embedded in the mapping
cardiac catheters using remote detection of decay in the mag- catheter tip detects and relays the strength of the composite
netic fields or drop in voltage of an electric current across the time-varying spatially coded magnetic field in its orientation.
subject’s body locally by the catheter tip; 2) computer gen- This information is used for computation of the spatial loca-
eration of a virtual spatial map of the 3-dimensional cardiac tion and orientation of the sensor by determining the distance
chamber anatomy from synthesis of point-to-point catheter from each of the 3 coils using the inverse-squared solution,
localization data as the catheters are moved along the intrac- triangulation by 3-dimensional trigonometric principles, and
ardiac or epicardiac surface; and 3) analysis, computation, vector summation. The catheter tip itself is a recording elec-
and display of electrophysiologic data, obtained coinciden- trode to sense local electrograms that are coupled with the
tally during point-to-point mapping, on the virtual map in 3-dimensional location and fed into the system for electro-
a meaningful way. This third step usually consists of 1 of 2 anatomic map generation by cataloging all such inputs (Heart
displays: 1) the arrhythmic activation sequence by a graded Rhythm. 2009 Aug;6[8]:1249–52; Catheter ablation of cardiac
color code of the 3-dimensional map to show the activation arrhythmias: a practical approach. Springer; c2006).
wave front sequentially reaching the mapped points using the
arrhythmic electrogram at each point compared to a reference The Carto System
or fiduciary point (activation mapping) or 2) the magnitude of
the unipolar or bipolar voltage of a near-filled component of The Carto XP Navigation System (Biosense Webster, Inc,
the arrhythmic electrogram at each point (voltage mapping), Diamond Bar, California) is probably the most widely used
with computer interpolation of the presumed intervening 3-dimensional electroanatomic mapping system in cardiac
surface (Europace. 2008 Nov 10;10 Suppl 3:iii28–34). electrophysiology practice. It is composed of a magnetic field
Other characteristics of point-to-point electrograms sensor in the tip of a quadripolar mapping and ablation cath-
can also be displayed, such as fractionated potentials, eter (NaviStar; Biosense Webster, Inc) and an external mag-
mid-diastolic potentials, and double potentials. The closer netic field emitter located under the patient and the operating
the points are to each other and the more points sampled, the table. The external magnetic field emitter has 3 coils that
better the resolution and accuracy of the actual surface elec- generate ultra-low-intensity magnetic fields (between 5×10−6
trogram of the interposed surface. Compatibility to merge and 5×10−5 T) that code the surrounding space with spatial
3. Electroanatomic Mapping for Catheter Ablation of Cardiac Arrhythmias 77
information sensed by the field sensor at the tip of the map-

ping catheter (Circulation. 1997 Mar 18;95[6]:1611–22). In
addition to the 3-dimensional location of the catheter, the
orientation (roll, yaw, and pitch) of the tip is also obtained. A
reference locator (RefStar with QwikPatch; Biosense Webster,
Inc) is placed on the patient’s back and serves a reference
location to correct for patient movement. The electroana-
tomic map is generated by navigating the mapping catheter
around the cardiac chamber as serial point-to-point electro-
physiologic data are collected and coupled with the temporal
information relative to the reference electrogram and spatial
information relative to the location of the reference locator
(Figures 3.1–3.4).
Figure 3.1 shows the Carto point-based activation map
obtained during monomorphic ventricular tachycardia in Figure 3.2 The activation sequence map, obtained with Carto,
a 42-year-old man with Marfan syndrome. The patient pre- of the right atrium during inappropriate sinus tachycardia.
viously had aortic valve replacement and coronary artery The sequence of activation, shown in graduated colors from
bypass graft (CABG) surgery for aortic dissection and right red to pink, progresses from the high right atrium (arrows) to
coronary artery occlusion that caused inferior myocardial the rest of the atrial chamber. Left panel, The activation map in
infarction. Afterward he had left ventricular endocardial anteroposterior orientation. Middle panel, The map is a right
ablation for ventricular tachycardia, but his condition sub- lateral projection. Right panel, The interface during registration of
a point with 2 surface electrocardiograms, a reference electrogram
sequently relapsed. Voltage mapping showed an extensive
from a stationary catheter in the coronary sinus, a local bipolar
scar involving the septum and the inferior and lateral walls electrogram, and a local unipolar electrogram.
of the left ventricle. Ventricular tachycardia originated in
the inferior wall near the apex of the left ventricle, and the
activation wave front spread to the rest of the myocardium. The ventricular tachycardia was entrained endocardially and
successfully ablated.
Figure 3.2 shows the activation sequence Carto map of the
right atrium during inappropriate sinus tachycardia as the
sequence of activation progresses from the high right atrium
to the rest of the atrial chamber. The tachycardia was not
RV endocardial LV endocardial entrainable and had features suggestive of triggered automa-
ticity. Although the earliest sinus activation site was discrete
from the earliest tachycardia activation site, it is impossible to
say whether the tachycardia focus was separate from or part
of the sinus node complex. The automatic focus was ablated
with successful tachycardia termination and restoration of
sinus rhythm.
Figure 3.3 is a Carto activation map showing the activa-
tion sequence of symptomatic monomorphic premature ven-
tricular contractions (PVCs) occurring in bigeminy. Local
Epicardial activation during mapping in the left coronary cusp (LCC)
was 8 ms ahead of the mitral-aortic region. However, pacing
RAO LAO caudal
at the LCC site was unable to capture the rest of the myocar-
Figure 3.1 These RV and LV endocardial and epicardial activation dium. Ablation at the mitral-aortic site terminated the PVCs.
maps, obtained with Carto during monomorphic ventricular Further ablation was done at the LCC site.
tachycardia, show the activation wave front spreading from the Figure 3.4 shows a left atrial voltage map of a patient who
endocardium of the inferior wall near the apex of the left ventricle, had recurrent atrial fibrillation after a previous pulmonary
depicted in red, to the rest of the myocardium, shown with vein isolation procedure. Notable are the pink areas that
graduated color coding. Left panel, The activation map in an RAO
designate locations with an activation potential of 0.5 mV
orientation. Middle panel, An LAO caudal view looking straight
or higher. Ablation lines were created across the electrically
at the LV apex. Right panel, The interface during registration of
an early point with 4 surface electrocardiograms (one of which active tissue to extend the previously established scar and
is the chosen reference electrogram with the fiduciary point), a reaccomplish pulmonary vein isolation.
local bipolar electrogram, and a local unipolar electrogram. LAO The Carto 3 System (Biosense Webster, Inc) is a 3-dimensional
indicates left anterior oblique; LV, left ventricular; RAO, right mapping system that builds on Carto, keeping the same
anterior oblique; RV, right ventricular. conceptual framework of magnetic mapping technology.
calculated using a proprietary algorithm. This current-based

technology is described in greater detail in sections to follow.
LCC The integration of data is designed to improve location accu-
racy and catheter visualization to within 1 mm on average. In
addition, improvements to the catheter tip and curve visual-
ization, rapid creation of high-resolution anatomic maps with
quick movement of the catheter within the cardiac chamber,
and a new patient interface unit serves as a central connection
point for all catheters and equipment.
Figure 3.5 shows left atrial anatomic mapping using the
Mitral-aortic
region Carto 3 System in a patient with atrial fibrillation. The fast
anatomic mapping technology allows detailed visual enhance-
ment of specific areas of interest. Wide area circumferential
pulmonary vein isolation lines were also created.
The Carto RMT Electroanatomical Mapping System
Figure 3.3 This Carto activation map shows the activation sequence (Biosense Webster, Inc) is designed to work in the intense
of a symptomatic monomorphic PVC, color coded from early red to magnetic environment that is generated for magnetic cath-
late pink. The earliest PVC activation was noted in the LCC and with eter navigation (stereotaxis). This system has been used reli-
an 8-ms delay in the mitral-aortic region below the aortic valve. Left
ably and extensively and validated for the navigation of all
panel, The Carto map seen in a posteroanterior view. Right panel,
cardiac chambers to map the various types of arrhythmias
An early point being registered with the display showing 5 surface
electrocardiograms, one of which served as the reference, a local studied in the electrophysiology laboratory, including ven-
bipolar electrogram, and a local unipolar electrogram. LCC indicates tricular and atrial tachyarrhythmias, and to identify electro-
left coronary cusp; PVC, premature ventricular complex. physiologic scar tissue in both the atria and ventricles using
voltage mapping (Catheter ablation of cardiac arrhythmias:
a practical approach. Springer; c2006; www.biosenseweb-
In addition to data garnered from magnetic mapping, Carto
ster.com/products/nagivation; Catheter ablation of cardiac
3 incorporates placement of 3 back and 3 chest patches to
arrhythmias. Saunders/Elsevier; c2006).
measure unique high-frequency, low-power currents released
An image integration soft ware module, CartoMerge
from each electrode of the corresponding catheters. The
(Biosense Webster, Inc), adds the functionality of inte-
strength of the currents is measured by each patch, creating
grated display of preacquired helical CT images or MRI
a current ratio unique to location. The electrode position is
views to the electroanatomic map acquired using the usual
Carto system. The merge technology imports the images,
processes them to identify and reconstruct the chambers of
Figure 3.4 A Carto left atrial voltage map from a patient with
recurrent atrial fibrillation after previous pulmonary vein isolation
is seen in a posteroanterior projection showing the posterior Figure 3.5 Th is left atrial anatomic map was created with the
left atrial wall and the 4 pulmonary veins. Areas of activation Carto 3 System with fast anatomic mapping technology by quick
potential ≥0.5 mV are depicted in pink. The contiguous red dots catheter movement across the left atrial space. The Carto 3 System
indicate ablation lines made across the electrically active tissue to has hybrid catheter localization technology using both magnetic
extend the previously established scar (red-yellow-green-blue) and fields and electrical impedance. The red dots indicate the wide area
reaccomplish pulmonary vein isolation. circumferential pulmonary vein isolation lines.
interest, and registers the images with the electroanatomic and QwikMap software (Biosense Webster, Inc) to acquire
map in the Carto environment using anatomic reference multiple distinct electroanatomic points simultaneously
points. Figure 3.6 shows mapping of the left atrial space using from multiple electrodes, thus reducing the required num-
CartoMerge soft ware in a patient with atrial fibrillation. The ber of point-to-point acquisitions to generate the electroana-
soft ware module imports preacquired CT images or MRI tomic map. Chauhan et al (Pacing Clin Electrophysiol. 2004
views, identifies the chambers of interest and processes the Aug;27[8]:1077–84) demonstrated that for large macroreen-
images, and applies registration techniques to merge the pro- trant tachycardias and for focal arrhythmias in patients with
cessed data with the electroanatomic data from the Carto sys- structural heart disease, this type of generated map can accu-
tem. Landmark registration of 3 anatomic points provides a rately guide electrophysiologic treatment.
rough merge, and surface registration of between 20 and 30
well-dispersed points provides a more accurate merge.
CartoSound (Biosense Webster, Inc), an image integra-
tion module, allows for real-time integration of intracar-
diac echocardiography imaging into the electroanatomic
map (www.biosensewebster.com/products/nagivation; Circ
Arrhythm Electrophysiol. 2008 Jun;1[2]:110–9). CartoSound
acquires the information of cardiac geometry using the
intracardiac echocardiographic catheter SoundStar (Biosense
Webster, Inc), located in the right atrium, and feeds it into the
Carto electroanatomic mapping environment (Figure 3.7).
Dyna CT (Siemens Medical Solutions USA, Inc, Malvern,
Pennsylvania) provides fast and accurate 3-dimensional
anatomic reconstruction of the cardiac chambers using
contrast-enhanced fluoroscopic image acquisition (Figure 3.8).
This technology allows 3-dimensional reconstruction of the
cardiac chambers like a CT image using simple fluoroscopic
image acquisition with contrast injection. The anatomic map
can then be merged with the electroanatomic maps in the
Carto or Ensite NavX (St. Jude Medical, St Paul, Minnesota)
environment using image registration.
QwikStar
The 26-electrode mapping and ablation catheter QwikStar

(Biosense Webster, Inc) is teamed with the Carto XP system
Figure 3.7 Top panels, The anatomic map of the right atrium
(yellow lines), left atrium (cyan lines), right ventricle (green
lines), and left ventricle (lavender lines) generated using
CartoSound in a structurally normal heart with episodic
monomorphic ventricular tachycardia. Top left is the left anterior
oblique (LAO) view; top right is the right anterior oblique (RAO)
view. Bottom left and middle panels, Point-based electroanatomic
activation maps during spontaneous ectopy with the earliest
activation site (arrows) in the right ventricular outflow tract
directly below the pulmonary valve that was successfully
ablated. Programmed ventricular stimulation, pace mapping,
and mapping in the aortic root were also done. Bottom right
panel shows the registration of the activation timing at the site of
origin relative to the fiduciary point. The top 3 electrograms are
Figure 3.6 Mapping of the left atrial anatomy using CartoMerge reference surface recordings; the middle image has the chosen
soft ware in a patient with atrial fibrillation. Here the CT-acquired fiduciary point at an easily identifiable deflection. The bottom 2
and processed geometry of the left atrium (blue) has been merged tracings are the bipolar and unipolar electrograms, respectively,
with the Carto 3 anatomic map to assist with accurate wide area showing the local activation timing at a sharp large-amplitude
circumferential pulmonary vein isolation (red dots). deflection and onset of a QS deflection.
Figure 3.8 Contrast fluoroscopy image acquisition and 3-dimensional reconstruction of the LA in a patient who underwent pulmonary
vein isolation for atrial fibrillation. Left panel, PA orientation showing the 3-dimensional reconstruction of fluoroscopic images obtained
during LA contrast injection and registration of the LA chamber in red. Middle panel, PA view of the imported LA chamber map. Right
panel, AP view of the map. AP indicates anteroposterior; LA, left atrium; PA, posteroanterior.
ELECTRICAL IMPEDANCE electric currents with slightly different frequencies of about

ELECTROANATOMIC MAPPING 30 kHz are applied across the patient. The electric currents
are delivered using standard electrocardiographic electrodes
The concept underlying the use of electrical impedance to for 2 of the 3 orthogonal axes by placing them in the fourth
calculate a spatial location is based on the following: A very intercostal space at the right and left midaxillary lines and at
low-voltage alternating current of a particular localization fre- the left shoulder and left leg. The anteroposterior axis is cre-
quency applied across a patient’s body using 2 skin electrodes ated by applying electrodes anteriorly on the chest just above
confers a relatively linear voltage gradient across the tissues the level of the heart and posteriorly on the back just below the
in the axis of the electrodes. The voltage can be detected by a level of the heart. Larger 15-cm skin patches are needed for
sensing electrode and can then be converted to the axial loca- this axis to create a homogenous axial field across the heart
tion of the sensor. Three such orthogonal electric currents because of its proximity to the patches. A Medtronic tem-
applied separately and detected by a sensor can thus be used porary pacing lead fi xed into the wall of the chamber being
to triangulate the 3-dimensional location of the sensor. studied is used as the intracardiac reference (Catheter abla-
Mapping using this concept requires fulfi llment of the tion of cardiac arrhythmias: a practical approach. Springer;
following 4 conditions: 1) 3 orthogonal currents with the c2006; Catheter ablation of cardiac arrhythmias. Saunders/
heart at the center need to be used to allow triangulation in Elsevier; c2006).
3-dimensional space; 2) the externally applied electric cur-
rent should be easily detectable but benign to the patient and EnSite NavX
not interfere with the recorded electrograms; 3) the voltage
gradient needs to be calibrated to interpret recorded voltages The EnSite NavX (St. Jude Medical, Inc, St. Paul, Minnesota)
for localization; and 4) spatial variations associated with the was first described for electroanatomic mapping and
cardiac and respiratory cycles need to be accounted for. Thus, navigation in atrial flutter ablation in 2004 (J Cardiovasc
stabilization of the whole localization apparatus throughout Electrophysiol. 2004 Oct;15[10]:1157–61). The system com-
the mapping and ablation procedure is important to limit prises 3 orthogonally placed body surface electrode pairs with
inaccuracies. the heart at the center: pair 1) back of the neck above C3–4
and upper medial left leg; pair 2) left and right lateral thorax at
LocaLisa Intracardiac Navigation System T5–6 level; and pair 3) anterior and posterior chest at T2 level.
A low electric current at 5.68 kHz is multiplexed with each
The LocaLisa Intracardiac Navigation System (Medtronic EP of these pairs of electrodes to create the navigational electric
Systems, Minneapolis, Minnesota) was the fi rst electroana- field across the heart. A fi xed intracardiac catheter (eg, in the
tomic mapping system using the electrical impedance con- coronary sinus) or a surface electrode serves as the reference.
cept for localization (J Electrocardiol. 1999;32 Suppl:7–12; The electrode position is averaged over 1 to 2 cardiac cycles to
Circulation. 1999 Mar 16;99 [10]:1312–7). The system allows reduce cyclic cardiac variation. However, because of the long
localization of the mapping and ablation catheters by mea- excursion of the respiratory cycle, eliminating respiratory
suring the characteristics of the local electromagnetic field by variations by averaging becomes impossible without compro-
the catheter electrodes while 3 small (≤300 μA) orthogonal mising the real-time localization and display.
Shown in Figure 3.9 is an anatomic map of the left atrium comprising 64 electrodes. The catheter is placed in the car-
in a patient with atrial fibrillation. The NavX system allows the diac chamber to be mapped, and its location and orientation
catheter position to be determined within an accuracy of 0.6 are derived by the electrical impedance method; the orthogo-
mm. The electroanatomic map is usually created by point-to- nal electric signals are detected by the ring electrodes proxi-
point mapping of the cardiac chamber, which requires an mal and distal to the multielectrode array. An inbuilt locator
electrophysiologically sustained and hemodynamically stable system also localizes the ablation catheter tip relative to the
arrhythmia, allowing individual point mapping on separate EnSite Array and is used to generate an accurate anatomic
arrhythmia cycles. However, NavX allows for real-time simul- endocardial model. The individual electrodes of the array
taneous electroanatomic acquisition from multiple conven- are electrically insulated with the exception of a 0.025-inch
tional electrophysiologic catheters (up to 12 catheters and 64 defect that allows them to function as unipolar sensors. The
electrodes). electrodes sense the far-field electrograms and feed these data
The EnSite NavX can be used with the EnSite Array into a multichannel recorder that amplifies the signals. The
noncontact mapping catheter, which is particularly use- system uses the inverse solution to the Laplace equation with
ful for mapping hemodynamically nonsustainable arrhyth- the boundary condition that describes how potentials at the
mias. The EnSite Verismo tool provides functionality to use endocardial boundary would appear at the individual elec-
preprocedural 2-dimensional CT or MRI data to generate trode locations, to formulate 3,360 virtual electrograms at the
3-dimensional spatial maps. The EnSite Fusion registration endocardial surface.
module is used for integration of these spatial maps with In addition to the mapping of the sustained atrial and
the conventional EnSite-generated electroanatomic maps ventricular arrhythmias, the EnSite Array noncontact map-
(Catheter ablation of cardiac arrhythmias: a practical approach. ping catheter can be used to map nonsustained or hemo-
Springer; c2006; www.sjmprofessional.com/Products/Intl/ dynamically unstable arrhythmias, because only a single
Mapping-and-Visualization/EnSite-System.aspx). electrophysiologic cardiac cycle is sufficient to formulate the
electroanatomic map. Moreover, multiple sequential electro-
physiologic cycles can be mapped to visualize the changes
NONCONTACT MAPPING in electrophysiologic characteristics, such as the activation
sequence, over time.
EnSite Array Shown in Figure 3.10 is a right atrial activation map cre-
ated using the noncontact EnSite Array catheter located
The EnSite Array noncontact mapping catheter (St. Jude within the right atrium during a single spontaneous prema-
Medical, Inc) was initially described as EnSite 3000 in 1998 ture atrial contraction (PAC). The earliest activation site can
(Circulation. 1998 Sep 1;98[9]:887–98). This is used with the be seen in the high lateral right atrium with the activation
EnSite NavX mapping system and facilitates sensing of the
electrogram signals from the whole cardiac chamber simul-
taneously. EnSite Array is a 9F catheter with an ellipsoid
7.6–mL balloon (18×40 mm) with a multielectrode array
Figure 3.10 Th is right atrial activation map was created using

a noncontact EnSite Array catheter located in the right atrium
during a single spontaneous premature atrial contraction.
Activation spreads out circumferentially from the earliest
site (arrows) in the high lateral right atrium. Left panel,
Figure 3.9 Anatomic map showing the posterior wall of the Anteroposterior view. Right panel, Right lateral view. Bottom
left atrium generated by point-to-point mapping using the NavX panel, The display for real surface and intracardiac electrograms
system. The red dots indicate where wide area circumferential and the deduced electrograms at virtual sites created by EnSite
ablation was performed around the right- and left-side pulmonary Array. CSO indicates coronary sinus ostium; IVC, inferior vena
veins and along the roof and the mitral isthmus line. cava SVC, superior vena cava; TV, tricuspid valve.
wave front spreading out centrifugally. This site of the symp- reference catheters are equipped with 4 ultrasound transduc-
tomatic monomorphic PACs was successfully ablated. ers, and the ablation-mapping catheter has 3 transducers.
The disadvantages of the noncontact mapping array The ultrasound transmitter sends a continuous cycle
include the inaccuracies of the map compared with the of ultrasound pulses at 558.5 kHz to the transducers of all
results of contact mapping, especially as the distance of the 3 catheters. The time delay between the transmitters and
endocardial surface mapped increases beyond 3 to 4 mm receivers is proportional to the distance between the trans-
(Circulation. 1998 Sep 1;98 [9]:887–98). Mapping of large ducers, assuming a constant speed of sound in blood of 1,550
chambers, eg, a large left ventricle, requires repositioning of m/s. This time delay information is used by the computer to
the multielectrode array to collect adequate data with some display real-time 3-dimensional information, and the cath-
accuracy. Conversely, in small areas under electrophysiologic eter positions are used to reconstruct the endocardial map.
study and intervention, the substantial volume of the array The RPM reference system is all internal, with no exter-
limits mobility of ablation and other catheters. Additionally, nal skin electrodes or patches, and interference by respiratory
weak electrograms might not create adequate far-field signals incursions and patient movement is reduced. By corollary,
to be picked up by the array, and mapping is complicated in during mapping this system requires 3 internal catheters in
areas with simultaneous atrial and ventricular far-field com- stable positions for spatial reference. The use of an ultrasound
ponents (Catheter ablation of cardiac arrhythmias. Saunders/ signal for localization limits the use of intracardiac ultra-
Elsevier; c2006; www.sjmprofessional.com/Products/Intl/ sound imaging during procedures.
Mapping-and-Visualization/EnSite-System.aspx).
MAGNETIC NAVIGATION SYSTEM

ULTRASOUND-BASED CATHETER
LOCALIZATION Niobe Magnetic Navigation System
Ultrasound-based electroanatomic mapping systems use Magnetic navigation technology began with a 1991 report
the concept of a relatively fi xed speed of an ultrasound pulse of catheter navigation in a neonate and has since evolved in
through blood within the heart, emitted and detected by ultra- the field of neurosurgery followed by cardiology (Cathet
sound transducers on intracardiac catheters to determine the Cardiovasc Diagn. 1991 Apr;22[4]:317–9; J Neurosurg. 2000
distances between them on the basis of time delay informa- Aug;93[2]:282–8; Med Klin [Munich] 2001 Dec 15;96[12]:
tion. This information is used to triangulate the spatial loca- 708–12). The Niobe Magnetic Navigation System (Stereotaxis,
tion of the catheters relative to each other, and manipulation St. Louis, Missouri), which can be used with the Carto RMT
of the mapping catheter on the endocardial surface is then electroanatomic mapping system and the Ensite NavX system,
used to generate the anatomic map. allows the navigation and positioning of the mapping-ablation
catheter within a cardiac chamber using energy from a mag-
Real-Time Position Management netic field. The computer-controlled catheter advancement
(RPM) System system allows remote catheter navigation without manual
manipulation. The catheter can be precisely advanced or
The Real-time Position Management (RPM) System (Boston retracted by 1-mm steps and oriented by 1° rotations controlled
Scientific, Natick, Massachusetts), initially described in 2000, through a workstation. Two magnets on either side of the table
is the first system that uses real-time ultrasound-based cath- create a uniform magnetic field of 0.08 T. A computer controls
eter localization for electroanatomic mapping (J Cardiovasc the direction of the magnetic field by changing the orientation
Electrophysiol. 2000 Nov;11[11]:1183–92). This system has the of the magnets relative to each other. The mapping-ablation
capability to simultaneously process 7 position management catheter has a magnet at the tip that aligns with the external
catheters and has 48 electrogram channels, in addition to a magnetic field. The catheter can thus be steered by a computer
12-lead surface electrocardiogram and 2 pressure channels. The algorithm by maneuvering the orientation of the magnetic
system is composed of a series of ultrasound transducers that field. All applied magnetic vectors can be stored and then reap-
transmit and receive ultrasound pulses on reference catheters. plied if necessary to repeat the procedure.
The system includes 3 proprietary, single-use intracardiac The advantages of this system are the absence of radiologic
catheters (Boston Scientific), 2 reference catheters, and 1 cath- exposure to the operator and minimal fluoroscopic exposure
eter for mapping and ablation. The first reference catheter is a for the patient, the ability to renavigate to a previously ablated
6F catheter placed in the right ventricle and has three 1-mm site using the stored magnetic field vector without fluoroscopy,
ring electrodes and one 4-mm tip electrode. The second ref- and improved stability and maneuverability during ablation.
erence catheter is also a 6F catheter placed in the right atrial
appendage, the lateral right atrium, or the coronary sinus and Sensei X Robotic Catheter System
has nine 1-mm ring electrodes and one 2-mm tip electrode
with 1-mm interelectrode distance. The ablation catheter is The Sensei X Robotic Catheter System (Hansen Medical,
a 7F bidirectionally steerable catheter with a 4-mm tip. The Inc, Mountain View, California) is a purely robotic catheter
control system that combines the EnSite mapping system for these systems has been to keep a log of and make manageable
3-dimensional localization, navigation, and generation of and interpretable the vast amount of information obtained
electroanatomic maps with computer-mediated robot-assisted during an electrophysiology study. These systems have made
control of an extended control catheter (Artisan Extend; possible the extensive intracardiac mapping that can now
Hansen Medical, Inc). The operator hand motion ensures be performed and applied during electrophysiologic proce-
accurate catheter manipulation. The capability to integrate dures. This enhanced mapping capability has been especially
tactile feedback has also been added by using a pressure sen- useful in the treatment of complex arrhythmias that require
sor at the catheter tip. extensive ablations in the cardiac chambers, eg, atrial fibril-
lation and ventricular arrhythmias. When used and applied
appropriately, these electroanatomic mapping systems can
SUMMARY portray the physiologic characteristics of the arrhythmia and
display the ablation points in 3 dimensions. They have also
The past 15 years have seen tremendous progress in the field of reduced the fluoroscopic exposure, and the most advanced
invasive interventional electrophysiology with catheter-based systems aim to eliminate the need for radiation exposure.
ablation for treatment of the usual arrhythmias as well as Further advancement in interventional electrophysiol-
those that are complicated and recalcitrant. This progress has ogy is intertwined with improvement in imaging technology.
occurred in part as a result of the simultaneous technologic Inexact input of data into the system and failure to appreciate
advancements in electrophysiologic catheters and mapping the requirements of the system specific to the physiology of
systems that facilitate the input and integration of complex the arrhythmia can magnify errors. As a first step, an under-
electrophysiologic and spatial signals from the catheter tips. standing of the technology involved with mapping systems
The electroanatomic maps that are generated using such tech- currently in use is needed and provided as an overview in this
nology have serious pitfalls inherent in the use of data from a chapter. In the accompanying illustrated examples are pre-
limited number of spatial points, the need for operator-driven sented the decision-making process and nuances of the map-
selection of reference electrograms, the fiduciary point, the ping systems.
signal window and arrhythmic beats to feed the map, as well
as the computer-inferred interpolation of the unassessed spa-
tial geometry. The inexperienced user can both misinform ABBREVIATIONS
and misinterpret the maps that are generated.
Independent of these limitations, the accuracy of localiza- CABG, coronary artery bypass graft
tion of ablation catheters based on the electroanatomic map- CPU, central processing unit
ping system needs further validation. Also, the diagnosis and CT, computed tomographic
localization of the ablation zone for successful arrhythmia LCC, left coronary cusp
resolution requires good conceptual understanding of the MRI, magnetic resonance imaging
physiologic characteristics of arrhythmia as well as familiarity PAC, premature atrial contraction
with the pitfalls in these procedures that cannot be replaced PVC, premature ventricular contraction
with modern electroanatomic mapping systems. The role of RPM, Real-Time Position Management
4
Diagnostic Maneuvers Commonly Used in the
Electrophysiology Laboratory: Understanding the
Rationale, Techniques, and Interpretation
Samuel J. Asirvatham , MD
INTRODUCTION Other maneuvers are performed when the patient is not

in tachycardia, primarily to assess the nature of the electrical
Among the keys to successful ablation are the correct interpre- connection between the atria and ventricles (atrioventricular
tation and thorough understanding of maneuvers commonly [AV] node, accessory pathway, or both).
applied in the electrophysiology laboratory. Throughout As a general rule, with narrow complex tachycardia, most
this textbook, these maneuvers appear integrated in cases information is obtained by placing sensed premature ven-
and in several of the other chapters. This chapter focuses tricular contractions (PVCs) during tachycardia, while with
on the maneuvers themselves rather than their particular a wide QRS tachycardia, sensed premature atrial contrac-
applications in given cases. The rationale for each maneu- tions (PACs) were placed, and the response was analyzed to
ver is described in some detail to allow the reader to antici- yield a great deal of information on the mechanism of these
pate and fully understand situations where the results from arrhythmias. When the patient is not in tachycardia, decre-
these maneuvers can be universally applied and to recognize mental pacing, differential pacing, parahisian pacing, and
exceptional circumstances. It should be apparent, after going related maneuvers usually allow quick recognition of the
through this chapter, that no single maneuver can be relied nature of conduction between the atria and ventricles. Other
on to be diagnostic of a particular arrhythmia or solely used specific maneuvers discussed in this chapter include diagnos-
to guide ablation. Important exceptions to the rules for these tic techniques for junctional tachycardia, maneuvers specifi-
maneuvers have to be kept in mind to fully evaluate a dif- cally related to the exact delineation of accessory pathways,
ficult case. Most often, however, when correctly applied and and analysis of variation in cycle lengths during tachycardia
in an appropriate sequence, a few of the described maneuvers (wobble).
quickly allow the ablationist to reach a diagnosis with near Specifically not discussed here but discussed elsewhere in
certainty. this book are the important electrophysiologic maneuvers
When a patient presents with tachypalpitation and a of entrainment mapping and delineation of pulmonary vein
diagnostic electrocardiogram (ECG) is obtained, much can potentials (Chapter 5).
be learned from the nature of the QRS complex and the Box 4.1 outlines the commonly used maneuvers in the
relationship of the QRS and P waves and is discussed fur- electrophysiology laboratory. Several maneuvers that are
ther in Chapter 6 as well as numerous examples in the case useful in narrow QRS tachycardia can also be used in wide
discussions throughout this book. In the electrophysiology QRS tachycardia. For example, a patient may have an anti-
laboratory, when tachycardia is induced, electrophysiology dromic reentrant tachycardia, but the retrograde activation
maneuvers are performed to perturb the circuit. The elec- to the atrium may have to be differentiated between AV node
trophysiologist then proceeds to interpret the sequelae of or another retrograde conducting accessory pathway. Thus,
these perturbations and from this information deduces the while the maneuvers described for wide QRS tachycardia may
mechanism of the tachycardia and predicts the successful site define the mechanism of antegrade conduction, maneuvers
of ablation. Even experienced ablationists continue to be fas- typically used for narrow QRS tachycardia need to be per-
cinated by the precision and logic that underlie these simple formed to understand retrograde conduction. Generally, the
maneuvers. electrophysiologist starts with the maneuvers most useful
for the type of arrhythmia (narrow QRS or wide QRS) and
Abbreviations are expanded at the end of this chapter. comes to an initial conclusion. If the information obtained is
85
of the arrhythmia. Subsequent observations analyze whether

Box 4.1 the tachycardia has been reset.
Maneuvers in the Electrophysiology Laboratory A typical example of this maneuver is illustrated in
Narrow QRS tachycardia Figure 4.1. The tachycardia cycle length is 340 ms. A sensed
Premature ventricular contractions during tachycardia PVC is placed shorter than the cycle length of the tachycardia.
Parahisian pacing
The PVC has been placed after the appearance of the ante-
Retrograde right bundle branch block
Morady maneuver grade His bundle deflection. The atrial electrogram following
Decremental pacing the sensed PVC is advanced by 25 ms. The PVC could not
Differential pacing have preexcited the atrium via the AV node as the antegrade
Wide QRS tachycardia His deflection rate is unchanged. Thus, a sensed PVC is deliv-
Premature atrial contractions during tachycardia
ered at the time of His bundle refractoriness and preexcites
Atrial pacing to entrain
Decremental atrial pacing the atrium.
Differential atrial pacing At this point, the only observation is that an accessory
Junctional tachycardia pathway is present, and it is not known whether the pathway
Pathway-related maneuvers participates in the tachycardia. The next step is to analyze the
Pathway potential
retrograde activation sequence. In this example, the retro-
Slant
Entrainment grade sequence is unchanged. If a change is noted, then an
accessory pathway is likely to be present, but it is unlikely that
it is one of several V-A connections responsible for the mech-
anism of the tachycardia (bystander pathway). Even if the ret-
not classical and multiple pathologies (pathway-to-pathway rograde activation sequence is unchanged, however, in order
tachycardia, bystander pathway, etc) are suspected, then a to demonstrate that the accessory pathway clearly partici-
more complete evaluation involving nearly all the described pates in the tachycardia, the subsequent A-H, A-V, and A-A
maneuvers is necessary in these exceptionally challenging intervals must be analyzed (reset). In Figure 4.1, after the pre-
situations. excited atrial activation, the A-H interval and the subsequent
A-A interval are increased. This effect on subsequent intracar-
diac intervals is termed resetting of the tachycardia. The initial
NARROW QRS TACHYCARDIA A is advanced, which gives rise to subsequent perturbations
in the circuit that increase the A-H interval and subsequently
The 3 principal causes of a narrow QRS tachycardia are atrial increase the next A-A interval. It is equally important to look
tachycardia, orthodromic AV reentrant tachycardia, and AV for both decrease and increase in the intracardiac intervals
nodal reentrant tachycardia. Most of the designed maneuvers following placement of a sensed PVC (Box 4.2).
are specifically used to distinguish between these 3 entities. The key difficulty with this maneuver occurs when a nega-
Much rarer are junctional tachycardias and relatively narrow tive result is obtained; that is, the sensed PVC does not pre-
QRS ventricular tachycardias that are discussed separately. excite the atrium. This situation poses 2 possibilities: either
Although these maneuvers are discussed sequentially, an accessory pathway is not present or the PVC has not been
there is no particular preferred order to perform them in delivered sufficiently early to penetrate the circuit (left free
the electrophysiology laboratory. For example, if tachycar- wall pathway, AV node reentry, decrementally conducting
dia has been induced, one might proceed directly to place retrograde pathway). Thus, PVCs with progressively shorter
sensed PVCs or perform entrainment of the arrhythmia coupling intervals have to be placed. The PVCs occur before
from the ventricle. If there is difficulty inducing the arrhyth- the anticipated antegrade His bundle electrogram, and it
mia initially as part of the routine electrophysiologic study, becomes difficult to know when the atrium is preexcited
parahisian pacing or induction of right bundle branch block and whether the early atrial activation has occurred via the
with ventricular extrastimuli may be performed first. In the AV node or an accessory pathway. To solve this difficulty,
interest of simplicity and common usage in this chapter, the 2 approaches are used in practice. The first is the use of the
commonly used maneuver of ventricular pacing to entrain a preexcitation index (Figure 4.2), and the second is analysis of
supraventricular tachycardia and analyze the effects of cessa- the retrograde His bundle deflection.
tion of pacing is referred to as the Morady maneuver. Retrograde His bundle deflection, described more than
Placement of sensed PVCs during narrow QRS tachycardia 2 decades ago, aims to tease out the retrograde limb of the
is a relatively simple maneuver to perform but may be among circuit by using the fact that the AV node is more difficult to
the most challenging to interpret. The essential principle is penetrate in a retrograde manner than most accessory path-
that during narrow QRS tachycardia, a sensed PVC of vary- ways. Progressively shorter coupled PVCs are placed during
ing coupling interval to the QRS is placed during tachycardia. tachycardia until the retrograde atrium has advanced by at
Observations are then made as to whether the atrial electro- least 10 ms. The extent of preexcitation, that is, the longest
gram is advanced as a result of the PVC and, if so, whether coupling interval for the PVC for the longest coupled PVC
this has occurred with a change in the activation sequence that can preexcite the atrium, is subtracted from the cycle
4. Diagnostic Maneuvers Commonly Used in the Electrophysiology Laboratory 87
II
V1
340 ms 315 ms
RA
H H H
HIS
CS PROX
CS MID
CS DIST
RV
Figure 4.1 Placement of sensed premature ventricular contractions (PVCs) during narrow QRS tachycardia. The PVC is placed after the
appearance of the antegrade His bundle deflection (H and arrow).
length of tachycardia (tachycardia cycle length minus cou- In all 3 common causes of supraventricular tachycardia,
pling interval for PVC) and yields the preexcitation index. antegrade conduction occurs via the AV node. In order for a
The higher the number for the preexcitation index, the shorter PVC to penetrate the atrium via the AV node during AV node
the coupling of a PVC is required to penetrate the circuit and reentry, very short coupling intervals (higher preexcitation
reset the tachycardia. index) are required to reset the tachycardia (Box 4.3).
Box 4.2
Pearls and Pitfalls Placing PVCs During Tachycardia
General considerations
1. Avoid placing PVCs from the right ventricular apex.
2. Carefully analyze the activation sequence in addition to checking if the retrograde A is advanced.
3. Changes in activation sequence imply fusion with more than 1 way to get from V to A.
4. Carefully analyze the His bundle electrogram before and after placing a sensed PVC.
Primary considerations when placing PVCs during narrow complex tachycardia
1. A PVC placed during narrow QRS tachycardia at the time of His bundle refractoriness that advances the retrograde atrial electrogram
without changing the activation sequence and resets the tachycardia is diagnostic of an accessory pathway–mediated tachycardia.
2. A PVC placed during tachycardia that postexcites (delays) the atrium is diagnostic of an accessory pathway–mediated tachycardia.
3. A PVC placed during tachycardia at the time of His bundle refractoriness that terminates the tachycardia without an atrial electrogram
is diagnostic of an accessory pathway–mediated tachycardia.
4. A PVC placed during narrow QRS tachycardia that preexcites the atrium only by preexciting the retrograde His bundle electrogram by
an amount greater than or equal to the preexcitation of the atrium, without a change in activation sequence, and resets the tachycardia
is diagnostic of AVNRT.
Abbreviations: AVNRT, atrioventricular nodal reentrant tachycardia; PVC, premature ventricular contraction.
120 PI=108 numbers that help distinguish one mechanism from another
have not been established in a large series.
100 PI=88 Perhaps a more precise interpretation of the data derived
80 from this maneuver occurs with analysis of the retrograde
His bundle deflection and the relationship between the extent
PI, ms
60 of preexcitation of the retrograde His bundle and the retro-

PI=38 grade atrial activation. When pacing from the right ventricu-
40
lar apex, it is very difficult to see the retrograde His bundle
20 PI=17 electrogram. At the level of the His bundle catheter (site A
in Figure 4.3), the ventricular wave front and the wave front
0 through the right bundle to the His bundle occur nearly
LFW PS AS AVNRT simultaneously.
n=20 n=21 n=7 n=3
If the ventricle is paced closer to the base of the heart (site
Figure 4.2 Preexcitation index (PI) in milliseconds. AS indicates A in Figure 4.4), then because of the insulation of the His
anteroseptal; AVNRT, atrioventricular nodal reentrant tachycardia; bundle and proximal right bundle branch, ventricular and
LFW, left free wall; PS, posteroseptal. (Data from Miles WM, His bundle activation occur independent of each other. Thus,
Yee R, Klein GJ, Zipes DP, Prystowsky EN. The preexcitation
the ventricular electrograms occur at the onset of pacing, but
index: an aid in determining the mechanism of supraventricular
tachycardia and localizing accessory pathways. Circulation. 1986
to activate the His, the ventricular wave front has to travel
Sep;74[3]:493–500.) to the entrance of the right bundle closer to the apex and
then up the right bundle and activate the His, giving rise to a
separation in the V and His electrograms. This anatomic fact
Although this technique can be beneficial, in many cases, can be used when placing PVCs during tachycardia; if they
limitations must be recognized. First, the initial studies were are placed at the base of the heart, the retrograde His bundle
done in a small number of patients with few decrementally deflection can be analyzed more readily.
conducting pathways or atypical AV node reentry. Second, When progressively shorter coupled PVCs need to be
the maneuver is not directly useful in identifying the type placed to preexcite the atrium, if the PVC has been placed
of AV node reentry or atrial tachycardia. Third, the ease of when the antegrade His bundle electrogram is seen (His
preexciting the atrium can vary with the site of ventricular bundle refractoriness), then no further detailed analysis
pacing and the presence or absence of left bundle branch is required. However, if very early PVCs are placed and the
block. For example, during orthodromic tachycardia PVC has been placed closer to the base of the heart, then
using a left-sided accessory pathway, if left bundle branch the retrograde His bundle deflection should be analyzed. If
block is present, the tachycardia circuit itself uses the the retrograde atrial electrogram is advanced to an amount
right interventricular septum. Thus, pacing from the right greater than the advancement of the retrograde His bundle
ventricular septum can preexcite the atrium with relative ease electrogram, an accessory pathway must be present. Without
compared with preexcitation when left bundle branch block advancing the retrograde His bundle electrogram, the AV
is not present (the pacing site is within the circuit). Finally, node cannot have been penetrated. If the PVC advances the
as with any arbitrary definition of mechanism, the exact retrograde A only when the retrograde His has been advanced
by an amount up to the extent of preexcitation of the A, then it
is highly likely that the retrograde limb of the circuit is the AV
Box 4.3
node. It is important to remember that subsequent analysis of
Preexcitation Index
1. Measure of how short the coupling interval of the sensed
PVC needs to be to penetrate the circuit.
2. PI is equal to tachycardia cycle length minus the coupling
interval (S1−S2). VH A
3. PI < 100 ms rarely occurs with AVNRT.
4. PI < 45 ms usually occurs with septal accessory pathways. VA 90 ms
5. PI > 75 ms usually occurs with left free wall pathways or
AVNRT.
6. In the presence of left bundle branch block, PI gives results
with a left free wall pathway similar to septal accessory
pathways.
7. Important exceptions occur with retrograde decremental
accessory pathways.
Figure 4.3 Ventricular pacing at apex. The yellow line shows
Abbreviations: AVNRT, atrioventricular nodal reentrant tachycardia; pattern of activation when pacing from near the right ventricular
PI, preexcitation index; PVC, premature ventricular contraction. apex. The His bundle is buried within the ventricular electrogram
recorded in the His bundle region.
His bundle electrogram terminates an arrhythmia or postex-

cites the atrium (delays the next atrial electrogram), acces-
sory pathway–mediated tachycardia can be diagnosed, even
V H A
without subsequent analysis for resetting the tachycardia.
VA 110 ms When the PVC preexcites the atrium, it may do so by occur-
ring earlier than spontaneous AV node reentry for another
tachycardia that is responsible for atrial activation. However,
with postexcitation, a delay in reaching the atrium delays
tachycardia, which means that no other mechanism is opera-
tive (Table 4.1).
Figure 4.4 Ventricular pacing at base. Pacing now near the base of
A common scenario in which the interpretation of
the heart shows early ventricular activation and late His activation PVCs delivered in tachycardia can be difficult is shown in
since the wavefront (yellow lines) needs to travel from the base Figure 4.6. This is an example of long RP tachycardia with P
toward the apex and then enter the right bundle to retrograde waves that suggest early activation of the proximal coronary
activate the His. sinus or posterior left atrium. Here, a decrementally conduct-
ing accessory pathway (permanent junctional reciprocating
tachycardia [PJRT]), as well as atrial tachycardia and atypical
perturbations in tachycardia (resetting) have to be done to AV node reentry should be considered. It can be very difficult
know whether the diagnosed retrograde limb is responsible to preexcite the atrium because of the decremental nature of
for tachycardia or is a bystander. both PJRT-related pathways and the AV node (Figure 4.7).
An equally important principle is illustrated in Figure 4.5. Frequently, PVCs are seen to either postexcite the atrium
Here, a PVC is placed during an induced narrow complex or terminate tachycardia without an atrial electrogram and
tachycardia. The His-to-His interval is unchanged, and thus, can be among the most straightforward maneuvers to apply
the PVC has not penetrated the AV node, yet tachycardia in these otherwise difficult arrhythmias. This maneuver and
terminates. Delaying the atrial activation sequence and its analysis of the relationship of the retrograde His and preex-
extreme manifestation of terminating tachycardia without an cited retrograde A can be used to distinguish between the
atrial electrogram is an even more powerful observation than types of AV node reentry and between atrial tachycardia and
preexciting the atrium. If a PVC delivered at the time of His other causes of supraventricular tachycardia. If the retro-
refractoriness or a PVC that does not affect the retrograde grade atrial electrogram is advanced without a change in the
Figure 4.5 A premature ventricular contraction is placed during induced narrow complex tachycardia. Premature ventricular extrasystole
delivered at the time of His bundle refractoriness terminates the tachycardia without retrograde activation to the atrium.
Table 4.1 atrial tachycardia is almost certainly present. These observa-

AVNRT Diagnosis tions are illustrated in Figure 4.8 and are repeatedly referred
Effective PVC Placed During Diagnosis to and used in the case discussions.
Tachycardia
PVC resets tachycardia when His is AVNRT

PARAHISIAN PACING
refractory
PVC resets tachycardia by advancing AVNRT Parahisian pacing is among the most useful maneuvers in
the retrograde His by an equivalent
cardiac electrophysiology when dealing with difficult cases.
amount without change in the
Parahisian pacing is primarily designed to distinguish
activation sequence
between retrograde activation from the ventricle to the atrium
PVC resets tachycardia by advancing Bystander fast pathway
the retrograde His with a change or bystander accessory
via an accessory pathway or the AV node. Unlike several of
in the retrograde atrial activation pathway the other maneuvers described below that also help in mak-
sequence ing this distinction, parahisian pacing is unique in that the
PVC resets the atrium by advancing Typical AVNRT site of pacing, as well as the rate of pacing, has not changed
the retrograde His by 10 ms during the maneuver. This fact greatly reduces the number
PVC resets the atrium when the His is Atypical AV node reentry of inaccuracies associated with interpreting maneuvers in the
preexcited by ≥30 ms electrophysiology laboratory.
PVC advances the A by a greater AVRT The anatomic fact that underlies this maneuver is that
extent than advancing the the His bundle is an insulated structure that carries a sleeve
retrograde His without change in of annular fibrous tissue around it. Because of this, pacing
the activation sequence at relatively low output, even very close to the distal His
Abbreviations: AV, atrioventricular; AVNRT, atrioventricular nodal reentrant bundle, does not directly capture this His bundle but cap-
tachycardia; AVRT, atrioventricular reciprocating tachycardia; PVC, premature tures only the local ventricular myocardium. In order for the
ventricular contraction.
activation to reach the His bundle itself, propagation toward
the apex to the entrance site of the right bundle occurs, and
atrial activation sequence and the retrograde His is advanced then retrograde propagation from the distal right bundle
by an amount less than the amount that the A is advanced, toward the His bundle occurs. Thus, there is a long V-H
an accessory pathway is diagnosed. If the retrograde A can be interval, and if retrograde conduction to the atrium is via
advanced consistently during tachycardia by advancing the the AV node, there is a delay in conduction to the atrium.
retrograde His, AV nodal reentrant tachycardia is very likely. If high-output pacing is performed at the same site and
Because of the anatomic circuit differences between typical cycle length, particularly in the region of the proximal right
and atypical AV node reentry, it is easier to preexcite typi- bundle branch, direct capture of the His bundle (proximal
cal AV node reentry (fast pathway in line with His bundle), right bundle branch) occurs, and propagation from this site
and preexciting the retrograde His by as little as 10 ms often to the AV node and atrium occurs sooner than it does with
preexcites the retrograde A without a change in activation lower-output pacing.
sequence. Because of the presence of a lower common path- As depicted in Figure 4.9, the insulation around the
way and the orthogonal orientation of the slow pathway to the His bundle causes a delay in activation of the atrium with
His bundle, preexcitation of more than 25 ms is often required low-output pacing near the base of the heart close to the His
to preexcite atypical AV node reentry. If the retrograde His is bundle. If retrograde activation of the atrium is occurring via
preexcited by pacing the ventricle with 1 or more premature an accessory pathway, whether or not the His bundle is cap-
beats placed at the base of the heart by greater than 50 ms and tured, the activation time to the atrium remains the same.
yet the retrograde atrium is not advanced (or delayed), then Thus, if a difference in activation time to the atrium (longer at
Figure 4.6 The interpretation of premature ventricular contractions delivered in tachycardia can be difficult.
I
II
V1
RVA
A A No A
HRA
H H
HBE
PCS
MCS
DCS
Figure 4.7 The red arrow indicates the His bundle deflection prior to ventricular extrastimulus delivery.
low output and less at high output) is seen with parahisian sequence when the QRS interval is widened from loss of
pacing, retrograde activation is via the AV node. direct His bundle capture.
In the parahisian maneuver depicted in Figure 4.10 the Although it is commonly assumed that an eccentric coro-
first QRS complex is narrow, likely because of direct capture nary sinus activation sequence is diagnostic of an accessory
of the His bundle along with the ventricular myocardium. The pathway, sometimes, distal to proximal coronary sinus acti-
second QRS complex is wider because at lower-output pacing, vation can be seen in AV nodal reentrant tachycardia or with
only the local ventricular myocardium is captured. With loss ventricular pacing, even though retrograde activation is via
of the direct His bundle capture, the interval from the pacing the AV node (Figure 4.12).
stimulus to the atrial electrogram at any site (in Figure 4.10 Usually, activation can progress from the fast pathway
measured to the proximal His bundle catheter) is longer. This exit site to the proximal coronary sinus, but in patients
suggests that retrograde activation is via the AV node. who have functional conduction block near the eustachian
As explained above with regard to PVCs and tachycar- ridge, activation may require the left atrium to complete the
dia, it is important to analyze the retrograde atrial activation circuit and activate the musculature of the coronary sinus
sequence. If the atrial activation sequence has changed, then (Figure 4.13).
there is fusion between 2 different mechanisms to activate the If the primary coronary sinus to atrial connections occur
atrium from the ventricular pacing. Thus, if pacing at higher more distally, even with retrograde AV node activation, the
output from a parahisian site results in a shorter V-A interval earliest coronary sinus electrogram may be found in the dis-
without changing the activation sequence in the atrium when tal coronary sinus. Thus, an eccentric activation in the coro-
compared to pacing from the same site at the same rate at nary sinus may be seen, mistakenly giving the impression of
lower output, then retrograde conduction is entirely through an accessory pathway. Parahisian pacing, combined with the
the AV node. fact that the fast pathway site is earlier than the earliest distal
As illustrated in Figure 4.11, sometimes with the use of coronary sinus site, helps in diagnosing the correct AV node
isoproteronol or for other reasons that change autonomic mechanism for retrograde activation (Figure 4.14).
tone, the activation sequence of the atrium during ventricular In Figure 4.15, the coronary sinus activation is highly
pacing can change. If this occurs, parahisian pacing must be unusual, with apparent “bracketing” in the middle of the
repeated to confirm that the newly seen activation sequence coronary sinus. This pattern strongly suggests an accessory
is also entirely AV node dependent. Figure 4.11 shows a lon- pathway, but the parahisian maneuver illustrated shows that,
ger stimulus to A interval with no change in the activation with His bundle capture, the V-A interval is shorter, with no
PVC during SVT
Capture
Atrium advanced
Activation unchanged Activation changed
Retrograde Retrograde His Retrograde His Fusion

His not advanced advanced less than A + A advanced bystander
Retrograde His Retrograde His

AP
≤15 ms change 30-50 ms
Reset Typical Atypical

Not reset
tachycardia AVNRT AVNRT
AVRT Bystander AP
Atrium not advanced

Retrograde His advanced ≥50 ms
Atrial tachycardia
Figure 4.8 Summary of salient features and fi ndings with premature ventricular contraction (PVC) delivered during supraventricular
tachycardia (SVT). AP indicates accessory pathway; AVNRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular
reciprocating tachycardia.
change in the retrograde activation sequence, thus diagnos- As illustrated in Figure 4.17, the most powerful application
ing AV node dependence for retrograde activation. Also, in for this maneuver is in septal pathways. A distinct change
the second paced beat with the wider QRS interval, the retro- occurs in the ventricle to His activation time (15 ms to 70 ms),
grade His bundle deflection can be seen, giving further evi- but no change is seen in the activation sequence or the stimu-
dence that the His bundle has not been captured. lus to atrial electrogram interval diagnostic of a septal acces-
In the example shown in Figure 4.16, there is no change sory pathway. However, even with left lateral pathways or
in the stimulus to atrial electrogram interval, and there is no right lateral pathways, as long as pacing from the parahisian
change in the atrial activation sequence with and without His region conducts to the atrium with the activation sequence
bundle capture. This is diagnostic of a retrograde conducting being analyzed, parahisian pacing can be used to determine
accessory pathway. Also in this example the change in width whether that activation is AV node or accessory pathway
of the QRS (wider with second beat when His bundle is not dependent. As with any pacing maneuver, if the pathway con-
captured) and the “release” of the retrograde His bundle elec- duction is not manifest with pacing from that site, a poorly
trogram with the wider beats are notable (Box 4.4). conducting or remotely located accessory pathway can be
A common misconception with regard to parahisian pac- overlooked. Thus, as long as conduction through the path-
ing is that it is useful only for septal accessory pathways. way is seen, parahisian pacing can be applied as a maneuver
His
Insulation
Sinus node
Right bundle exit
AV
node
RV
Low-output pacing
(RV capture only)
High-output pacing
(RV and His capture)
Figure 4.9 The insulation around the His bundle delays activation of the atrium when pacing at low output near the base of the heart close
to the His bundle. AV indicates atrioventricular; RV, right ventricle.
Figure 4.10 The duration of the first QRS complex is shorter (175 ms) than that of the second QRS complex (203 ms).
Figure 4.11 A longer stimulus-to-A interval occurs with no change in activation sequence when the QRS interval is widened from 57 ms to
67 ms from loss of direct His bundle capture.
Figure 4.12 Eccentric activation noted in the coronary sinus during an arrhythmia with near-simultaneous ventricular and atrial
activation.
bundle capture is lost, are atrial sites dependent on AV node

activation, whereas sites that show no change in the stimulus
to atrial electrogram interval, even with loss of His bundle
capture, are sites that are activated via an accessory pathway.
As with any maneuver, parahisian pacing is associated with
some pitfalls that need to be avoided (Box 4.5). Sometimes,
high-output pacing, when performed too close to the annu-
lus, results in direct atrial capture and gives the mistaken
impression of earlier activation of the atrium with high-out-
put pacing (masking an accessory pathway). Similarly, at very
high-output pacing, direct capture of the contralateral bundle
(left bundle or left ventricular myocardium) can create earlier
activation via a left-sided pathway, with high-output pacing
giving a mistaken impression of retrograde AV node activa-
tion. If very proximal right bundle branch block is present,
then both high- and low-output pacing results in only ven-
tricular myocardial capture (wide QRS), and parahisian pac-
Figure 4.13 The yellow lines indicate activation proceeding from ing cannot be performed. A similar situation occurs when a
the fast pathway exit site. fasciculoventricular tract with retrograde conduction is pres-
ent. Because of the loss of insulation around the His bundle,
both high- and low-output pacing results in direct His bundle
to confirm or refute the possibility that this is an accessory capture, and a wide QRS is not seen again, negating the basic
pathway–mediated sequence. premise of parahisian pacing. Finally, in rare circumstances,
A second misconception with parahisian pacing is related direct capture of the His bundle may occur without capture
to changes in activation sequence in the atrium when pac- of the overlying ventricular myocardium. This is usually with
ing at high and low output. When the activation sequence small electrodes placed directly at the His–right bundle junc-
changes fusion between the AV node, an accessory pathway tion. Interpretation of the retrograde sequence, in this situ-
(or pathways) is present. This information can be used to ation, is difficult, and it is best to repeat the maneuver at a
identify the site of pathway activation. In other words, when slightly different location.
the activation sequence changes, with loss of His bundle cap- Figure 4.18 summarizes the features related to the correct
ture, some sites in the atrium have delayed activation while interpretation of the parahisian pacing maneuver. This algo-
others do not. The sites with delayed activation, when His rithm is referred to repeatedly in the case discussions.
INDUCTION OF RETROGRADE RIGHT

BUNDLE BRANCH BLOCK TO DIFFERENTIATE
RETROGRADE AV NODE AND ACCESSORY
PATHWAY CONDUCTION
Another maneuver, in some ways related to parahisian pac-

ing, that can be useful to diagnose the nature of retrograde
ventriculoatrial (VA) conduction is the induction of retro-
grade right bundle branch block. The underlying principle
behind this maneuver is that, with pacing from the ventricu-
lar apex, there is usually simultaneous activation of the His
bundle and ventricular myocardium at the base of the heart
(Figure 4.19). However, when placing a ventricular extrastim-
ulus at certain coupling intervals, retrograde right bundle
branch block occurs. Since ventricular myocardial activation
is unchanged, but the retrograde His bundle gets activated
after transseptal conduction and activation of the retrograde
Figure 4.14 The yellow lines indicate activation proceeding
from the fast pathway exit site. (Adapted from Asirvatham SJ.
left bundle, the V-H interval increases suddenly, as measured
Cardiac anatomic considerations in pediatric electrophysiology. near the His bundle. This usually is manifested as the sudden
Indian Pacing Electrophysiol J. 2008;8 [Suppl 1]:S75–S91. Used appearance of a clearly discernible His bundle electrogram.
with permission of Mayo Foundation for Medical Education and This fact, once appreciated, can be used to analyze the nature
Research.) of VA activation.
Figure 4.15 The coronary sinus activation is highly unusual with apparent bracketing in the middle of the coronary sinus. In the second
paced beat with the wider QRS interval (109 ms), the retrograde His bundle deflection can be seen, giving further evidence that the His
bundle has not been captured.
Figure 4.16 No change in the stimulus to atrial electrogram interval (174 ms to 175 ms) or the atrial activation sequence with and without
His bundle capture, which is diagnostic of a retrograde conducting accessory pathway.
Box 4.4 Box 4.5

Salient Features of Parahisian Pacing Pitfalls With Parahisian Pacing
Steps in parahisian pacing 1. Direct atrial capture
1. Pace at high and low output from near the proximal right 2. Proximal right-bundle branch block
bundle. 3. Fasciculoventricular tracts
2. Using the width of the QRS and the presence or absence of a 4. Direct left bundle or left ventricle capture
retrograde His bundle deflection ascertain which beats show 5. Very rapid intraventricular conduction
His bundle capture and ventricular myocardial capture and
which beats show ventricular myocardial capture alone.
3. Measure the stimulus to any atrial electrogram and com-
pare the same interval between beats with and without His but when retrograde right bundle branch block is induced,
bundle capture. there is a corresponding delay in getting to the atrium, show-
4. Analyze each atrial electrogram to look for changes in acti- ing that VA activation is via the AV node. Although obvious
vation sequence. similarities exist between this maneuver and parahisian pac-
ing (Table 4.2), important differences should be appreciated.
Because of the change in the rate of pacing (coupling interval)
If, with induction of retrograde right bundle branch block, with the retrograde right bundle branch block technique, a
the retrograde V-A interval increases to the extent of increase possibility of decremental conduction or block in an acces-
of the retrograde V-H interval, then retrograde activation sory pathway exists. Thus, this maneuver is useful only when
is via the AV node. If there is an increase in the retrograde there is continued VA conduction with a similar activation
V-H interval with no associated change in the V-A interval sequence. Despite this important limitation, however, in
(negative retrograde H-A interval), then an accessory path- cases where parahisian pacing is difficult to perform or when
way is present. Here again, the retrograde activation sequence the finding is seen during routine electrophysiologic testing,
must be analyzed, and if there is a change in the activation important information can be learned that could otherwise
sequence, then, as before with parahisian pacing, fusion with be difficult to obtain.
both AV node and pathway (or pathways) is present.
With routine electrophysiologic testing, retrograde right
MORADY MANEUVER
bundle branch block is frequently seen. In this example, there
is delay in atrial activation when there is delay in reaching the The Morady maneuver, along with PVCs placed in tachycar-
His bundle, showing that retrograde conduction is probably dia, is the one of the most useful and common techniques to
via the AV node (Figure 4.20). identify the tachycardia mechanism. During supraventricular
In Figure 4.21, there is eccentric activation of the coronary tachycardia, ventricular pacing is performed at a cycle length
sinus that is usually seen when an accessory pathway is present, slightly shorter than the cycle length of the tachycardia. After
ensuring ventricular capture, whether the atrial electrograms
are continuously advanced (entrainment of the tachycardia)
has to be determined. Once this determination is made,
ventricular pacing is stopped. The tracing is analyzed to see
whether the next ventricular electrogram is preceded by 2
atrial electrograms (V-A-A-V) or a single atrial electrogram
(V-A-V).
The utility of this maneuver in atrial tachycardia is illus-
trated in Figure 4.22. During atrial tachycardia, conduction to
the ventricle occurs via the AV node. Then, during tachycar-
dia, ventricular pacing at a shorter cycle length is performed.
Retrograde activation occurs to the atrium at the cycle length
of ventricular pacing. With most atrial tachycardias, there is
an abrupt change in the atrial activation sequence (an excep-
tion is if the site of origin of atrial tachycardia is at the AV
node exit site). After pacing for several beats, ventricular pac-
100 ms ing is terminated. Now, the last ventricular electrogram from
pacing is followed by an atrial electrogram that occurs from
Figure 4.17 Parahisian pacing. (Adapted from Hirao K, Otomo K,
Wang X, Beckman KJ, McClelland JH, Widman L, et al. Para- retrograde conduction to the atrium from that paced beat.
Hisian pacing: a new method for differentiating retrograde Following this, the next atrial electrogram results from the
conduction over an accessory AV pathway from conduction over atrial tachycardia focus, which then conducts to the ventricle
the AV node. Circulation. 1996 Sep 1;94[5]:1027–35. Used with via the AV node (V-A-A-V pattern on stopping ventricular
permission.) pacing). For this maneuver to be applicable, the tachycardia
High- and low-output pacing
Narrow QRS Wide QRS

V and His capture V capture
Activation Activation
sequence unchanged sequence changed
V-A V-A longer Fusion

unchanged with wide QRS
AP-dependent
AP AV node sites unchanged
Caveats: • Atrial capture • Left bundle capture

• His-only capture • Change with isoproterenol/rate
Figure 4.18 Algorithm for correct interpretation of the parahisian pacing maneuver. AP indicates accessory pathway; AV, atrioventricular.
should not be terminated by ventricular pacing but either electrogram is followed by the retrograde advanced atrial
entrained or transiently suppressed. electrogram, and then, because antegrade activation via the
In Figure 4.23, the use of this maneuver in AV nodal reen- slow pathway can still occur, that same advanced atrial elec-
trant tachycardia is illustrated. During AV node reentry (the trogram is followed by a ventricular electrogram as a result
slow-fast form is illustrated in this figure), activation of the of antegrade conduction via the slow pathway, AV node, and
ventricle is antegrade through the AV node. When ventricular His-Purkinje system (V-A-V pattern). The electrogram that
pacing is performed at a slightly faster rate than the tachycar- usually immediately follows the V-A electrograms is the His
dia, tachycardia is entrained, with the atrial activation occur- bundle deflection (V-A-H-V) sequence.
ring at the rate of ventricular pacing. There is no change in the The sequence observed with the Morady maneuver in
retrograde activation sequence, and the exit site to the atrium patients with orthodromic AV reciprocating tachycardia and,
in this example continues to be the retrograde fast pathway. in this instance, a left lateral accessory pathway is illustrated
When ventricular pacing is stopped, the last paced ventricular in Figure 4.24. During orthodromic reciprocating tachycardia
(ORT), antegrade activation is via the AV node to the ventri-
cle. Ventricular pacing at a cycle length shorter than the ORT
cycle length is performed. The tachycardia is not terminated
but continuously reset (entrained), with no change in the ret-
V H A rograde activation sequence and tachycardia occurring at the
ventricular pacing cycle length. On cessation of ventricular
VA 110 ms
pacing, the last paced ventricular electrogram is followed by
the last advanced atrial electrogram, and as it is possible for
this advanced atrial electrogram to reenter the ventricle via
the AV node, another ventricular electrogram follows (V-A-V
sequence). Again, with ORT (unlike most atrial tachycar-
dias), there is no change in the activation sequence, and the
Figure 4.19 Ventricular pacing at apex with right bundle branch last paced ventricular electrogram and the return ventricular
block. Arrows indicate wave fronts of activation. electrogram are separated by a single atrial electrogram.
Figure 4.20 There is delay in atrial activation when there is delay in reaching the His bundle, showing that retrograde conduction is
probably via the atrioventricular node.
Figure 4.21 Retrograde right bundle branch block with eccentric activation of the coronary sinus, usually seen when an accessory pathway
is present.
Table 4.2
Comparing Parahisian Pacing and Induction of Retrograde Right Bundle Branch Block in Distinguishing
Retrograde Atrioventricular Nodal From Accessory Pathway Conduction
Parahisian Pacing Retrograde RBBB
Pacing from same site Pacing from same site

Pacing at same cycle length Different cycle length and coupling interval
Different pacing output Same pacing output
Can be interpreted with change in activation sequence Best used when activation sequence unchanged
Cannot be performed if proximal RBBB present Can be performed with proximal RBBB
Can be performed with poorly conducting accessory pathways If the pathway blocks at shorter coupling interval, maneuver
cannot be performed
Abbreviation: RBBB, right bundle branch block.
Figure 4.25 is an example of AV nodal reentrant tachycar- conduction, the second atrial electrogram following the last
dia from the publication that first systematically analyzed this paced V is the last atrial electrogram advanced by the last
finding (J Am Coll Cardiol. 1999 Mar 1;33[3]:775–81). With paced ventricular beat. Thus, this is in fact a V-A-V pattern,
AV node reentry, the last paced ventricular beat is followed by as is illustrated in Figure 4.27. In the same patient, slower ven-
an atrial electrogram that is entrained by the ventricular pac- tricular pacing giving less VA decrement illustrates the true
ing and then a His bundle deflection followed by a ventricular pattern.
electrogram (V-A-H-V pattern). Other situations where the Morady maneuver must be
Figure 4.26 illustrates one of the pitfalls to avoid when per- interpreted with caution include suppression of atrial tachy-
forming a Morady maneuver. This patient had a decremen- cardia with pacing the ventricle too fast where a junctional
tally conducting retrograde pathway. Yet, on first glance, the escape on cessation of ventricular pacing may occur prior to
maneuver shows the last ventricular paced beat to be followed the return of the atrial tachycardia, giving rise to a V-A-V pat-
by 2 atrial electrograms and then the return ventricular beat tern despite the diagnosis of atrial tachycardia. Other difficult
(V-A-A-V pattern). However, because of the slow retrograde situations include atypical forms of AV node reentry where
Sinus
node
AV
node
V pacing
(...A-V)
Stop V pacing (V-A...)

Figure 4.22 The Morady maneuver in atrial tachycardia. AV indicates atrioventricular.
Sinus
node AV node
FP
SP
V pacing
(...V)

Figure 4.23 The Morady maneuver in atrioventricular nodal reentrant tachycardia. AV indicates atrioventricular; FP, fast pathway; SP,
slow pathway; V, ventricular.
Sinus
node AP
AV
node
V pacing
(...V)

Figure 4.24 The Morady maneuver in atrioventricular reentry tachycardia. AP indicates accessory pathway; AV, atrioventricular.
V1
II
A
HRA
V
HBE
S S
RVA
III
100 ms
Figure 4.25 Atrioventricular nodal reentry tachycardia, V-A-V response. (Adapted from Knight BP, Zivin A, Souza J, Flemming M,
Pelosi F, Goyal R, et al. A technique for the rapid diagnosis of atrial tachycardia in the electrophysiology laboratory. J Am Coll Cardiol.
1999 Mar 1;33[3]:775–81. Used with permission.)
Figure 4.26 Morady maneuver, V-A-V pattern.

Figure 4.27 Slower Morady maneuver, V-A-V pattern.
atrial activation occurs much before ventricular activation or Second, close attention must be paid to the retrograde acti-
even much before the His bundle deflection. These examples vation sequence because a pathway may block with a change
and their exceptions are described as part of several of the in activation sequence followed by decremental properties
ensuing case discussions. and eventual block in the AV node, giving rise to the mis-
Figure 4.28 summarizes the interpretation of the effect of taken impression that only retrograde AV nodal conduction
resetting supraventricular tachycardia with ventricular pac- was present. Third, considerable intraventricular or infra-
ing and then stopping pacing. hisian delay may occur with rapid ventricular pacing in some
patients. Thus, a type of gap phenomenon may manifest and
give an appearance of lack of decrement via AV nodal con-
DECREMENTAL PACING duction. Finally, rapid ventricular pacing may cause repeated
initiations of tachycardia, making it difficult to assess the
Decremental pacing from the ventricle to assess VA activa- nature of VA conduction.
tion is among the most common maneuvers performed in In Figure 4.29, a PVC coupled at 360 ms shows conduction
the electrophysiology laboratory. Although this maneuver is to the atrium with a VA interval of 112 ms. In Figure 4.30,
easy to perform, it is relatively nonspecific unless interpreted with the coupling interval shortened to 340 ms, the VA inter-
with great caution. The underlying premise is that retro- val increases to 129 ms, with no change in the retrograde atrial
grade AV nodal conduction exhibits decremental properties, activation sequence. While this finding is most consistent
whereas retrograde accessory pathways do not. Thus, ventric- with retrograde conduction via the AV node, the possibility
ular pacing shows early activation in the anteroseptal region of a decrementally conducting accessory pathway cannot be
consistent with either a retrograde accessory pathway or ret- excluded. With the observation that the activation sequence
rograde conduction via the AV node and fast pathway, but did not change, then when only 1 method of conducting from
with increasing the ventricular pacing rate, there is gradual the ventricle to atrium is present, there is no fusion. Further
decrement (delayed conduction) to the atrium. Unless the VA maneuvers are required to know whether that 1 sequence is an
sequence changes, retrograde conduction is assumed via the accessory pathway or the AV node. In Figures 4.29 and 4.30,
AV node. despite the bracketed sequence in the coronary sinus, the ear-
Several important caveats must be kept in mind. First, cer- liest atrial activation is in the His bundle catheter region, a
tain accessory pathways show retrograde decremental prop- finding consistent with retrograde fast pathway conduction
erties. At times, they exactly parallel the patterns seen with and a variable entrance into the coronary sinus, as explained
AV nodal conduction and decremental ventricular pacing. above. With the premature ventricular extrastimulus, there
Tachycardia continues
Tachycardia entrained
Stop pacing
V-A-A-V V-A-V
AVNRT
Atrial tachycardia
AVRT
But But
Atach suppressed Very long RP
V-A-V V-A-A-V
Pace slower Pace slower
Figure 4.28 Ventricular pacing during supraventricular tachycardia. Atach indicates atrial tachycardia; AVNRT, atrioventricular nodal
reentrant tachycardia; AVRT, atrioventricular reciprocating tachycardia; RP, R wave to P wave interval.
is no discernible retrograde His bundle electrogram. Thus, vs left ventricular pacing to distinguish left-sided accessory
retrograde right bundle branch block has not occurred. If ret- pathways from right-sided accessory pathways, and AV nodal
rograde right bundle branch block occurs and by increasing conduction and differential site right ventricular pacing.
the V-H interval the V-A interval is increased by a similar This chapter discusses differential site right ventricular pac-
amount, an accessory pathway can be excluded. This is the ing. Analogous inferences, including those of the limitations
fundamental difference between simple pacing at a shorter involved, can be made to the various other differential pacing
cycle length and specific induction of retrograde right bundle techniques. Many of these techniques are illustrated as part of
branch block. the case discussions elsewhere in this book.
The fundamental premise for differential site right ventric-
ular pacing is that accessory pathways tend to insert to the
DIFFERENTIAL PACING ventricle close to the annulus, whereas the entrance or exit
site for the right bundle branch is closer to the apex. Thus,
Differential pacing is also a common maneuver performed if retrograde conduction is via the AV node, pacing near the
in the electrophysiology laboratory and, like pacing at faster apex is likely to result in a shorter VA conduction time than
rates, must be interpreted carefully. Various forms of differ- pacing the right ventricle from the base (nearer the annulus).
ential pacing exist that include differential atrial site pacing Similarly, one would expect that if retrograde VA conduction
to deduce whether antegrade conduction is via an accessory is via an accessory pathway, then pacing the right ventricle
pathway or AV node, differential atrial site pacing to identify near the base (closer to the pathway) results in a shorter VA
the site of the atrial insertion of an accessory pathway, right conduction time than pacing from the apex.
Figure 4.29 Ventricular extrastimulus with prolongation in the retrograde ventriculoatrial activation time.
The top panel of Figure 4.31 shows pacing from the right between the ventricular electrogram and the retrograde His
ventricular apex (site C). As noted previously, because of the bundle electrogram, as seen with a catheter at the His bun-
near-simultaneous propagation of the ventricular wave front dle (site A). In the bottom panel, however, pacing at about
toward the annulus and via the right bundle and the conduc- two-thirds the distance to the apex is closer to the entrance of
tion system wave front toward the His bundle, there is fusion the right bundle, and the VA conduction time is less than that
Figure 4.30 Ventricular extrastimulus with prolongation in the retrograde ventriculoatrial activation time.
the shortest V-A interval occurs when pacing closer to the

apex. Several important caveats must be kept in mind.
VH A 1. The entrance site for the right bundle is variable and
VA 90 ms may be at the true apex, at the moderator band exit on
the lateral wall of the right ventricle, or relatively closer
to the base at the mid septal region. Thus, if a more
proximal than usual site for a right bundle exit exists
and if when attempting to pace at the base one is forced
to move slightly further into the ventricle to obtain
stable capture (a frequent occurrence), then equivocal
findings result from the maneuver.
2. There can be significant variation in the ventricular
HV A insertion site of an accessory pathway. Sometimes, the
ventricular insertion of an accessory pathway may be fur-
VA 70 ms ther into the ventricle (Ebstein anomaly), and in addition,
even a pathway with an annular insertion may be rela-
tively far from a basal pacing site. For example, a posterior
lateral accessory pathway may be further away from an
anterior basal site for pacing than the entrance site for the
right bundle, again giving rise to equivocal results.
Figure 4.31 Top panel, Ventricular pacing at the apex. Bottom 3. When a fasciculoventricular tract that conducts in
panel, Ventricular pacing at mid septum. A shows pacing from the retrograde direction is present, pacing at the site
site B near the right bundle exit. Yellow lines indicate patterns of of the fasciculoventricular tract (usually closer to the
activation. base) results in a shorter V-A interval than pacing at
the apex, even though with these tracts, conduction to
the atrium is via the AV node and not a true accessory
at the true right ventricular apex. The retrograde conduction
pathway. Thus, while differential site pacing is useful,
to the His bundle is favored, and the retrograde His bundle
it is best used in conjunction with other maneuvers,
deflection occurs prior to the local ventricular electrogram at
as described above, to differentiate conduction via an
the base (site A).
accessory pathway and the AV node.
Figure 4.32 reillustrates the point that pacing near the His
bundle without actually capturing the His bundle results in In the examples shown in Figures 4.33 and 4.34, an accessory
a long V-H interval and a long V-A interval when conduc- pathway is likely responsible for VA conduction. The VA conduc-
tion from ventricle to atrium is via the AV node. If an acces- tion time is longer when pacing from the right ventricular apex
sory pathway has its ventricular insertion near the annulus, than pacing from the right ventricular base, without a change in
pacing at site A results in a short V-A interval. As seen on the activation sequence. This patient, however, had retrograde
Figures 4.31 and 4.32, however, with retrograde AV nodal conduction via the AV node shown clearly with parahisian pac-
conduction, the true shortest V-A interval occurs when pacing as well as other maneuvers. The reason for this paradoxical
ing is close to the right bundle entrance, not necessarily the finding is that the RV apical pacing catheter was placed deep in
apex. Thus, the generalization is that with retrograde acces- the apex, and the patient had a previous myocardial ischemic
sory pathway conduction, the V-A interval is shortest when event that probably slowed conduction from the true apex to the
pacing at the base, and with retrograde AV nodal conduction, right bundle entrance, thus making it easier to get to the right
bundle entrance from sites that were relatively close to the base.
Therefore, whenever varying the pacing site or pacing rate, vari-
ous factors, including myocardial conduction velocities, need to
be considered when making a judgment regarding the nature
V H A of VA conduction. Thus, the value of a maneuver such as para-
VA 110 ms
hisian pacing can be interpreted without such considerations,
as neither the pacing rate nor the pacing site is changed when
performing the maneuver.
WOBBLE
Figure 4.32 Pacing from the base of the heart (A). The yellow Wobble, or spontaneous variation in the cycle length of a
arrows indicate the pattern of activation. tachycardia, frequently occurs when attempting to perform
Figure 4.33 Pacing at the right ventricular base.
various maneuvers. Although wobble is not a maneuver per arrhythmia, just prior to termination, when placing PVCs
se, important information regarding the mechanism of the or PACs into tachycardia, and when performing the Morady
arrhythmia can be determined with a careful and reasoned maneuver.
analysis of a wobbling arrhythmia. Changes in the cycle The key feature of analyzing wobble is trying to ascertain
length of the arrhythmia may be seen at the initiation of an the driver for the tachycardia. In other words, if there is a
Figure 4.34 Pacing at the right ventricular apex.

spontaneous variation in the A-A interval but a previous change in subsequent changes in other intracardiac intervals. If
in the A-H interval gave rise to the subsequent change in the changes in the A-H interval always result in changes in the
A-A interval, an AV node-dependent arrhythmia is present. If tachycardia cycle length, including the A-A interval, an AV
marked variations in the A-H interval are not associated with node-dependent arrhythmia is present. If a change in the
changes in the A-A interval, then an atrial tachycardia is likely. H-V interval or intraventricular conduction interval (V-V)
Figure 4.35 shows a significant change in the A-A interval with affects the subsequent A-A interval in the context of a nar-
a consistent finding that shortening of the A-H interval in the row complex supraventricular tachycardia, orthodromic AV
prior beat causes shortening of the A-A interval, and lengthen- reciprocating tachycardia can be diagnosed. This is because
ing of the A-H interval in the prior beat causes lengthening of among atrial tachycardia, AV node reentry, and orthodromic
the A-A interval. This would be an unusual finding for atrial AV reentrant tachycardia, only the latter has the infrahisian
tachycardia and suggests an AV node-dependent arrhythmia conduction tissue and ventricular myocardium as part of
such as AV node reentry or orthodromic AV reentrant tachy- its circuit. If the change in the His bundle to atrial electro-
cardia as the mechanism of the arrhythmia. gram interval results in subsequent changes in the atrial cycle
The first step in analyzing an arrhythmia that shows spon- length, then an AV nodal reentrant mechanism is highly
taneous cycle length variation is to identify a constant inter- likely because this finding suggests that the retrograde fast
val, that is, a constant A-A interval with marked changes in pathway is part of the tachycardia circuit. The principle find-
other intervals, suggesting an atrial tachycardia. Similarly, a ings useful in analyzing a wobbling arrhythmia are summa-
constant His bundle to His bundle interval, despite changes in rized in Table 4.3.
the A-A interval, is consistent with a junctional tachycardia.
A clearly fi xed interval (except in certain atrial tachycardias
and atrial flutters) is found rarely to allow this immediate WIDE QRS TACHYCARDIA
clarification of the nature of the arrhythmia.
The second step, when all intervals are changing, is to Chapter 6 discusses a detailed approach to the patient with
try to find the primary interval that, when changed, results wide QRS tachycardia. This chapter focuses on the main
Figure 4.35 Shortening of the A-H interval in the prior beat causes shortening of the A-A interval, and lengthening of the A-H interval in
the prior beat causes lengthening of the A-A interval.
Table 4.3
Importance of the Primary Interval Change That Drives Box 4.6
Subsequent Changes During Tachycardia Causes of Wide QRS Tachycardia
Drivera Likely Arrhythmia Wide QRS because of bundle branch block

AV node reentry
A-A interval Atrial tachycardia Orthodromic AV reentry
A-H interval AV node–dependent arrhythmia, Atrial tachycardia
either AVNRT or AVRT Junctional tachycardia
H-V interval AVRT Sinus tachycardia
Atrial flutter/fibrillation
V-V conduction interval If SVT, then AVRT
If VT, then not bundle branch reentry Wide QRS because of antegrade preexcitation
Preexcitation secondary to bystander accessory pathway
H-H interval If SVT, then likely junctional
AV node reentry
tachycardia Orthodromic AV reentry
If VT, then likely bundle branch Atrial tachycardia
reentry Junctional tachycardia
H-A interval AV node reentry Sinus tachycardia
Atrial flutter/fibrillation
Abbreviations: AV, atrioventricular; AVNRT, atrioventricular nodal reentrant
tachycardia; AVRT, atrioventricular reciprocating tachycardia; SVT, Pathway part of tachycardia circuit
supraventricular tachycardia; VT, ventricular tachycardia. Antidromic tachycardia
a
Either the constant interval during a changing tachycardia or the interval whose Mahaim-related tachycardia
change predicts subsequent changes in the tachycardia intervals. Pathway-to-pathway tachycardia
Others
maneuvers used in the electrophysiology laboratory aiding in Nodal ventricular tachycardia
the differential diagnosis of wide QRS tachycardias. The num- Nodal fascicular tachycardia
Ventricular tachycardia
ber of causes for a wide QRS tachycardia is much greater than
those for a narrow QRS tachycardia, making the differential Abbreviation: AV, atrioventricular.
diagnosis in these arrhythmias more difficult. A thorough
understanding of the common electrophysiology maneuvers
used in this setting simplifies and streamlines the approach
for patients with this condition. retrograde limb of the circuit and identify the exact nature of
All causes described for supraventricular tachycardia with the rhythm disorder.
a narrow QRS complex may present with a wide QRS tachy- Before using the maneuvers described below, it is worth-
cardia either because of coexisting bundle branch block or while analyzing the clinical situation and the electrocardio-
antegrade preexcitation. In addition to this diverse group of gram during tachycardia to try to narrow the differential
disorders, antidromic tachycardia, the various forms of ven- diagnosis.
tricular tachycardia, and certain unusual causes of a wide For example, in Figure 4.36, a wide QRS tachycardia is
QRS must be considered, including fasciculoventricular tract seen showing positive concordance at the precordial leads.
and nodal ventricular tracts. What this means is the first site to activate the ventricle is
The principal causes and a clinically useful classifica- close to the annulus on the left side of the heart. The entire
tion for wide QRS tachycardias are summarized in Box 4.6. wave front is moving toward the apical leads as well as lead
The electrophysiologist must have 2 goals in applying the V1 on the right side. This would effectively exclude either
relevant maneuvers in these patients. First, the cause of the right or left bundle branch block aberrancy as whether the
wide QRS must be identified; that is, is there preexcitation, right or left bundle is blocked. The bundle that conducts is
is there bundle branch block, or is it ventricular tachycardia? closer to the apex than the base. Thus, either an accessory
Second, once the first has been determined, the exact cause of pathway is responsible for the wide QRS or this arrhythmia is
the arrhythmia is determined. If a stepwise approach is not a ventricular tachycardia. If this were ventricular tachycardia,
taken, too many possibilities remain and can confuse even the then the site of origin is somewhere along the mitral annulus
most experienced electrophysiologist. The principal unique anterolaterally. If the patient has a structurally normal heart,
maneuvers in wide QRS tachycardia diagnosis are place- the anteroseptal mitral annulus would be an uncommon
ment of sensed PACs during the tachycardia and pacing the site for ventricular tachycardia, and while it still needs to be
atrium faster than the tachycardia to entrain the tachycardia excluded, this simple analysis allows the electrophysiologist
and then analyze the return beats after cessation of pacing. to hone in on accessory pathway conduction as the cause of
Usually with these 2 maneuvers completed, the cause of wide wide QRS. If this cause is quickly established with the maneu-
QRS and a great deal of information on the actual circuit are vers described above, the next determination is whether the
known. The job, however, is half fi nished at this point. As in pathway participates in the tachycardia. If this is also estab-
all patients with wide QRS tachycardia, maneuvers described lished fairly quickly, then the possibilities are antidromic
for a narrow QRS tachycardia must be used to analyze the tachycardia or pathway-to-pathway tachycardia. The nature
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure 4.36 Wide QRS tachycardia.
of retrograde conduction to the atrium is then determined, a lateral and a septal antegrade conducting accessory pathway
and by using the maneuvers described above under narrow or, in rare circumstances, distinguishing between a Mahaim
QRS tachycardia (parahisian pacing, PVCs during tachycar- fiber and a nodal ventricular tract (see Chapter 6). As with
dia, etc), retrograde activation is in fact identified as another PVCs in narrow QRS tachycardia, both late and early coupled
accessory pathway (if this is the case), and in a relatively short PACs are placed to also assess whether the excitable gap for
time, the ablationist has concluded that pathway-to-pathway the tachycardia is narrow (AV nodal reentrant tachycardia
tachycardia, generally considered a difficult diagnosis in the with bundle branch block) or wide antidromic tachycardia.
electrophysiology laboratory, is present. The next major step after placing the PACs and seeing
whether the ventricular electrograms are advanced is to
PACs Placed During Wide QRS Tachycardia analyze the ventricular activation sequence. As in many of
the other maneuvers described above, if the ventricular acti-
Just as one of the principal maneuvers for narrow QRS tachy- vation sequence changes, then the bystander phenomena
cardia is the placement of sensed PVCs during tachycar- should be considered, for example, ventricular tachycardia
dia, sensed PACs placed during wide QRS tachycardia are with a bystander antegrade accessory pathway or fusion from
extremely informative. Once the sensed PAC has been placed more than 1 method of getting from A to V (eg, 2 accessory
and capture ascertained, whether the ventricular electro- pathways or an accessory pathway and AV node).
grams have been advanced must be determined. If a sensed If the PAC that has been placed in tachycardia is seen to
PAC advances the ventricular electrograms, then it remains to capture and advance the V and not change the ventricular
be determined whether this was done via an accessory path- activation sequence, then the question is whether the ante-
way or through the AV node. In the case of placing PVCs in grade His has been advanced. A critical part of these cases is
narrow QRS tachycardia, an analogous determination is done to determine before placing the PACs whether the His bundle
by comparing the extent of advancement of retrograde A with deflection that is being recorded is antegrade or retrograde. As
retrograde His. In this inverse situation (with PACs in wide discussed elsewhere, using a multipolar, closely spaced cath-
QRS tachycardia), the question is whether the antegrade His eter that spans the His bundle and right bundle and pacing
is advanced. Because of the difficulty of knowing whether the the atrium more rapidly (further decrement to His suggests
His is antegrade or retrograde, the analysis must also include antegrade), no further change in A-H interval despite faster
whether the atrium near the AV node has been advanced. To pacing suggests retrograde His activation. If an antegrade His
do this effectively, the pacing site should not be near the atrial bundle electrogram is not present and the PAC with the char-
septum. Thus, when putting in PACs during tachycardia, it is acteristics just described does not advance the antegrade His,
critical to choose a pacing site on the free wall of either the yet was able to preexcite the tachycardia, then an accessory
right or the left atrium. In certain instances, septal vs later- pathway is the mechanism for getting the V. If the tachycar-
ally placed PACs may be compared to assess the ease of pre- dia is reset, then an antidromic tachycardia is present. If the
exciting tachycardia, for example, in distinguishing between tachycardia is not reset, then the accessory pathway is present
but is a bystander (eg, AV nodal reentrant tachycardia with change in the activation sequence by advancing the ante-
bystander accessory pathway). grade His, but the tachycardia is not reset. If, on the other
Because of the difficulty associated with knowing whether hand, a PAC advances the tachycardia by advancing the His
the His bundle electrogram is antegrade or retrograde, a use- but the A-H interval is found to be short, the His bundle may
ful observation is to look at whether the septal atrial elec- in fact be retrograde. For example, in an atriofascicular path-
trogram is advanced. If the assumption is to reach the His way (Mahaim), a PAC advances the V and may also advance
bundle, the atrium must be reached near the AV node. Thus, the His bundle–right bundle electrogram. However, the PAC
if a laterally placed PAC is found to advance the V but the sep- wave front travels toward the septum at about the same time
tal atrial electrogram is not advanced on the beat for the PAC, that the His bundle electrogram is being advanced, giving
then an accessory pathway is present. The septal A, however, rise to a short A-H interval.
may be advanced in the next beat from resetting of the tachy- Finally, if a PAC is placed and found to advance the V
cardia via retrograde conduction either through the AV node but the activation sequence changes and the His bundle
or septal accessory pathway. Thus, both analysis of the His electrogram has not been advanced, then a bystander acces-
bundle electrogram and the septal A is of paramount sig- sory pathway is present while the primary diagnosis is
nificance in the correct interpretation where PACs are placed probably ventricular tachycardia. If the His bundle is nec-
during wide QRS tachycardia. essarily advanced to advance the V with a change in acti-
A further utility to analyzing the septal atrial electro- vation sequence, then AV node conduction is present in the
gram is to differentiate between a laterally placed antegrade antegrade direction but is not associated with the tachycar-
conducting bypass tract like a Mahaim fiber and a nodoven- dia circuit. Here again, ventricular tachycardia is a strong
tricular tract. If the laterally placed PAC can preexcite a consideration although other rare possibilities, including
tachycardia only by preexciting the septal atrial electrogram pathway-to-pathway tachycardia with bystander AV node,
but without preexciting an antegrade His, then a nodoven- cannot be entirely excluded with this maneuver (but can be
tricular tract should be suspected because with a nodoven- differentiated with PVCs during tachycardia in addition to
tricular tract, atrial activation penetrates the AV node, the placing PACs during tachycardia).
His bundle is bypassed, and the ventricular myocardium is Figure 4.37 summarizes the salient findings and outlines
preexcited without preexciting the His. Because the nodoven- a stepwise approach to interpreting the maneuver of placing
tricular tract involves the compact AV node, the pathway PACs in wide QRS tachycardia.
shows decremental antegrade properties. On the other hand,
a septally placed atrioventricular bypass tract does not typi- Atrial Pacing to Entrain Wide QRS Tachycardia
cally show decremental properties. Since Mahaim fibers are
located more laterally (usually), a laterally placed PAC can The second most important maneuver to correctly identify
preexcite the tachycardia (or postexcite) without advancing the circuit responsible for wide QRS tachycardia is atrial
the septal atrial electrogram. There is no known maneuver pacing that entrains the tachycardia and then assessing the
that can distinguish between a very septal Mahaim fiber with sequence of atrial to ventricular activation on cessation of
a connection to the ventricular myocardium and a nodal ven- pacing (Box 4.7). Just as the placement of PACs in wide QRS
tricular tract. Some electrophysiologists question whether tachycardia is analogous to placing PVCs in narrow QRS
these 2 entities are truly different. tachycardia, this maneuver is, in some ways, the inverse of
If a PAC advances the V without changing the ventricular the Morady maneuver.
activation sequence and does so only by advancing the ante- After ascertaining capture of the atrium during atrial
grade His, then the cause for wide QRS is most likely from pacing at a cycle length slightly shorter (25–40 ms) than
bundle branch block. Now what needs to be determined is the the cycle length of the tachycardia, the tachycardia is being
nature of the supraventricular arrhythmia that is conducting continuously reset, that is, the ventricular electrograms are
with bundle branch block. While this is best done by plac- occurring at the atrial rate of pacing. Next, as with so many
ing PVCs and analyzing the data as described above under other maneuvers described, whether the activation sequence
narrow QRS tachycardia, useful clues may appear on further has changed must be assessed. If during atrial pacing the
analysis of the PAC placed during wide QRS rhythm. If the ventricular rate does increase to the atrial rate but the acti-
His needs to be advanced to advance the ventricular electro- vation sequence changes, ventricular tachycardia must be
gram and if the A-H interval with the PAC that advances the considered as the most likely possibility although conduc-
His and then the V is similar to the tachycardia, then it is tion via a bystander pathway or a bystander AV node remain
likely that an orthodromic AV reentrant tachycardia or AV possibilities. The electrogram sequence is analyzed when
nodal reentry tachycardia is present with bundle branch pacing is stopped. For the last paced beat, an atrial electro-
block. For this to be the diagnosis, the tachycardia needs to gram from pacing is present. If this conducts down to the
be reset. If the tachycardia is not reset, antegrade AV nodal ventricle and then before the next atrial electrogram occurs,
conduction is present; however, it serves as a bystander for another ventricular electrogram is seen with the activation
the tachycardia. For example, if a bundle branch reentrant sequence of the second ventricular electrogram identical to
tachycardia is present, a PAC may advance the V with no that of the tachycardia (A-V [changed activation sequence]-V
PAC in wide QRS tachycardia
A captured
V advanced
Activation sequence Activation sequence

unchanged changed
His advanced His unchanged His unchanged
Septal A Septal A not

A-H same A-H short advanced advanced Bystander
No ? Retrograde Nodo- ART

Reset reset His ventricular Mahaim His advanced
AVNRT By-
ORT stander VT
Figure 4.37 Stepwise approach to treating premature atrial contractions in wide QRS tachycardia. ART indicates antidromic reciprocating
tachycardia; AVNRT, atrioventricular nodal reentrant tachycardia; ORT, orthodromic reciprocating tachycardia; PAC, premature atrial
contraction; VT, ventricular tachycardia.
[identical activation sequence]-A), then ventricular tachycar-

Box 4.7 dia can be diagnosed.
Atrial Pacing to Entrain Wide QRS Tachycardia If, after pacing is stopped, the atrial electrogram from the
Ascertain capture last paced beat conducting to the ventricle shows no change
Confirm resetting of tachycardia in the activation sequence and a return electrogram to the
Assess activation sequence atrium occurs without an intervening second ventricular elec-
Stop pacing
A-V-V-A→ trogram, then antidromic tachycardia, pathway-to-pathway
VT tachycardia, or orthodromic reentrant tachycardia with
A-V-A→ aberrancy is likely. With AV node reentry and aberrancy, an
Antidromic tachycardia A-V-A pattern may be seen; however, as the atrial electrogram
Pathway-to-pathway tachycardia associated with the last paced beats conducts through the
ORT with aberrancya
A-A-V→ ventricle at about the same time, a return electrogram to the
AVNRT with aberrancya atrium occurs. Thus, the second atrial electrogram may occur
slightly before the ventricular electrogram (A-A-V) sequence
Abbreviations: AVNRT, atrioventricular nodal reentrant tachy- or simultaneous with the ventricular electrogram (A-V = A)
cardia; ORT, orthodromic reciprocating tachycardia; VT, ventri- or slightly after the ventricular electrogram (A-V-A) sequence,
cular tachycardia.
a
Near septum to His interval is similar to or longer than the A–H but regardless, the HA and VA intervals are short, as is typi-
interval in sinus rhythm. cal of AV node reentry. Analysis of the return AV activation
sequence, with specific attention to the timing between the
last ventricular and atrial electrograms, can clarify details on represents the Mahaim pathway potential on the ablation
the mechanism of the arrhythmia. catheter (arrow). With arrhythmias associated with Mahaim
Figure 4.38 summarizes the phenomena and related fibers, this pathway potential is the ideal target for ablation,
explanations associated with the maneuver of atrial pacing to and its recognition and analysis can greatly simplify the
entrain wide QRS tachycardia. These principles are applied in maneuvers required to arrive at the correct diagnosis.
many examples dispersed through the case studies discussed It should be noted, however, that some patients have
in this book. bystander Mahaim-like potentials on the lateral tricuspid
Among the most difficult diagnoses in the set of situations annulus. Figure 4.41 shows the sharp potential approximately
with wide QRS tachycardia is the presence of a Mahaim fiber, midway between the atrial and ventricular electrograms on
which either is responsible for an antidromic tachycardia or the ablation distal catheter (arrow) placed on the lateral tri-
is present as a bystander. The reason for this inordinate dif- cuspid annulus. It is obvious that this potential is from a
ficulty is the decremental nature of antegrade conduction of bystander tract or is occurring with infrapotential block
the Mahaim fiber, making it difficult to distinguish from the to the ventricle; in the first 3 preexcited beats, this electro-
AV node. Although not typically considered a maneuver, the gram actually occurs after the onset of the QRS complex and
identification and correct interpretation of pathway poten- after the earliest ventricular electrogram seen in the catheter
tials with Mahaim fibers are very important. labeled IS 9,10. Further evidence that this is not the culprit
Figure 4.39 shows the ablation catheter (arrow) in the pos- pathway is seen in the last beat where there is no change in the
terolateral region of the tricuspid annulus far from the His characteristics or intervals associated with this potential, but
bundle, yet in Figure 4.40, the large His bundle–like potential there is loss of preexcitation.
Wide QRS with 1:1, A:V
A paced faster than tachycardia
V entrained
Changed QRS/activation QRS/activation unchanged

sequence
His His Stop pacing

advanced unchanged
VT Bystander A-V-V-A A-V-A A-A-V
AVNRT
A-H A-H
VT short same
Bystander
But
Decrement ORT
ART
antegrade AVNRT
Figure 4.38 Atrial pacing to entrain wide QRS tachycardia. ART indicates antidromic reentrant tachycardia; AVNRT, atrioventricular
nodal reentrant tachycardia; ORT, orthodromic reciprocating tachycardia; VT, ventricular tachycardia.
Prior to the induction of tachycardia, atrial pacing maneu-

vers, including decremental atrial pacing and atrial extrastim-
ulus testing, is performed primarily to distinguish between
conduction via the AV node and antegrade conduction via an
accessory pathway. The main intervals of concern are the A-H
interval, the H-V interval, the pacing stimulus to the earliest
V, and the presence and extent of preexcitation.
The principal differences between AV node conduction,
accessory pathway conduction, and uncommon situations
such as Mahaim fibers and fasciculoventricular tracts are
outlined in Table 4.4.
In the tracing shown in Figure 4.42, minimal preexcitation
with a short H-V interval is noted. However, with increas-
ing the atrial pacing rate, the A-H interval increases with no
change in the preexcitation or the H-V interval.
With further increase in the pacing rate in Figure 4.43, a
Figure 4.39 Ablation catheter (arrow) in the posterolateral region long A-V interval and a long A-H interval are seen again with
of the tricuspid annulus far from the His bundle. no change in the extent of preexcitation.
With adenosine (Figure 4.44), there is an abrupt loss of AV
Decremental Atrial Pacing conduction with no preceding or subsequent changes in pre-
excitation or the short but stable H-V interval.
The utility of decremental as well as differential atrial pacing In the same patient shown in Figure 4.44, the effect of pac-
is similar to that of decremental ventricular and differential ing from the coronary sinus vs the right atrium again shows
ventricular pacing discussed above in the diagnosis of nar- no effect on preexcitation or the H-V interval (Figure 4.45).
row complex tachycardia. A few specific differences are rel- All these findings suggest that to get to the ventricular myo-
evant to the interpretation of these maneuvers in wide QRS cardium despite the short H-V interval and minimal preexci-
tachycardia. tation, the AV node needs to be activated first. Thus, the A-H
Figure 4.40 The large His bundle–like potential represents the Mahaim pathway potential on the ablation catheter (arrow).
Figure 4.41 The sharp potential approximately midway between the atrial and ventricular electrograms on the ablation distal catheter
(arrow) placed on the lateral tricuspid annulus.
interval increases without change in the H-V interval. There and the His bundle, rather than needing a delay to exit to the
is also no difference in the degree of preexcitation with differ- myocardium from the exit site of the right bundle, earlier acti-
ent sites of pacing. vation of relatively more basal ventricular myocardium occurs
Findings characteristic of a fasciculoventricular tract are (Figure 4.46). No clinically significant arrhythmias are associ-
typically observed insulation on the proximal His, and the right ated with this finding, and the primary reason for identifying
bundle is absent in these patients. After reaching the AV node this type of tract is to avoid unnecessary therapy or ablation.
Table 4.4
Effect of Decremental/Incremental Atrial Pacing
Observation AV Node Conduction Accessory Pathway Mahaim Fiber Fasciculoventricular Tract
Conduction
Preexcitation on the QRS No Yes Yes, often minimal Yes

Effect of increased pacing No change Increased preexcitation Usually increased No change
rate on preexcitation preexcitation
Pacing stimulus to earliest V Increases No change No change or increases Increases
A-H interval Increases Increases Increases (may stop Increases
increasing when
retrograde His is
present)
H-V interval No change Shortens and then Variable response No change
becomes progressively usually shortens and
negative becomes negative
until retrograde His is
present
Effect of adenosine during No change in QRS, Increase in preexcitation Variable response No change in
atrial pacing AV block preexcitation, AV block
Abbreviation: AV, atrioventricular.
Figure 4.42 Minimal preexcitation.
It is useful to have a clear understanding of the terms His bundle, and may also have direct connections to the
associated with the types of pathways being developed while ventricular myocardium. Th is connection represents a true
performing maneuvers in patients with suspected acces- bypass tract, as atrial tissue connects to the ventricle with-
sory pathways (Figure 4.47). A Mahaim fiber is the eponym out passing through the AV node or His bundle. Retrograde
for an atriofascicular bypass tract. Thus, the atrium con- conduction is not present in these pathways, and patients
nects to the right bundle branch, sometimes close to the may have preexcited tachycardias or antidromic tachycardia.
Figure 4.43 Increased pacing rate.

Figure 4.44 An abrupt loss of atrioventricular conduction with adenosine.
A nodoventricular or nodofascicular tract, on the other tract being thought responsible for the arrhythmia. Finally,
hand, does not have a direct connection from atrium to a fasciculoventricular tract is a simple early exit from the
either the conduction tissue or the ventricle. Instead, a por- conduction system (breach in the insulation) to reach the
tion of the AV node bypasses the His bundle, and the tract ventricular myocardium earlier than the usual right bundle
connects either to the right bundle or to the ventricular exit. Th is may represent a continuum of conditions with
myocardium. Tachycardias have been reported, with this exits anywhere from the usual right bundle exit to exits close
Figure 4.45 The effect of pacing from the coronary sinus vs the right atrium again shows no effect on preexcitation or the H-V interval.
electrophysiology laboratory, this may be especially confus-

ing when junctional tachycardia or an accelerated junctional
A HV rhythm is seen following slow pathway ablation, particularly
when using isoproteronol for postablation testing. Junctional
tachycardia or accelerated junctional rhythm must be dis-
tinguished from recurrent but slower AV nodal reentrant
tachycardia.
In general, where suprajunctional rhythms placing PVCs
are most useful in finding the cause of arrhythmia and during
infrajunctional rhythms, the PACs placed during tachycardia
Figure 4.46 Fasciculoventricular tract in sinus rhythm. A, A
are useful. For junctional tachycardia itself, 2 useful primary
recording site near the His bundle at the base of the heart; B, techniques are placing late coupled PACs as well as careful
a recording site near the right bundle exit; and C, a recording analysis of wobble and noting the mechanism of termination
site near the apex. The yellow arrows indicate a usual pattern of of tachycardia.
activation, and the green arrow indicates an activation pattern with Figure 4.48 illustrates the principle of using atrial pacing
a fasciculoventricular tract. to identify junctional tachycardia and junctional rhythm.
The essential difference between typical AV node reentry
to the His bundle. No notable arrhythmias arise from this and junctional rhythm or tachycardia exiting to the atrium
condition. via the fast pathway is the extent of the excitable gap. In
AV nodal reentrant tachycardia, primarily an intra-atrial
rhythm that happens to involve AV node tissue, there is a
JUNCTIONAL TACHYCARDIA relatively smaller excitable gap. Thus, to reset AV nodal reen-
trant tachycardia, either a very early coupled PAC should
Junctional tachycardia is a relatively common cause of nar- be placed or the atrium paced significantly faster than the
row complex tachycardia in fetuses and children. Junctional tachycardia. When the PAC or atrial pacing does reset the
tachycardia may occur also in the immediate postoperative tachycardia, conduction usually occurs via the slow pathway
setting, especially after valve-related cardiac surgery. In the (the antegrade limb of the arrhythmia), and thus the A-H
Mahaim Nodoventricular/nodofascicular
Sinus
node
AV
node
Mahaim
fiber
Fasciculoventricular
Figure 4.47 Types of accessory pathways. AV indicates atrioventricular.
Figure 4.48 Use of atrial pacing to identify junctional tachycardia and junctional rhythm.
interval is long. In fact, because of the decremental prop- atrium may advance the next His without resetting the tachy-
erties of some of the critical elements of AV node reentry, cardia. Distinguishing this arrhythmia from junctional tachy-
rapid pacing or early coupled PACs reset the tachycardia by cardia exiting via the slow pathway is best made by analyzing
delaying the next His bundle electrogram (longer A-H than the change in the activation sequence. With fast/slow AV
tachycardia). Junctional rhythm, even late coupled PACs, nodal reentrant tachycardia, the PACs that advance the His
can advance the next His, often suppressing or terminating or delay the subsequent His do not change the tachycardia’s
the junctional rhythm/tachycardia. Thus, when the His is early site. Once a junctional rhythm/tachycardia is advanced,
advanced following the pacing of the atrium, the A-H inter- the retrograde activation sequence abruptly changes.
val is short (normal). Another situation, although distinctly unusual, that can be
A second situation that may yield confusion is differen- confusing occurs when a junctional rhythm/tachycardia has
tiating atypical AV nodal reentrant tachycardia (retrograde a retrograde block to the atrium, but a bystander left-sided
slow pathway) from a junctional rhythm/tachycardia that accessory pathway is present. Thus, an eccentric activation
exits to the atrium via the slow pathway. Again, with atypi- sequence is found, and one needs to distinguish this rhythm
cal AV nodal reentrant tachycardia, it is difficult to reset the from orthodromic reciprocating tachycardia. Once again,
tachycardia from the atrium, and when this is done, the A-H PACs or atrial pacing clarify the situation because PACs, even
interval tends to increase in comparison with the tachycardia. late coupled, advance the His during a junctional rhythm with
Further, the activation sequence of the tachycardia when pac- a normal A-H interval and an abrupt change in the activa-
ing the atrium in the posterior annular region is unchanged tion sequence. With orthodromic reciprocating tachycardia,
from the tachycardia; that is, the site of earliest activation con- relatively earlier coupled PACs are required (although not as
tinues to be the region of the coronary sinus. With junctional early as with AV node reentry), and in several atrial locations
tachycardia, however, although the PACs may reset the tachy- (left atrium), the reset beats show no significant change in the
cardia with a longer than normal A-H interval as antegrade activation sequence (concealed fusion) (Box 4.8).
conduction can now be down the fast pathway (junctional Analyzing termination of tachycardia, particularly if it
beats were exiting via the slow pathway), the A-H interval is occurs in a consistent fashion, can also be greatly illuminating.
shorter than that observed during tachycardia. Further, the Figure 4.48 illustrates a rapid tachycardia that was easily
activation sequence of the rhythm changes as early activation inducible and also occurred spontaneously with the use of
at the site of the slow pathway exit no longer occurs. isoproteronol in a young patient. The tachycardia itself can
It should be noted that when attempting to reset the fast/ be difficult to distinguish between junctional tachycardia
slow variant of AV nodal reentrant tachycardia, the fast path- and AV node reentry. However, termination of the tachycar-
way itself may be a bystander to the circuit. Thus, pacing the dia consistently occurred after a His bundle deflection and
the tachycardia. A slow pathway ablation was successful in

Box 4.8 eliminating the arrhythmia. A less extreme form of a simi-
Junctional Tachycardia lar phenomenon is wobble occurring during tachycardia, and
Differentiation from typical AVNRT prolongation of the retrograde H-A interval repeatedly results
Late coupled PACs reset His with normal A-H interval in delaying the next His or next A of the tachycardia. This
Differentiation from atypical AVNRT
phenomenon suggests that the cardiac structures responsible
Late coupled PACs reset His with long A-H interval
Atypical AVNRT may reset His and not tachycardia for conduction during the H-A interval (AV node retrograde
Differentiating junctional tachycardia with bystander accessory fast pathway) are critical to the circuit of the arrhythmia and
pathway from ORT favor AV node reentry as the diagnosis. An example of this
Late coupled PACs preexcite the His with a normal A-H phenomenon is illustrated in Figure 4.49.
interval
Abbreviations: AVNRT, atrioventricular nodal reentrant

tachycardia; ORT, orthodromic reciprocating tachycardia; PAC,
PATHWAY-RELATED MANEUVERS
premature atrial contraction.
The differential diagnosis of pathway-related syndromes
(ORT, antidromic reciprocating tachycardia, etc) are dis-
cussed extensively in the illustrative cases elsewhere in this
a ventricular electrogram. If this arrhythmia is a junctional book. Because of the importance of specific maneuvers used
tachycardia, the same beat where the junctional tachycar- in the electrophysiology laboratory, this section describes
dia stops is probably the one that occurred when retrograde pathway potentials by identifying specific characteristics of
block in the atrium also occurred. This sequence is analogous accessory pathways (pathway potential and pathway slant).
to the situation where a supraventricular tachycardia stops These techniques and concepts are used in various areas of
with antegrade AV block, making atrial tachycardia unlikely. electrophysiology whenever an electrical signal is recog-
This type of termination was repeatedly seen during the case nized during mapping, but its origin is obscure. Diagnosing
and strongly favored AV node reentry as the mechanism of pulmonary vein potentials, coronary sinus potentials, and
Figure 4.49 Supraventricular tachycardia stops with antegrade atrioventricular block, making atrial tachycardia unlikely.
fragmented atrial and ventricular signals employ similar rea- and it is not A, from the prior maneuver, then the poten-
soning and maneuvers. tial is likely to be a pathway potential. In the third beat, an
even earlier ventricular extrastimulus further dissociates
Identifying Pathway Potentials the ventricular signal from the accessory pathway as well as
the atrial signal. If retrograde conduction via the pathway
The principle behind the maneuvers to diagnose a pathway was present in this patient, the accessory pathway poten-
potential is to effectively associate or dissociate a candidate tial would be visible just after (rather than before, as seen
signal (signal under question as to whether it is a pathway previously) the ventricular electrogram. Th is situation is
potential) from/with other known causes of signals in that illustrated in Figure 4.52.
region (atrium, ventricle, His bundle, coronary sinus, etc). If In Figure 4.53, during ventricular pacing, eccentric activa-
a particular potential can be distinguished from the atrium, tion of the coronary sinus is noted. Multiple signals are seen
ventricle, His bundle, and, in some instances, the coronary between the ventricular electrogram and what is clearly the
sinus muscle, no matter how different or unusual the poten- atrial electrogram. These signals may represent fragmented
tial is, it is highly likely that it is a pathway potential. Box 4.9 V, fragmented A, or a pathway potential (for simplicity, the
summarizes these steps. possibility of coronary sinus musculature, which is unlikely
As illustrated in Figure 4.50, a multielectrode catheter is in this location, is not discussed).
placed on the annulus where both atrial and ventricular sig- During more rapid ventricular pacing, VA block occurs
nals can be identified. The first 2 beats show preexcitation. (Figure 4.54). When VA block occurs, one of the candidate
A candidate potential is evident between the atrial and ven- potentials between V and A remains with the V and likely
tricular signals. By pacing the atrium at a more rapid rate, the represents a fragmented ventricular electrogram (although V
pathway blocks, and a normal QRS with a longer AV interval to pathway conduction and pathway to fragmented A block-
results. With accessory pathway block, the candidate poten- ing cannot be excluded). The second candidate potential is
tial is no longer seen. Thus, the potential is related to pathway not seen when VA block occurs.
conduction. Further, when total AV node block occurs, as During ventricular pacing, sensed PACs are being placed.
with the last paced beat, the signal is not seen. This maneuver The electrogram in the coronary sinus begins to advance in
effectively dissociates the signal from the ventricular elec- the second beat (Figure 4.55).
trogram as well as the atrial electrogram in most instances. With earlier atrial pacing, the atrial electrograms in the
Rarely, severely diseased atria, such as from prior ablation, coronary sinus are advanced, but the candidate potential is not
may show intra-atrial block, but all atrial signals are expected (Figure 4.56). Thus, the potential has been differentiating from
to be fragmented in that instance. both a ventricular electrogram and an atrial electrogram, diag-
In Figure 4.51, sensed ventricular pacing is performed nosing this potential as a pathway potential. Once this has been
during atrial pacing. The goal of this maneuver is to assess established, the ablation catheter should be placed to obtain a
the relationship of the candidate potential to the ventricu- similar electrogram and target the site of the pathway poten-
lar electrogram. In the second beat, the PVC that had been tial for ablation. The principal observations related to pathway
placed advances the ventricular electrogram with no signifi- potentials and pacing maneuvers are summarized in Table 4.5.
cant effect on the candidate potential. Th is strongly suggests
that the candidate potential is not part of V; if it is not V
PATHWAY SLANT
Box 4.9 Another important maneuver in the electrophysiology labo-

Steps to Identify Pathway Potential ratory used during the analysis of supraventricular tachy-
Antegrade preexcitation cardia is elucidation of pathway slant. Accessory pathways,
1. Pace A until pathway blocks which are generally musculature connections between the
2. Pace A until AV node conduction blocks atrium and ventricle bypassing the fibrous annulus, are rarely
3. Sensed PVCs during atrial pacing
4. Access difference in decrement between atrium and candi-
perpendicular to the annulus. Because of this anatomic ori-
date potential in comparison with other signals (His, etc) entation, the course of the accessory pathway from its atrial
to ventricular insertion (or vice versa) occurs at an angle or
Retrograde conduction via pathway
1. Pace V until pathway blocks
slant to multielectrode catheters placed parallel to the annu-
2. Pace V until AV node blocks retrograde lus (for example, the coronary sinus catheter). Any electrode
3. Sensed PACs during ventricular pacing placed on the annulus, such as via the coronary sinus, records
4. Access difference in decrement during ventricular pacing electrograms from the ventricular myocardium and atrial
between V and candidate electrogram with other decre- myocardium immediately adjacent to the annulus since the
menting intervals (retrograde His, etc)
annulus itself is not associated with any electrogram. This
Abbreviations: AV, atrioventricular; PAC, premature atrial
anatomic relationship allows for some pacing and mapping
contraction; PVC, premature ventricular contraction. maneuvers that define the direction the pathway is slanted.
Once defined, the pathway slant recognition can greatly
AP AVN-only Atrial capture with

conduction conduction block in AP and AVN
Surface ECG
Stim Stim Stim Stim
440 ms 430 ms 420 ms
A V A V A V A
Annular EGM
AP AP
Atrium Atrium Atrium

Conduction
Schematic AVN AVN AVN

Recording Recording
catheter catheter
Pathway Pathway Pathway
Ventricle Ventricle Ventricle
Pathway AVN-only Block in

conduction conduction AVN and AP
Figure 4.50 A multielectrode catheter is placed on the annulus where both atrial and ventricular signals can be identified. AP indicates
accessory pathway; AVN, atrioventricular node; ECG, electrocardiogram; EGM, electrogram; Stim, stimulus.
enhance the ability to recognize the best and safest sites to 1 site may find the site of earliest activation but may need to
ablate accessory pathways. be advanced further along the annulus to locate the site of
One manifestation of pathway slant is an anatomic sepa- earliest ventricular activation during sinus rhythm or atrial
ration in the site of earliest ventricular and earliest atrial pacing. When a closely placed multielectrode catheter is posi-
activation in pathways that exhibit bidirectional conduction. tioned along the annulus (mitral or tricuspid or coronary
Thus, a bipolar mapping electrode placed on the annulus at sinus), 1 pair of electrodes may show the earliest ventricular
Surface ECG
Stim Stim Stim Stim
A V AV V A
Annular EGM
AP AP AP
Anterograde Ventricular signal Very early PVC

AP conduction advanced by PVC dissociates VEGM
from A and AP
Figure 4.51 Sensed ventricular pacing is performed during atrial pacing. AP indicates accessory pathway; ECG, electrocardiogram; EGM,
electrogram; PVC, premature ventricular contraction; Stim, stimulus; VEGM, ventricular electrogram.
Surface ECG
Stim Stim Stim
A V A V V A
Annular EGM
AP AP APR
Antegrade AP A single PVC advances the VEGM;

conduction during there is a retrograde pathway potential (APR)
fixed-rate atrial with atrial block; atrial stimulation is followed
pacing by the atrial EGM alone
Figure 4.52 With retrograde conduction via the pathway, the accessory pathway potential occurs just after the ventricular electrogram.
A indicates atrial electrogram; AP, accessory pathway; APR, retrograde pathway potential with atrial block; ECG, electrocardiogram; EGM,
electrogram; Stim, stimulus; PVC, premature ventricular contraction; VEGM, ventricular electrogram.
electrogram during atrial pacing, and another pair of elec- the exact annular location of a roving or mapping catheter is
trodes may show the earliest atrial electrogram during ven- difficult to maintain. Thus, when a catheter is advanced fur-
tricular pacing. The pathway potential in both the antegrade ther along the annulus from the site of earliest atrial activa-
and retrograde direction may be found between these 2 sets tion, it may have slipped to a more ventricular location, giving
of bipolar electrodes and is typically in the same location for rise to an earlier ventricular site even if the pathway had no
both antegrade and retrograde conduction. It is often difficult significant slant. Further, many pathways exhibit unidirec-
to ascertain the slant using these simple maneuvers because tional conduction, and in these common situations, it is not
Figure 4.53 Eccentric activation of the coronary sinus during ventricular pacing.
Figure 4.54 The second candidate potential (arrow) is not seen when VA block occurs.
possible to define both sites of earliest atrial and ventricular retrograde-only connecting pathway is found, a multielec-
activation. trode catheter placed along the annulus does not have the
access of the electrodes perpendicular to the body (functional
Defining Slant With Differential Pacing or anatomic) of the accessory pathway. A bipolar electrode
placed exactly at the site of the accessory pathway records a
Using differential site pacing, pathway slant can be defined pathway potential, but the ventricular and atrial electrograms
even when conduction occurs in only 1 direction. Thus, if a recorded on this same electrode depends on the timing of
Figure 4.55 During ventricular pacing, sensed premature atrial contractions are being placed. The electrogram in the coronary sinus
begins to advance in the second beat.
Figure 4.56 With earlier atrial pacing, the atrial electrograms in the coronary sinus are advanced, but the candidate potential is not.
the local ventricular myocardial and local atrial myocardial pacing site is located septally in panel A and more laterally in
activation. panel B. Because the ventricular insertion of this retrograde
Figure 4.57, adapted from Otomo et al (Circulation. 2001 conducting pathway is located septally in this example, when
Jul 31;104[5]:550–6), clearly illustrates this concept. In the pacing from a septal site, the local ventricular electrogram
electrograms labeled A, the pathway is located closest to the near electrode 3 is activated after the wave front has already
set of electrodes CS3 (in this case, orthogonal electrodes). Thus, begun to climb up the pathway toward the atrium. Thus, the
a pathway potential is clearly seen on CS3. The ventricular timing from the local ventricular electrogram to the accessory
Table 4.5
The Pathway Potential
Maneuver Observation Interpretation
Pace V until VA block Candidate potential not seen once Candidate potential is not V
VA block occurs May be A or pathway potential
During VA pacing place PACs Early PACs dissociate atrial signal from the Candidate potential is not A
candidate potential May be pathway potential or V
Pace A until loss of preexcitation Candidate potential not seen when Candidate potential is not A
preexcitation lost May be pathway potential or V
Pace A during preexcitation until AV block Candidate potential no longer seen Potential is not A
May be pathway potential, His, or V
Pace A during preexcitation until AV block Potential is still seen May be part of A or pathway potential
Pace V until VA block in patient with Candidate potentials still seen May be V or pathway potential
retrograde conducting pathway
Abbreviations: AV, atrioventricular; PAC, premature atrial contraction; VA, ventriculoatrial.
A B C D
LA LA
p 4 3 2 d p 4 3 2 d p 4 3 2 d p 4 3 2 d
CS CS
LV LV
A1 A2 B1 B2 C1 C2 D1 D2
V1 V1
A A A A
V V V V
CSp CSp
AP AP
CS4 CS4
AP AP
CS3 CS3
CS2 CS2
AP AP AP AP
CSd CSd
A A A A
V V V V
Figure 4.57 Slant used to uncover accessory pathway potentials. A, The pathway is located closest to the CS3 electrodes. B, The pacing site
is located more laterally than in A. C, Atrial pacing site from the coronary sinus (lateral). D, The same phenomenon during differential
atrial pacing with pathways that are slanted and conduct in the antegrade direction. (Adapted from Otomo K, Gonzalez MD, Beckman KJ,
Nakagawa H, Becker AE, Shah N, et al. Reversing the direction of paced ventricular and atrial wavefronts reveals an oblique course in
accessory AV pathways and improves localization for catheter ablation. Circulation. 2001 Jul 31;104(5):550–6. Used with permission.)
pathway potential is short. Further, the local atrial electro- CS3, the local atrial myocardium is activated nearly simul-
gram recorded on CS3 occurs after activation of the pathway taneously as the pathway itself gives rise to a short interval
potential, then the local atrial tissue that is now lateral to CS3 between the local atrial electrogram and the pathway on CS3.
(CS2), then the wave front comes back toward CS3, giving rise When the wave front is reversed, pacing the atrium from a
to a discernible interval between the pathway potential and septal site such as the right atrium, the local atrial electro-
the local atrial electrogram. Thus, the ventricle to pathway gram occurs earlier than the time when the wave front inserts
potential interval is short, and while the ventricle to atrial
electrogram is also fairly short, most of the discernible iso-
electric period is between the pathway potential (labeled AP)
and A.
Box 4.10
In panel B, however, the ventricular pacing site is lateral.
Pathway Slant
Thus, the local ventricular tissue adjacent to electrode 3 gets
activated before the wave front reaches the more septally 1. Pathways are rarely perpendicular to the annulus.
2. Electrodes on the annulus located at the pathway site can
located insertion of the accessory pathway, and the wave front
identify pathway slant with differential site pacing.
travels up the pathway to give rise to the pathway potential 3. The local V-A interval on an electrode at the site of an acces-
recording. A clear discernible interval between the local ven- sory pathway is not a measure of conduction via the pathway
tricular electrogram and the accessory pathway electrogram but is a pseudointerval.
is now seen. The V-A interval is now also longer because, from 4. For a retrograde conducting pathway, if pacing from a lateral
ventricular site gives rise to a longer V-A interval (and local
the time of local ventricular electrogram activation by pole 3,
V-AP interval) than septal site ventricular pacing, the path-
the pathway needs to reach the septally located pathway inser- way is likely to be located septally.
tion, travel up the pathway, exit through the atrial insertion, 5. For a pathway slanted to have the ventricular insertion more
and then travel back toward pole 3. Therefore, the local V-A lateral than the atrial insertion septal site, pacing gives rise
interval, when recorded through an electrode placed along to longer V-A and V-AP intervals than with lateral ventricu-
lar site pacing.
the annulus with pathways that are slanted, is a pseudointer-
6. With antegrade conducting pathways, if the atrial insertion
val and does not reflect the actual conduction time through is more septal than lateral, atrial pacing (coronary sinus)
the accessory pathway. To perform this maneuver, the pacing results in a longer A-V (A-AP) interval and vice versa.
rate should not be changed, and only the pacing site (septal vs 7. Pathway slant can also be identified in an anteroposterior or
lateral) should be varied. superoinferior orientation.
8. The pacing maneuver that causes the maximum separation
Panels C and D demonstrate the same phenomenon dur-
of local myocardial electrograms with a pathway potential
ing differential atrial pacing with pathways that are slanted should be used to facilitate identification of the pathway
and conduct in the antegrade direction. In panel C, the atrial potential as a target for ablation.
pacing site is from the coronary sinus (lateral). Thus, in pole
Figure 4.58 Local electrograms compared with the ablation electrode oriented along a previously defi ned slant on the pathway.
into the atrial end of the pathway near CS2. Thus, a longer AV ablation electrode oriented along a previously defined slant
interval and specifically a longer interval between the local on the pathway.
atrial electrogram near CS3 and the pathway potential on the
electrode at the site of the accessory pathway are noted. By ABBREVIATIONS
examining the intervals between the local myocardial elec-
trograms and the pathway potential as well as the local A-V AV, atrioventricular
and V-A intervals between septal and lateral pacing, the slant ECG, electrocardiogram
can be defined. The salient findings associated with pathway ORT, orthodromic reciprocating tachycardia
slant are summarized in Box 4.10. PAC, premature atrial contraction
In Figure 4.58, the marked differences in the local elec- PJRT, permanent junctional reciprocating tachycardia
trograms on the coronary sinus (parallel to the annulus and PVC, premature ventricular contraction
off axis with a slanted pathway) can be compared with the VA, ventriculoatrial
5
Reentry, Transient Entrainment,
and Concealed Entrainment
Win-Kuang Shen , MD
INTRODUCTION
The primary objective of this chapter is to provide essential

information as a reference to dissect the arrhythmogenic
mechanisms useful in clinical practice.
PL ≥ V × R
REENTRY
Definition
Reentry is a cardiac reentrant rhythm in an electrical wave

propagating over a circuitous pathway (2-dimensional in
the simplest form, like the wave front moving around a cen-
tral anatomic obstacle that does not allow conduction) and
returning to its site of origin to reactivate the circuit in the
same sequence. The wavelength (WL) of the reentrant circuit
can be calculated by the product of the pathway tissue con-
duction velocity (V) and refractoriness (R), ie, WL = V×R. PL ≥ V × R
In order for any reentry rhythm to occur, the physical
length of the cardiac tissue pathway (pathway length [PL])
must be ≥WL. When PL>WL, an excitable gap is theoreti-
cally present but may not always be accessible. A fully excit-
able gap is not present or possible when PL=WL (Figure 5.1).
On the basis of these concepts, the reentry rhythm termi-
nates when the propagating wave front “catches” the wave
tail by either increasing the V or prolonging the R of the
tissue. Therapeutically, the latter scenario is possible when
the excitable gap is not very large because class III antiar-
rhythmic drugs mediate R prolongation, thereby prevent-
ing recurrent reentrant arrhythmias. When the excitable
PL ≥ V × R
gap is large, mere prolongation of tissue R by drugs may
not be sufficient to render prevention of recurrent arrhyth-
mias. Reentrant arrhythmias also can be prevented by cre-
ating conduction blocks along the circuit pathway by either
tissue-specific drugs (class I, II, IV, adenosine, or digoxin) or Figure 5.1 Scenarios where continuation of reentrant tachycardia
is possible with or without a zone of slow conduction and the
presence of varying degrees of an excitable gap. PL indicates
Abbreviations are expanded at the end of this chapter. pathway; R, refractoriness in reentry; V, conduction velocity.
129
physical interruption (ablation or surgery). These simple ana-

tomic concepts provide foundations for better understand- Box 5.1
ing of multidimensional reentry, functional reentry (no fi xed Four Criteria for (Transient) Entrainment
anatomic pathways), and treatment of reentry arrhythmias, 1. Pacing during tachycardia yields constant fusion on the
with ever-increasing sophistication of electrophysiologic and electrocardiogram except for the last captured beat, which
is not fused
pharmacologic technology.
2. Progressive fusion while pacing at different rates
3. Pacing termination of tachycardia yields localized conduc-
Types of Reentrant Rhythm tion block followed by activation of that site with a shorter
conduction time
Several types of reentrant models and related key characteris- 4. Change in conduction time and electrogram morphology
when pacing at 2 different rates
tics are summarized in Table 5.1. Most of the concepts devel-
oped from responses to program stimulation for entrainment
are derived from anatomic reentrant models with an acces-
sible excitable gap and for concealed entrainment from ana-
tomic models where a critical zone of conduction (central CONCEALED ENTRAINMENT
common pathway in the figure-of-8 model) is present.
Definition
TRANSIENT ENTRAINMENT Pacing that entrains the tachycardia without changing the
morphology of the surface electrocardiogram (ECG) (P wave
Definition for atrial arrhythmias and QRS for ventricular arrhyth-
mias) demonstrates the presence of concealed entrainment
Entrainment is broadly defined as any stable condition with a (also known as entrainment of concealed fusion or exact
definable periodicity resulting from interactions of 2 rhythms entrainment; Figure 5.3). For concealed entrainment to
(ie, paced rhythm by programmed stimulation and intrinsic occur, the site of pacing must be protected (ie, concealed;
rhythm). The presence of entrainment suggests the underly- fusion between orthodromic and antidromic wave fronts
ing rhythm is of a reentrant nature. occurs within scars, not apparent on the ECG) from the
main body of myocardium, and the paced wave front must
Criteria propagate (orthodromic wave front) to depolarize the
myocardium at the same exit site as the underlying spon-
Four criteria have been proposed to recognize the presence taneous tachycardia. The site of pacing demonstrating
of entrainment (Box 5.1 and Figure 5.2). Demonstration of 1 concealed fusion suggests that the pacing site is within the
or more of the 4 criteria proves the presence of entrainment reentrant circuit (central common pathway or critical zone
and supports a reentrant mechanism, but their absence does of slow conduction) or at a bystander site (nearby but not
not exclude entrainment or reentry (ie, programmed stimula- participating in the reentrant arrhythmia), communicat-
tion from the site and cycle length cannot reset or get into the ing with the reentrant circuit and sharing the same exit site
circuit). within scars.
Table 5.1
Types of Reentrant Models
Reentrant Model Substrate PL-WL Relationship Excitable Gap Examples and Comments
Anatomic reentry
Circus movement Around valves, special conduction PL ≥WL + Atrial flutter, WPW, bundle
pathways or isthmus branch reentry
Figure-of-8 Scars PL ≥WL + Scar-dependent AT or VT
Anisotropic Tissue-fiber orientation PL ≥WL + AVNRT
Functional reentry
Leading circle Dynamic interactions between tissue PL=WL − AF
conduction and refractoriness
Spiral waves Initiates in an excitable tissue (a core PL=WL − Some experimental models of
or an organizing center), with AF and VF
formation of spiral waves when there
is interruption of the wave front
Abbreviations: AF, atrial fibrillation; AT, atrial tachycardia; AVNRT, AV nodal reentrant tachycardia; PL, pathway length; WL, wave length; VF, ventricular fibrillation; VT,
ventricular tachycardia; WPW, Wolff-Parkinson-White; +, present; −, absent.
5. Reentry, Transient Entrainment, and Concealed Entrainment 131
A
Spontaneous Paced (x) Paced (x + 1)
ART ORT ART ORT
* * *
x+
1
+
x
1
x
f x−1 x
* Paced * Spontaneous *
ART ORT
* *
1
x+
+
1
x
x x+1
ORT ART ORT ART ORT

1 1
x
x
* * + * +
+
+
x x
1
f x x
* * *
Figure 5.2 Characteristics of criteria for entrainment. A, Entrainment criterion 1. Top panel, Schematic depiction of constant fusion. The letter
f represents the wave front of activation. Similar areas are marked with an asterisk in the lower panels with the electrograms. Arrows indicate
the patterns of activation in the electrograms in the right and left ventricle that result from that paced beat. The white segment is the excitable
gap, and the asterisks indicate the timing reference. The letter x represents the specific paced beat of interest, with x+1 being the next beat and
x–1 the prior beat. Wavy lines indicate slow conduction, and dashed arrows indicate continuing activation. Middle panel, Last paced beat,
entrained but not fused. Bottom panel, Electrocardiographic and intracardiac (electrogram) recordings. The letter s represents pacing stimulus.
Note fusion of the QRS complexes with pacing. Circled numbers represent the timing interval from the adjacent stimulus to the electrogram
indicated by the arrow. B, Entrainment criterion 2. Top panel, Progressive fusion. Bottom panel, Electrocardiographic and intracardiac (elec-
trogram) recordings. Note the effect of pacing on the tachycardia specifically showing progressive fusion on the surface QRS. (Continued)
C
Paced Paced
* x+2
ART ORT
x+
+
x
1
x
*
D
Paced 300-ms CL Paced 250-ms CL
* *
ART ORT ART ORT
* *
1
x+
x+
+
x
1
1
x+
x
x
* *
I I
Figure 5.2 (Continued) C, Entrainment criterion 3. Top panel, Localized block. The curved blue lines represent electrical activation unre-
lated to the circuit for the tachycardia. The notation x+2 represents the activation resulting from 2 beats after tachycardia terminates. Bottom
panel, Electrocardiographic and intracardiac (electrogram) recordings. D, Entrainment criterion 4. The letter x indicates the referenced beat
of interest. Bottom left panel, Electrocardiographic and intracardiac (electrogram) recordings. The letter S represents the pacing stimulus.
Bottom right panel, Electrocardiographic and intracardiac (electrogram) recordings. ART indicates antidromic reciprocating tachycardia;
CL, cycle length; ECG, electrocardiogram; ORT, orthodromic reciprocating tachycardia.
I * V1 S *
S
350 ms 420 ms 350 ms 420 ms
II V2
III V3
AVR V4
AVL V5
AVF V6
Figure 5.3 Concealed fusion as seen on electrocardiographic and intracardiac (electrogram) recordings. The letter S represents the pacing
stimulus, and the asterisk indicates the last beat affected by pacing.
Site of Pacing and Relationship to the

Outer loop
Reentrant Circuit
Dead-end
Although the demonstration of concealed entrainment dur- pathway
Scar
ing programmed stimulation provides information local- QRS onset
izing key components of the reentrant circuit useful for
ablative therapy, program stimulation to find the critical
ECG CP CP entrance
zone of slow conduction is inherently tedious and difficult. *
Generally, identifying endocardial sites with concealed
entrainment occurs in fewer than half of all patients, while CP exit
successful ablation to eliminate ventricular tachycardia (VT)
Inner loop
(less known in atrial arrhythmias) occurs in fewer than half
of these identified sites with demonstration of concealed Scar
entrainment.
ECG
Key Components of Concealed Entrainment
Following are definitions of the key components of concealed Figure 5.4 The exit site of the tachycardia is indicated by the
entrainment according to the figure-of-8 model and termi- asterisk, and the arrows represent the wave front of activation in
the various parts of the circuit. The point of exit corresponds to
nologies in response to program stimulation (Figure 5.4).
the onset of the QRS complex on the surface ECG. CP indicates
The common central pathway is a critical zone of slow con- common pathway; ECG, electrocardiogram.
duction participating in the tachycardia circuit, within scars,
concealed from the main body of myocardium. Along the
orthodromic depolarization wave front, the common path- The dominant loop is the circuit loop outside the com-
way has an exit and entrance in reference to the scar (con- mon pathway with the shortest conduction time. Thus, it
cealed) zone. establishes the tachycardia cycle length (CL). If the conduc-
The inner loop is a conduction pathway within scars, com- tion time through the inner loop is slower than the conduc-
municating with the common central pathway forming a tion time through the outer loop, the inner loop serves as a
circuit. bystander and the outer loop is dominant. If the conduction
The outer loop is a pathway outside scars, communicating time is faster in the inner loop, it becomes an obligatory com-
(and not concealed) with the main body of myocardium, con- ponent of the reentrant circuit and is designated the dominant
necting to the common pathway and forming a circuit. inner loop. Differentiation of a dominant inner loop from the
ECG 391 391 369 391

S
EG-QRS 248 248 S-QRS 444 444 396 444
ECG
Site 15 S
391 391 391
393 412
Postpacing interval
Site 6
444 337 463 444
350 350 350 391 391
ECG Postpacing interval
S S S 248 S-QRS 248
Site 15
391
Postpacing interval
391 391 356 391

463 463 429 463 ECG
ECG S
S 193 299
412 412
Site 6 Site C
463 429 463 463 391 250 497 391
Postpacing interval Postpacing interval

Figure 5.5 The electrocardiograms (ECGs) and intracardiac electrograms that correspond to activation at the site marked by the asterisk
in each panel. The asterisk is a point in the circuit at the entrance into a bystander pathway. All other arrows and asterisks are same as above
as for Figure 5.2.
Table 5.2
Response to Programmed Stimulation With Respect to
Pacing Site in the Reentrant Circuit
* Site ECF PPI=VTCL S-QRS=EG-QRS S-QRS–VTCL

Outer loop Common pathway + + + 1%-70%
Dominant inner loop + + ± >70%a
Dominant outer loop − + − 0
Bystanders
Inner loop
Dead-end pathway ± − − >70%a
Nondominant loop ± − − >70%a
Abbreviations: ECF, electrogram of concealed fusion; EG-QRS, local electrogram
(on the pacing channel)–QRS interval; PPI, postpacing interval; S-QRS, stimulus-
QRS interval; VTCL, ventricular tachycardia cycle length; +, present; −, absent.
a
Some exceptions may occur depending on the pacing location in relation to the
ECG 463 380 412 483 common pathway.
S
Site L 463 329 463 463
Postpacing interval
loop, dominant inner loop, and outer loop are shown in
Figure 5.5 (Continued) Figure 5.5. A summary of these responses in terms of QRS
morphology (concealed or not), PPI vs VTCL, and S-QRS vs
EG-QRS intervals is provided in Table 5.2. When pacing at
common pathway can be difficult because responses to pro- the common pathway, the difference between the PPI and
grammed stimulation are similar between the 2 locations. VTCL, PPI–VTCL, is expected to be within 30 ms, while
The dead-end pathway (a blind pouch) is a pathway that S-QRS–EG-QRS is expected to be within 20 ms. When pac-
connects to an inner loop or to the common pathway without ing is done near the exit site, central common pathway, and
other exits. entrance site, the S-QRS is expected to be ≤30%, 31%-50%,
The bystander/dead-end pathway is a pathway communi- and 51%-70%, of the VTCL, respectively. When pacing is
cating with the common pathway or any inner loop without done from a dead-end bystander location, S-QRS–VTCL is
being an obligatory component of the reentrant circuit. expected to be >70%.
The S-QRS interval for VT (S-P interval for atrial arrhyth-
mia) occurs between the stimulus (S) artifact to the onset of
QRS on the surface ECG. ABBREVIATIONS
The EG-QRS interval for VT (EG-P interval for atrial
arrhythmia) occurs between a local (on the stimulus channel) CL, cycle length
electrogram (EGM) to the onset of QRS on the surface ECG. ECG, electrocardiogram
The postpacing interval (PPI) occurs from the stimulus to EGM, electrogram
the succeeding activation (local EGM) at the stimulus site. PL, pathway length
PPI, postpacing interval
Site of Pacing and Response to Programmed R, refractoriness
Stimulation S, stimulus
V, conduction velocity
In the setting of VT, examples of pacing responses from the VT, ventricular tachycardia
common pathway, dead-end pathway, nondominant inner WL, wavelength
6
Approach to Wide QRS Tachycardias
Yong-Mei Cha , MD, and Samuel J. Asirvatham , MD
INTRODUCTION prolonging the QRS duration. When an accessory pathway is

present, antegrade conduction results in activation of the ven-
Among the most difficult set of arrhythmias to analyze, tricular myocardium rather than the His-Purkinje network.
diagnose, and treat appropriately in the electrophysiology Sequential ventricular activation without the benefit of con-
laboratory are wide QRS tachycardias. The reasons for this duction through the specialized conducting network leads to a
difficulty include the relatively rare occurrence of some of wide QRS rhythm. Finally, if the site of origin of the tachycar-
these conditions (pathway-to-pathway tachycardia, preex- dia (or exit) is in the ventricular myocardium itself (ventricular
cited atrioventricular [AV] nodal reentry, etc) and the fact tachycardia), for similar reasons the QRS is wide (Figure 6.2).
that the differential diagnosis for a wide QRS rhythm includes Any of the known causes of supraventricular tachycardia
all the possibilities for a narrow QRS rhythm and, in addi- (SVT) can be associated with bundle branch block or the pres-
tion, arrhythmias related to antegrade pathway conduction ence of an antegrade conducting bypass tract, and all causes
and ventricular tachycardia. This wide range of possibilities of SVT may present as wide QRS tachycardia. Thus, all the
can be confusing even to experienced electrophysiologists, maneuvers described in Chapter 4 for narrow QRS tachycar-
and a complex case may lead to inappropriate diagnoses and dia need to be applied to analysis of wide QRS tachycardia; in
maneuvers, including a wrong ablation sequence. Chapter 4 addition, the mechanism for the wide QRS rhythm has to be
discusses the correct execution and application of pacing determined. Finally, unique, challenging, and, for the electro-
maneuvers, with reference to wide QRS tachycardias. This physiologist, interesting diagnostic possibilities arise in ana-
chapter focuses on the overall approach to wide QRS tachy- lyzing wide QRS tachycardia because of multiple mechanisms
cardias. A brief description of the clinical and electrocardio- that may be operative in a given case. For example, antidro-
graphic (ECG) features is followed by an in-depth discussion mic tachycardia may be the primary diagnosis, but retrograde
of diagnostic maneuvers and approaches in the electrophysi- conduction may be present intermittently through a second
ology laboratory. Finally, representative electrograms and accessory pathway, or with variation in the tachycardia
case studies follow to illustrate some of the more involved cycle length, a second tachycardia (AV node reentry) may be
principles discussed in this chapter. induced, with the antegrade pathway serving as a bystander.
Although these situations may be complex, thorough knowl-
edge of the possibilities that need to be considered, systematic
CAUSES AND CLINICAL FEATURES analysis of the electrograms, and appropriate application of
OF WIDE QRS TACHYCARDIA pacing maneuvers usually lead to the correct and complete
diagnosis. The main causes of wide QRS tachycardia that
Most supraventricular rhythms have a narrow QRS complex
need to be considered in the electrophysiology laboratory are
because of the near simultaneous and efficient depolariza-
summarized in Table 6.1.
tion of both ventricles by both bundle branches and their
The main distinguishing clinical feature of patients with
respective Purkinje networks (Figure 6.1).
SVTs and wide QRS rhythm, either from bundle branch block
Disruption in this orderly activation pattern may occur if
or antegrade preexcitation, is their younger age. Ventricular
one of the bundle branches is blocked, thus leading to sequen-
tachycardia typically occurs in older patients with structur-
tial rather than simultaneous biventricular activation and
ally abnormal hearts, although considerable overlap may exist
between conditions and age groups. For example, in younger
Abbreviations are expanded at the end of this chapter. patients, fascicular tachycardia with rapid ventriculoatrial
137
Narrow QRS
Left anterior
fascicle
Right bundle
branch exit
Moderator band
Figure 6.1 Simultaneous right and left ventricular stimulation. Arrows indicate breakout sites for activation from the conduction system to
the ventricular myocardium.
conduction is often confused with AV node reentry. Certain ANALYSIS OF ECG AND MONITORING DATA
clinical features, however, are useful when anticipating the BEFORE WIDE QRS TACHYCARDIA ABLATION
types of maneuvers required in the electrophysiology labora-
tory. For example, abrupt termination of tachycardia with a This text assumes that the reader is familiar with the general
Valsalva maneuver or carotid sinus massage strongly impli- use of the ECG in distinguishing bundle branch aberrancy
cates the AV node as part of the circuit. Adenosine sensitivity and ventricular tachycardia. The purpose of this section is to
has similar implications, although ventricular outflow tract emphasize the specific details that can be obtained from the
tachycardia and left posterior fascicular tachycardia are often ECG to facilitate mapping and ablation in the electrophysiol-
adenosine sensitive as well. ogy laboratory.
LV RV RV LV LV RV
Figure 6.2 Left panel, Right bundle branch block delays ventricular activation. Middle panel, The presence of an accessory pathway on
the right leads to early and late LV activation. Right panel, Left ventricular tachycardia leads to early LV and late RV activation and slow
ventricular conduction. Arrows with wavy lines indicate slow conduction. LV indicates left ventricle; RV, right ventricle.
6. Approach to Wide QRS Tachycardias 139
Table 6.1
Causes of Wide QRS Tachycardia
Primary Diagnosis Mechanism for Comments
Wide QRS Tachycardia
Atrial tachycardiaa Bundle branch block The atrial activation sequence is determined
Antegrade conduction over a bystander by the typical sites of origin of the atrial
accessory pathway tachycardia and is usually different from
retrograde activation of the atrium during
ventricular pacing
With antegrade preexcitation, pacing the
atrium preexcites the ventricle but does not
reset tachycardia
AV node reentrant tachycardia Bundle branch block Difficult to distinguish from antidromic
Antegrade conduction via a bystander tachycardia
accessory pathway Short H-A interval may also be seen in
fascicular ventricular tachycardia
Systematic application of PACs in tachycardia
to identify the mechanism of the wide QRS
complex followed by placement of PVCs to
define the mechanism of ventriculoatrial
activation and the arrhythmia
Junctional tachycardia Bundle branch block Junctional tachycardias, particularly those
Origin in the His bundle/bundle branch originating from the distal His, can be
junction difficult to distinguish from AV node reentry
Rarely antegrade preexcitation and aberrancy or fascicular tachycardia
Via atrial activation and antegrade Both the application of PACs during
accessory pathway tachycardia and PVCs to distinguish from
Nodoventricular connection AV node reentry is necessary (see Chapter 4)
Orthodromic reciprocating tachycardia Bundle branch block PVCs placed in tachycardia identify the
Antegrade conduction via an accessory retrograde accessory pathway and thus
pathway define the arrhythmia as ORT
PACs in tachycardia define the presence of
the second antegrade bystander accessory
pathway
Antidromic reciprocating tachycardia Early ventricular myocardial activation via PACs placed in tachycardia preexcite the
the accessory pathway that participates in ventricle and reset the tachycardia without
the tachycardia a change in ventricular or the subsequent
retrograde atrial activation sequence
Important to defi ne the mechanism for
ventriculoatrial conduction (AV node or a
second accessory pathway)
Ventricular tachycardia Initial myocardial activation without use of Difficulty arises when rapid and consistent
the conduction system ventriculoatrial activation is present,
particularly with fascicular tachycardia
Intermittent late coupled PVCs can also be
difficult to distinguish from intermittent
preexcitation
Abbreviations: AV, atrioventricular; ORT, orthodromic reciprocating tachycardia; PAC, premature atrial contraction; PVC, premature ventricular contraction.
a
Sinus tachycardia, atrial flutter, atypical atrial flutter, etc, can be analyzed as recommended for atrial tachycardia.
Specific attention should be paid to the onset and termi- unlikely. When dissociation between the atria and ventricles
nation of tachycardia. PR prolongation just prior to the ini- is clearly observed and the ventricular rate is greater than
tiation of tachycardia strongly suggests a supraventricular the atrial rate, ventricular tachycardia is likely. However, AV
mechanism, with the wide complex probably related to bun- node reentry as well as junctional tachycardia with aberrancy
dle branch aberrancy. Termination of tachycardia with ven- or a bystander accessory pathway may present with ventricu-
triculoatrial delay and then block also suggests a reentrant loatrial dissociation.
mechanism, either AV node reentry or a pathway-related Although the presence of fusion beats during tachycardia
tachycardia, and makes ventricular tachycardia highly is generally considered diagnostic of ventricular tachycardia,
in the context of wide QRS tachycardia, caution is required

in interpreting this phenomenon. Bystander pathways may Box 6.1
show intermittent or varying degrees of preexcitation, and Wide Complex Tachycardia With Right Bundle Branch
Block Morphology
some patients may have both bundle branch aberrancy and
a bystander pathway, giving rise to varying degrees of QRS Supraventricular tachycardia with right bundle branch block
fusion. Not uncommonly, rapid tachycardia from any mecha- Preexcited supraventricular tachycardia with a left-sided acces-
sory pathway
nism may induce bundle branch reentrant or intraventricular Antidromic tachycardia with a left-sided accessory pathway
reentrant echo beats that also give rise to fusion beats. In the conducting in an antegrade direction
electrophysiology laboratory, however, fusion during tachy- Ischemic ventricular tachycardia with exit in the left ventricle
cardia in the ventricular activation sequence, when placing Fascicular ventricular tachycardia (left posterior fascicle most
premature atrial contractions (PACs), or in the atrial activation common)
Left ventricular outflow tract tachycardia
sequence, when placing premature ventricular contractions
(PVCs), specifically signifies more than 1 method to get from
the atrium to the ventricle or ventricle to atrium, respectively. 2. With antegrade preexcitation via a left-sided accessory
This fusion in the intracardiac activation sequence is seen as pathway, certain specific axes or morphologies are less
fusion in the surface ECG as well. likely to be seen. For example, a strongly positive R wave
in lead II, III, or aVF, with an initially positive R wave
in lead I, suggests early activation of the left anterior
QRS Morphology wall of the ventricle and is unlikely from a preexcitation
mechanism. This is because accessory pathways are rare
Careful analysis of the wide QRS complex, paying attention
in the region of the aortic mitral continuity although
to whether the most abnormal segment is in the initial or later
this location is not an uncommon site for ventricular
portion of the QRS complex or affects the entire QRS, can
tachycardia in patients with relatively normal hearts.
be helpful in understanding the mechanism behind the wide
3. Although ischemic ventricular tachycardia may have any
QRS complex. When bundle branch aberrancy is present,
QRS morphology or axis associated with it, depending
because initial ventricular activation is via the normal con-
on the location of associated infarction and slow conduc-
duction system (left bundle, for example, during right bundle
tion zones, certain morphologies are highly suggestive of
branch block) (Figure 6.2), the initial part of the QRS deflec-
ischemic ventricular tachycardia. For example, right axis
tion is relatively normal. When the mechanism behind a wide
deviation tachycardia with right bundle branch block,
QRS tachycardia is antegrade preexcitation via an accessory
particularly in a patient with a known inferior wall myo-
pathway, the initial QRS deflection is the most abnormal
cardial infarction, suggests mitral isthmus ventricular
(delta wave later conduction is via the normal conduction
tachycardia (left bundle branch block and left axis devia-
system). Thus, a slurred initial deflection and relatively rapid
tion may also be seen, as discussed in Case 14).
later portions of the QRS are seen. With ventricular tachycar-
4. Because the most common type of fascicular ventricular
dia, unless it arises close to the conduction system, typically
tachycardia originates and exists close to the usual exit
a uniformly (early and late) wide QRS (greater than 160 ms,
of the left posterior fascicle, right bundle branch block
almost always diagnostic of ventricular tachycardia) and
is seen with a left anterior fascicular block pattern. The
often bizarre complexes are seen.
axis is typically left ward and superior. Whenever this
The ablationist should look further at the QRS morphology
specific morphology is seen in young patients, in whom
to see if that particular morphology and axis are consistent
a bifascicular block pattern aberrancy is seen rarely
with one of the more common sites for ventricular tachycar-
during SVT, fascicular ventricular tachycardia must
dia or with the usual exit location of the bundle branch system
not be confused with AV node reentrant tachycardia.
(right bundle exit in left bundle branch block tachycardia).
5. Left ventricular outflow tract tachycardia usually has a
Box 6.1 summarizes the main causes of wide QRS tachy-
strong inferior axis, with large R waves in leads II, III,
cardia with a right bundle branch block pattern. The ablation-
and aVF and a QS complex in leads aVR and aVL. This
ist should pay specific attention to the following details:
axis is unusual for a preexcited tachycardia because
1. When right bundle branch block is present (aberrancy), pathways in this location are rare (trigone pathways)
the exit may be through the left anterior fascicle or the and exclude the possibility of right bundle branch block
left posterior fascicle or both. Although the exact loca- aberrancy. The fascicular exits are much more apical
tion of these exits may vary considerably, they are never than this morphology suggests.
at the base of the heart or at the true apex of the left
Box 6.2 summarizes the causes of wide complex tachycar-
ventricle. Thus, if the precordial leads around the apex
dia with a left bundle branch block pattern. The ablationist
(V3, V4, V5, V6) are all negative (suggesting an origin
should pay specific attention to the following details:
near the apex) or most of the chest leads are positive
(suggesting an origin near the base), aberrancy from 1. With left bundle branch block aberrancy during
right bundle branch block is unlikely (Figure 6.3). supraventricular tachycardia, the exit is through the
Figure 6.3 Left panel, Exit through the left anterior and left posterior fascicles between base and apex after right bundle block. Middle
panel, Pathways exit at base (arrows). Right panel, Ventricular tachycardia can exit anywhere, but if from the apex, it would result in
negative concordance in the chest leads. Arrows represent conduction; wavy lines represent slow conduction.
right bundle. Although this exit may vary, the right almost always excludes an accessory pathway because
bundle is never at the true right ventricular apex or near even anteriorly located accessory pathways do not usu-
the base, with the exit typically higher than two-thirds ally show a QS complex in aVR and aVL. Very rarely
the distance to the apex. In the anteroposterior axis, the accessory pathways have been described connecting
right bundle usually exits slightly anterior to the mid the right atrial appendage to the right ventricular out-
portion of the right ventricular septum. Thus, neither flow tract, and in this situation, the QRS analysis can-
an apical (QS complexes in V2 to V6) nor a basal (all R not differentiate this rare entity from common right
waves in V2 to V6) morphology is seen. Further, because ventricular outflow tract tachycardia.
of the slightly anterior location of the usual right bun- 3. With a Mahaim-type fiber, left bundle branch block
dle exit, the entirely negative QS complexes in leads II, pattern is seen, and the QRS axis can be very difficult
III, and aVF are not seen. If morphologies that are not to distinguish from left bundle branch block aberrancy.
consistent with left bundle branch block aberrancy are The reason for this difficulty is that some Mahaim
noted, ventricular tachycardia is present, or in the case fibers connect to the right bundle and thus exit to the
of a basal (tall R waves in V2 to V6) morphology, both ventricular myocardium via the right bundle exactly
ventricular tachycardia and preexcited tachycardia at the location where exit occurs during left bundle
should be considered. branch block. Sometimes a glitch or notching of the
2. Ventricular tachycardia from the right ventricle in downstroke of the QS complex in lead I may be seen
patients with structurally normal hearts (no evidence with Mahaim-related tachycardia.
for dysplasia) usually arises from the outflow tract and 4. Rarely a left bundle branch block morphology may
has a strong inferior axis (R waves in leads II, III, and be seen with left ventricular tachycardia (Figure 6.4).
aVF and QS complexes in leads aVR and aVL). This Mitral isthmus ventricular tachycardia seen in patients
morphology excludes the possibility of left bundle with a prior inferior wall myocardial infarction may
branch block aberrancy because of the relatively more exhibit a left bundle branch block with left access devia-
apical exit of the right bundle. This morphology also tion morphology. Ventricular tachycardia with a suc-
cessful ablation site in the supravalvular aortic outflow
region may show a left bundle branch block pattern, but
Box 6.2 usually a small R wave is seen in lead V1.
Wide Complex Tachycardia With Left Bundle Branch
Block Morphology Precordial QRS Concordance
Supraventricular tachycardia with left bundle branch block
Supraventricular tachycardia with preexcitation via a right-sided Because neither the right bundle nor the left bundle exits
accessory pathway (including a Mahaim-type fiber) at the apex or the base, apical or basal QRS morphology/
Antidromic tachycardia using a right-sided accessory pathway axis during wide QRS tachycardia makes SVT with bundle
(including Mahaim-type fiber)
branch aberrancy unlikely. As most of the precordial leads
Right ventricular tachycardia
Left ventricular tachycardia (aortic cusp, mitral isthmus ven- tend to drape around the ventricular apex when positive con-
tricular tachycardia) cordance (R waves in all chest leads) is seen, a basal exit or
focus is suggested. Such a basal exit or focus may be seen in
A H V
2
43
2
AP 1 1
(antidromic
tachycardia)
Figure 6.4 Distal-to-proximal His bundle activation represents retrograde His bundle activation. Wide QRS tachycardia is a result of
antidromic tachycardia, with an antegrade conducting accessory pathway. Conduction through the His bundle and atrioventricular (AV)
node is retrograde, and the His bundle electrograms are earliest on the distal His electrode (1) and latest on the proximal His bundle
electrode (4). The pattern of His bundle electrograms is as expected, given the direction of conduction through the His-Purkinje and AV
nodal conduction system. The lines represent electrical conduction and are explained in the text. AP indicates accessory pathway.
ventricular tachycardia arising near the mitral annulus or in free wall, septum, or slow pathway region. The right ventricu-
preexcited tachycardia because accessory pathways typically lar pacing catheter is best placed at a slightly more basal loca-
insert close to the base. Negative concordance (QS complex tion rather than at the ventricular apex so the retrograde His
in all precordial leads, especially V3 to V6) suggests an apical bundle deflection is more likely to be seen during ventricular
exit or origin for tachycardia and is almost always diagnostic pacing. When pacing at the apex, the ventricular activation
of ventricular tachycardia. This is because neither the bundle wave front and His bundle activation occur almost simulta-
branch exit nor the typical accessory pathway insertions are neously, obscuring the His deflection.
at or near the apex. When a right-sided pathway, including a Mahaim-type
fiber, is in the differential diagnosis (left bundle branch block
tachycardia), a multielectrode catheter placed along the tri-
APPROACH TO WIDE QRS TACHYCARDIA IN cuspid annulus (with care to avoid “bumping” the pathway)
THE ELECTROPHYSIOLOGY LABORATORY can be useful.
To maximize the accuracy of diagnosis in sometimes highly AV Relationship

complex situations, meticulous attention to detail is required,
from the selection of the types of catheters to their placement If AV dissociation is obvious on the intracardiac electrogram
during pacing maneuvers. during a wide QRS tachycardia analysis and if there are more
atrial than ventricular electrograms, atrial tachycardia with
Catheter Placement and Recording of either aberrancy or antegrade accessory pathway (bystander)
Electrograms conduction is likely. Similarly, if there are more ventricu-
lar than atrial electrograms, then ventricular tachycardia
Because of the importance of recording the His bundle electro- becomes more likely. If differing QRS morphologies are
gram and knowing the His bundle activation sequence (distal observed during wide QRS tachycardia (some beats are nar-
to proximal or proximal to distal), a closely spaced multielec- row, but the tachycardia cycle length is unchanged), then SVT
trode catheter (1 or 2 octapolar catheters) should be placed with bystander pathway (or AV node or multiple pathways)
for His bundle and proximal right bundle branch recording. conduction is likely. With antidromic tachycardia, maximal
A deflectable catheter is advisable in the atrium because PACs preexcitation with the same ventricular activation sequence
must be placed at various atrial locations, including the atrial is usually seen, except in the rare situation when a second
antegrade conducting bystander pathway is present. Here, pacing maneuvers to determine whether the His bundle is
changes in the QRS morphology and the associated ventricu- being activated antegrade via the AV node or retrograde as in
lar activation sequence may be seen without a change in the antidromic tachycardia and ventricular tachycardia. A mul-
tachycardia cycle length. Very rarely junctional tachycardia tielectrode catheter that spans the His bundle and proximal
or AV node reentry may present with more ventricular elec- right bundle can be useful to make this determination. If the
trograms (with wide QRS) than atrial electrograms (upper His bundle activation sequence is clearly from proximal to
common pathway block) and mimic ventricular tachycar- distal, retrograde activation is highly unlikely. Similarly, if
dia. The more common AV dissociation seen with AV node distal His bundle activation (proximal right bundle) precedes
reentry occurs with infrahisian block, and in that situation, proximal His bundle activation, retrograde activation from
its differentiation from atrial tachycardia with intermittent ventricular tachycardia, antidromic tachycardia, or atrio-
AV conduction and bundle branch block or intermittent fascicular bypass tract activation is likely. The intrahisian
preexcitation must be made. activation sequence can at times be misleading, particularly
if most of the recording electrodes have been placed fairly
Intracardiac Intervals (A-H, H-V, and distally. If retrograde right bundle branch block that is fairly
V-H Intervals) distal is present, then even ventricular tachycardia with retro-
grade conduction via the left bundle and antegrade conduc-
If the A-H interval is shorter during wide QRS tachycardia
tion in the proximal His bundle region are misinterpreted as
than during sinus rhythm, either fast-slow AV node reentry
antegrade His bundle activation (Figure 6.5). The concept of
tachycardia with bundle branch block or preexcited tachy-
direction of His bundle activation and its relationship to the
cardia should be considered. A shorter A-H interval during
type of tachycardia are illustrated in Figures 6.4 through 6.7.
tachycardia may also be seen in junctional tachycardia and
Figure 6.5 shows a wide QRS tachycardia caused by left
with atriohisian pathways (variant of Mahaim). When the
bundle branch block during atrial tachycardia. This scenario
A-H interval during tachycardia is considerably longer than
is common to several SVTs with bundle branch block. A mul-
that seen in sinus rhythm, typical AV node reentry or anti-
tipolar His bundle catheter is placed in the region of the His
dromic tachycardia with a retrograde His bundle deflection
bundle and proximal right bundle branch. During tachycar-
should be considered.
dia, antegrade activation of the AV node and His-Purkinje
If the H-V interval is considerably shorter during wide
system occurs. This results in early activation at the proximal
QRS tachycardia than during sinus rhythm, His bundle
His bundle electrode or progressively later activation through
tachycardia, ventricular tachycardia, or antidromic tachycar-
subsequent more distal electrodes. Thus, proximal-to-distal
dia should be considered. In the latter 2 situations, the H-V
His bundle activation is seen representing antegrade His bun-
interval is often negative. With bundle branch reentrant ven-
dle activation.
tricular tachycardia, the H-V interval may be shorter than,
In Figure 6.4, the His bundle electrodes are similarly
similar to, or slightly longer than the H-V interval during
placed as in Figure 6.5. Wide QRS tachycardia is a result of
sinus rhythm and depends on the conduction characteristics
antidromic tachycardia with an antegrade conducting acces-
antegrade in the right bundle and retrograde conduction from
sory pathway at the right free wall. Conduction through the
the left bundle–His bundle junction to the portion of the His
His bundle and AV node is retrograde. As expected, this
bundle being recorded by the mapping catheter. If the H-V
retrograde conduction is reflected in the His bundle electro-
interval is longer during tachycardia than in sinus rhythm,
grams, earliest on the distal His electrode and latest on the
bundle branch aberrancy with conduction abnormality in the
proximal His bundle electrode. The pattern of His bundle
conducting bundle (eg, left bundle with right bundle branch
electrograms is expected, given the direction of conduction
block) should be considered. Sometimes the appearance of
through the His-Purkinje and AV nodal conduction sys-
antegrade H-V conduction presents when the retrograde His
tem. Unfortunately, this simple method of trying to iden-
bundle electrogram is very late (a long V-H interval mimick-
tify whether the His bundle is being activated antegrade or
ing a shorter H-V interval).
retrograde is far from foolproof.
If the H-A interval is shorter during tachycardia than with
Figure 6.6 shows a disjoint between His bundle activation
ventricular pacing at a similar cycle length, AV node reen-
and the true direction of conduction through the AV conduc-
try, particularly the type associated with a lower common
tion system. Atrial tachycardia with proximal right bundle
pathway, is likely. The H-A interval during tachycardia is also
branch block produces wide QRS tachycardia. The His bun-
shorter than ventricular pacing in patients with atriohisian or
dle electrodes are distal to the site of right bundle branch
atriofascicular connections, with a connection being close to
block. The His bundle electrograms are earlier distal and later
the proximal right bundle and antidromic tachycardia.
proximal. The right bundle branch distal to the site of right
Recognizing Retrograde His Bundle bundle branch block is activated retrograde, with activation
Activation first occurring via the left bundle and then with transseptal
conduction up the right bundle. Since the recording elec-
Often the key to ablation of complex wide QRS tachycardia is trodes are distal to the proximal site of right bundle branch
the His bundle electrogram. It is useful prior to performing block, retrograde activation of the His bundle electrograms
A H V
4
Atrial
tachycardia
3
2
43
2 LBBB
1 1
Figure 6.5 Proximal-to-distal His bundle activation represents antegrade His bundle activation. A multipolar His bundle catheter
(4, 3, 2, 1) is placed in the region of the His bundle and proximal right bundle branch. During tachycardia, antegrade activation of the
atrioventricular node and His-Purkinje system occurs. This results in early activation at the proximal His bundle electrode (4) and
progressively later activation through subsequent more distal electrodes (3, 2, 1). Yellow arrow represents the electrical conduction
wavefront. LBBB indicates left bundle branch block.
A H V
Atrial 4
tachycardia
3
Proximal
RBBB 2
43 1
2
1
Figure 6.6 Distal-to-proximal His activation represents antegrade His bundle activation. A disjoint between His bundle activation and
the true direction of conduction through the atrioventricular (AV) conduction system can occur. Atrial tachycardia with proximal right
bundle branch block (RBBB) produces wide QRS tachycardia. The His bundle electrodes are placed more distally and are distal to the RBBB
site. The His bundle electrograms are earlier distal and later proximal (1→4) because the right bundle branch distal to the site of RBBB is
activated retrograde, with activation first occurring via the left bundle and then with transseptal conduction up the right bundle. Since the
recording electrodes are placed distal to the proximal site of RBBB, retrograde activation of the His bundle electrograms is seen despite
antegrade conduction of the AV node and His bundle. The lines represent electrical conduction and are explained in the text.
is seen despite antegrade conduction of the AV node and His increases (decremental compact AV nodal conduction). When
bundle. antegrade conduction blocks the AV node and the His bun-
Figure 6.7 shows an analogous situation to Figure 6.6 dle is being activated retrograde via an accessory pathway,
where retrograde conduction via the His bundle and AV node ventricular myocardium, and the conduction system, fur-
occurs, yet the His bundle electrodes show antegrade activa- ther decrement is not seen. This plateau in the A–H interval
tion. Antidromic tachycardia occurs with distal right bundle with decreasing A-A intervals strongly suggests that the His
branch block. The His recording electrodes are all proximal bundle electrogram being recorded is activated in a retrograde
to the site of right bundle branch block. The His electrograms fashion. Once retrograde activation of the His has been con-
show proximal-to-distal activation because activation of the firmed, if the V-H interval changes and gives rise to changes
proximal right bundle branch is in the antegrade direction in the tachycardia cycle length, antidromic tachycardia can
despite the fact that activation of the His bundle and AV node be diagnosed (see case examples below). If the V-H interval
is in the retrograde direction. This situation of retrograde dis- (His bundle activated retrograde) changes without affecting
tal right bundle branch block is fairly frequently seen during the tachycardia cycle length, ventricular tachycardia is the
Mahaim and other antidromic tachycardias. Thus, using the likely diagnosis.
direction of activation on multipolar His bundle recordings
requires cautious interpretation in the context of right bundle What Is the “Driver”?
branch block and precise location of the recording electrodes.
Relative fi xity of the A-H interval, despite variation in the During wide complex tachycardia, if the cycle length of
atrial cycle length (tachycardia cycle length), suggests a ret- tachycardia varies spontaneously (often seen at initiation or
rograde His bundle electrogram. The same phenomenon is just prior to termination), careful analysis of the intracardiac
seen during atrial pacing on electrophysiologic study and is intervals can be useful to see which change in interval (the
important to recognize. With antegrade His bundle activa- “driver”) results in subsequent changes in other intracardiac
tion, as the atrial pacing rate is increased, the A-H interval intervals and the tachycardia cycle length.
A H V
3
Distal
RBBB 2
AP 43 1
(antidromic 2 1
tachycardia)
Figure 6.7 Proximal-to-distal His activation represents retrograde His bundle activation. In an analogous situation to Figure 6.6,
retrograde conduction via the His bundle and atrioventricular (AV) node occurs, yet the His bundle electrodes show antegrade activation.
Antidromic tachycardia occurs with distal right bundle branch block (RBBB). The His recording electrodes are all proximal to the RBBB
site. The His electrograms show proximal to distal activation (4→1) because activation of the proximal right bundle branch is in the
antegrade direction despite activation of the His and AV node in the retrograde direction. The wave front blocks in the distal right bundle
and through transseptal conduction ascends the left bundle, simultaneously progressing up the His and AV node and down the proximal
right bundle branch where the His recording catheters have been placed. Retrograde distal RBBB is seen fairly frequently during Mahaim
and other antidromic tachycardias. Using the direction of activation on multipolar His bundle recordings requires cautious interpretation
in the context of RBBB and precise location of the recording electrodes. AP indicates accessory pathway. The lines represent electrical
conduction and are explained in the text.
H-H Interval A-H Interval
When changes in the H-H interval result in subsequent If the A-H interval is seen to vary first, thus being the driver
changes in wide QRS tachycardia, junctional tachycardia for tachycardia, the interpretation depends on whether the
and AV node reentry or bundle branch reentrant tachycar- His bundle is activated antegrade or retrograde. If the A-H
dia should be considered. Further analysis can determine interval is the driver and the His bundle is being activated
whether changes in the H-H interval cause changes in both antegrade, then antegrade AV nodal conduction is critical to
the atrial and ventricular cycle lengths. If the H-H interval the circuit. Thus, even if an antegrade conducting accessory
varies and causes variation in the atrial cycle length but not pathway has been found, it is a bystander. Reentrant SVTs
the ventricular cycle length (dissociation from ventricle), with bundle branch block also show this type of response
junctional tachycardia or AV node reentry with infrahisian (ie, A-H is the driver).
disease or block is possible. With fascicular tachycardia and If the His bundle is known to be activated retrograde and
rapid ventriculoatrial conduction, if the left ventricular map- changes in the A-H interval cause subsequent changes in the
ping catheter is not placed at the site of earliest activation near tachycardia cycle length, then the examiner should determine
the left posterior fascicle, the His bundle deflection is seen as if the ventricular electrogram changed before or after the ret-
the first recorded deflection, and H-H variation causes subse- rograde His bundle electrogram changed. If the A-retrograde
quent change in the atrial cycle length. However, importantly His interval is the driver without intervening change in the
the tachycardia is not reset. With bundle branch reentrant intervening ventricular electrogram, then antidromic tachy-
tachycardia, changes in the H-H interval do predict changes cardia with an atrial fascicular bypass tract is likely. If the
in the subsequent V-V interval, but with dissociation from A-retrograde His interval is the driver but a ventricular elec-
the atrium (no predicted changes in the A-A interval). trogram change precedes the His bundle electrogram change,
then antidromic tachycardia with an atrioventricular bypass
V-V Interval tract is likely.
When the V-V interval changes, subsequent changes in the H-A Interval
atrial cycle length occur, and tachycardia is reset, there is
likely SVT with either antegrade preexcitation or aberrancy. Any changes in the H-A interval measured from the end of
For example, in orthodromic tachycardia with right bundle the His bundle electrogram to the earliest atrial electrogram,
branch block, a PVC or spontaneous ventricular cycle length if determined to be the driver of the circuit, strongly suggest
variation causes atrial cycle length variation and subsequent AV node reentry as the mechanism of tachycardia. However,
changes via antegrade conduction in the next ventricular if the His bundle recording is retrograde with antidromic
activation. If, however, the V-V changes cause changes in tachycardia, the retrograde H-A interval reflects conduction
either the retrograde His or the atrium without resetting the via the compact AV node, and such changes are consistent
tachycardia, then ventricular tachycardia is likely. with antidromic tachycardia. Determining whether a His
bundle recording is antegrade or retrograde is important
before these maneuvers are applied and analyzed.
A-A Interval
If changes in the A-A interval are dissociated from changes in H-V Interval
the His electrogram or ventricular electrograms, atrial tachy-
cardia is likely. If changes in the A-A interval cause subse- If the His bundle being recorded is antegrade and the H-V
quent changes in the V-V interval, similar changes in the H-H interval is found to be the driver of the circuit (that is, the
interval may occur. If the A-A interval changes and causes H-V interval predicts changes in the atrial and ventricular
changes in the V-V interval only when changing the ante- cycle lengths, with reset of the tachycardia), orthodromic
grade His bundle cycle length without resetting the tachycar- reciprocating tachycardia is likely, and the cause of the wide
dia, then atrial tachycardia with aberrancy, as the cause of QRS interval may be either a second bypass tract acting as a
the wide QRS rhythm, is likely (it should first be determined bystander or bundle branch block. If the His bundle is acti-
whether the His bundle electrogram is in fact activated ante- vated retrograde and the H-V interval is positive and found to
grade). If the A-A cycle length causes changes in the V-V be the driver of the circuit, then pathway-to-pathway tachy-
cycle length, but without first affecting the H-H interval or cardia with an antegrade atrial fascicular pathway and retro-
resetting the tachycardia, then atrial tachycardia with antegrade conducting accessory pathway is highly likely. The H-V
grade preexcitation via a bystander pathway is likely. If the interval is the driver and implicates the His-Purkinje network
A-A interval does affect the V-V interval (without affecting and ventricular myocardium, necessary for retrograde activa-
the H-H interval) and the tachycardia is reset, then a reen- tion of the atrium. This situation occurs only when an acces-
trant mechanism that involves both the atrial and ventricular sory pathway forms the retrograde limb of the circuit. With
myocardium (antidromic tachycardia, pathway-to-pathway this conclusion, along with the determination that the His
tachycardia) is likely present. bundle is being activated retrograde (antegrade preexcitation)
and with the positive H-V interval (unlikely with regular infrahisian conduction) are expected, with rapid pacing prior
atrioventricular bypass tracts), pathway-to-pathway tachy- to termination of the atrial arrhythmia.
cardia with the antegrade pathway being an atriofascicular If, during wide QRS tachycardia, incremental atrial pacing
tract can be diagnosed. is found to entrain the tachycardia (ie, preexciting the V and
resetting the tachycardia) without a change in the activation
V-H Interval sequence, then a reentrant mechanism that likely involves
both the atrium and ventricle is usually present (antidro-
If retrograde activation of the His bundle has been deter- mic tachycardia, orthodromic tachycardia with bystander
mined and changes in the V-H interval predict changes in the antegrade or retrograde accessory pathways). Careful atten-
atrial cycle length and reset the tachycardia, then antidromic tion should be paid to the ventricular and atrial activation
tachycardia, either with an atrioventricular bypass tract or an sequences during entrainment of the tachycardia from the
atriofascicular tract, is present. Changes in the V-H interval atrium. If tachycardia is entrained but there are changes in
that cause changes in the A-A interval but do not reset the either the antegrade ventricular activation sequence or the
tachycardia suggest ventricular tachycardia as the mecha- retrograde atrial activation sequence, then bystander acces-
nism of the wide complex rhythm. sory pathways in the antegrade or retrograde direction,
respectively, are likely present.
If pacing from the atrium during wide QRS tachycardia
PACING MANEUVERS entrains the atrium with no effect or dissociation from the
ventricular electrograms, then a macro-reentrant atrial tach-
Chapter 4 on maneuvers used in the electrophysiology labo- yarrhythmia with bystander accessory pathway or bundle
ratory discusses the common pacing maneuvers pertinent branch block is likely present.
to wide QRS tachycardia ablation. Here we highlight the If atrial pacing during tachycardia entrains the tachycar-
main principles and common issues encountered when the dia, then when pacing is stopped, the return electrogram
maneuvers are used with these often complex wide QRS sequence can be analyzed, as summarized in Figure 6.8.
tachycardias. After determining with atrial pacing that the tachycardia
has been entrained, the ventricular activation sequence and
Incremental/Decremental Atrial Pacing QRS morphology are analyzed. If entrainment of the tachy-
cardia occurs with a change in the ventricular activation
In patients with suspected antidromic tachycardia, atrial sequence, either a bystander accessory pathway or ventricular
pacing at the cycle length of tachycardia typically results in tachycardia is present. If the entrainment with QRS morphol-
maximal preexcitation and QRS morphology similar to that ogy change occurs only with advancing the antegrade His
seen in tachycardia. Maximal preexcitation does not always bundle electrogram, then the underlying arrhythmia is likely
occur, however, especially if the pacing is done from a site far to be ventricular tachycardia that can be entrained from the
removed from the atrial insertion of the accessory pathway. atrium (ischemic ventricular tachycardia with atrial pacing
During tachycardia, if atrial pacing results in either loss results in the equivalent of ventricular pacing, with the stim-
of the wide QRS complex (normalization of QRS) or AV ulation site being the bundle branch exit). If the tachycardia
block with continued tachycardia, on cessation of pacing, can be entrained with a change in the activation sequence but
atrial tachycardia is likely, with bystander activation via an without preexcitation of the atrial electrogram near the AV
accessory pathway and AV node conduction to the ventricle. node or the His bundle, then an accessory pathway is pres-
If atrial pacing results in termination of tachycardia without ent but likely does not participate in tachycardia as otherwise
prolongation of the A-H interval or preexcitation of the ven- a similar QRS morphology results (antidromic tachycardia
tricular electrograms, then antidromic tachycardia is likely. with atrial pacing).
The most likely way atrial pacing can disrupt a tachyarrhyth- If entrainment is established from the atrium and the
mia without affecting the AV node (the A-H interval does not QRS morphology is identical (similar ventricular activation
change) or affect the ventricular myocardium (no preexcita- sequence), then the electrogram sequence after cessation of
tion of V) is by penetrating and delaying conduction in the pacing is analyzed next. If the atrial paced beat enters the ven-
accessory pathway. This is similar to the situation in which tricle and the next electrogram is another ventricular electro-
ventricular pacing during SVT terminates tachycardia with- gram with retrograde activation of the atrium subsequently,
out affecting atrial activation or the retrograde His. ventricular tachycardia is likely (A-V-V-A sequence). An
When atrial pacing terminates tachycardia without affect- A-A-V sequence is unusual with any of the causes described
ing the AV node or the ventricle, atrial tachycardia cannot for wide QRS tachycardia but may be seen rarely in AV node
be excluded as the primary arrhythmia. Tachycardia may reentry as the atrial pacing may be going antegrade through
be overdrive suppressed, or reentrant tachycardia may ter- the slow pathway. On cessation of pacing, retrograde activa-
minate with the atrial pacing. These situations, however, are tion of the atrium via the fast pathway may precede ante-
unlikely as changes in the QRS morphology (from differing grade conduction of the ventricle through the His-Purkinje
fusion with AV node and an accessory pathway or changes in system.
Wide QRS with 1:1, A:V
A paced faster than tachycardia
V entrained
Changed QRS/activation
sequence QRS/activation unchanged
His His
advanced unchanged Stop pacing
VT Bystander A-V-V-A A-V-A A-A-V
AVNRT
A-H A-H
VT short same
Bystander
But
Decrement ORT
ART
antegrade AVNRT
Figure 6.8 Atrial pacing to entrain wide QRS tachycardia. ART indicates antidromic reciprocating tachycardia; AVNRT, atrioventricular
node reentry tachycardia; ORT, orthodromic reciprocating tachycardia; VT, ventricular tachycardia.
If, on cessation of pacing, the last paced atrial electro- This maneuver is in many ways analogous to the introduc-
gram is followed by a ventricular electrogram of similar QRS tion of PVCs during narrow complex tachycardia. The main
morphology and there is a return atrial electrogram with an feature that should be specifically sought is whether the ven-
unchanged atrial activation sequence (compared to tachycar- tricular electrograms are advanced and, if so, whether the
dia), several possibilities exist. First, antidromic tachycardia activation sequence is changed. If the ventricular electro-
is possible as the last paced beat travels down the accessory grams are advanced, then it should be ascertained whether
pathway and then up the AV node, identical to the activa- the next set of atrial electrograms is also advanced and, if so,
tion in tachycardia. The paced atrial complex (particularly if whether the activation sequence has changed (resetting the
placed close to the pathway) travels directly down the acces- tachycardia). An additional piece of information that should
sory pathway, and the wave front then travels to reach the be obtained is whether the atrial electrograms on the septum
atrial myocardium near the His bundle catheter. Thus, the (near the AV node) are advanced by placing the PACs on the
A-H interval from the last paced beat may be shorter than that lateral right or left atrium prior to advancing the next ven-
seen in tachycardia (Figure 6.8). If the A-H interval is the same tricular electrogram.
or there is a consistent decrement in the AV node noted with
atrial pacing that entrains the tachycardia, then orthodromic Does Tachycardia Terminate?
reciprocating tachycardia or AV node reentry is likely.
If a PAC placed during wide QRS tachycardia terminates tachy-
Introduction of PACs During Wide QRS cardia without advancing the atrial electrogram near the AV
Tachycardia node, the His bundle electrogram, or the next ventricular elec-
trogram, then antidromic tachycardia, pathway-to-pathway
Figure 6.9 summarizes the interpretation of the response seen tachycardia, or atrial tachycardia can be diagnosed. Since
when PACs are introduced during wide complex tachycardia. the atrium near the AV node and the His bundle are not
A captured
V advanced
Activation sequence Activation sequence

unchanged changed
His advanced His unchanged His unchanged
Septal A Septal A not

A-H same A-H short advanced advanced Bystander
No ? Retro Nodo- ART

Reset reset His ventricular Mahaim His advanced
AVNRT By-
ORT stander VT
Figure 6.9 Premature atrial contractions in wide QRS tachycardia. ART indicates antidromic reciprocating tachycardia; AVNRT,
atrioventricular node reentry tachycardia; ORT, orthodromic reciprocating tachycardia; VT, ventricular tachycardia.
advanced, tachycardia is not terminated because of penetra- the ventricle without reaching the AV node or the His bundle
tion into the AV node, making AV node reentry or ortho- (the His bundle may be preexcited but only after preexcitation
dromic tachycardia unlikely. Since tachycardia is terminated of the ventricle). Once the ventricle has been activated, the
without entering the ventricle, once again orthodromic PAC functions like a PVC placed in tachycardia and resets
tachycardia is unlikely (it would have to reach the ventricle the atrial electrogram. The electrophysiologist ascertains
to get to the retrograde conducting accessory pathway) and whether the advanced V has advanced the next A, with or
excludes ventricular tachycardia. With antidromic tachycar- without advancing the retrograde His bundle electrogram
dia or pathway-to-pathway tachycardia (antegrade accessory by a similar amount. If the V that is advanced by the PAC
pathway), PACs may penetrate into the pathway and termi- advances the next A without advancing the retrograde His,
nate tachycardia. This phenomenon of concealed penetration then retrograde activation is via another accessory pathway,
is analogous to termination of tachycardia by PVCs without and pathway-to-pathway tachycardia can be diagnosed.
affecting the retrograde His bundle electrogram or the next If the PAC placed during tachycardia advances the next
atrial electrogram. Finally, a PAC may terminate atrial tachy- retrograde His electrogram, even before the next ventricular
cardia without necessarily affecting AV conduction, be it electrogram is advanced, without a change in the QRS mor-
through a bystander accessory pathway or the AV node. phology, and resets the tachycardia, then antidromic tachy-
cardia, using an atriohisian or atriofascicular connection
Is the Next V Advanced Without a Change in inserting in the proximal right bundle branch, is present.
the QRS Morphology and Is the Subsequent
A Advanced Without a Change in the Atrial Is the V Advanced Without Advancing the
Activation Sequence? Next Atrial Electrogram and Without a
Change in the QRS Morphology?
If this response is observed without preexcitation of the sep-
tal atrial electrogram or the His bundle electrogram, then This response is similar to that described above and is diag-
antidromic tachycardia is present. Thus, the PAC has reached nostic of an accessory pathway conducting in the antegrade
direction. To reach the ventricle without advancing the septal generally believed that Mahaim fibers do not occur in the
atrial electrogram or antegrade His bundle electrogram, an septum, and congenital duplication of the AV node is usu-
accessory pathway must be present. However, as the tachy- ally located on the left side of the septum. No maneuvers
cardia is not reset, it is not known whether that accessory have been described to distinguish among these 3 rare dis-
pathway is a bystander or the PAC failed to advance the V orders; further mapping identifies the Mahaim potential
early enough to penetrate either the retrograde AV node or (Mahaim-related His bundle) in a location separate from the
another pathway. The situation can be clarified by simply His bundle recording. Similarly, if a duplicate AV node and
placing earlier PVCs during tachycardia to analyze the retro- His bundle are present, further mapping identifies this struc-
grade preexcitation and activation sequence. ture to be spatially distinct from the initially recorded His
bundle electrogram.
Is the Next V Advanced Without Changing
the Septal Atrial Electrogram or Antegrade Is the Next Ventricular Electrogram Delayed
His but With a Change in the QRS by the Inserted PAC Without Affecting the
Morphology? Septal Atrial Electrogram or the His Bundle
Electrogram?
If this response is observed, then an antegrade conducting
accessory pathway that is a bystander is diagnosed. The actual This finding is diagnostic of antidromic tachycardia either
tachycardia mechanism may be ventricular tachycardia or using a usual AV connecting pathway or a Mahaim-type
AV node reentry orthodromic reciprocating tachycardia or fiber. This postexcitation, in its extreme form, is the termina-
antidromic reciprocating tachycardia using a second ante- tion of the tachycardia described above. A bystander pathway
grade accessory pathway. In other words, the ventricle is acti- is excluded when conduction is delayed, and it is not neces-
vated from a ventricular source (ventricular tachycardia), the sary to demonstrate reset of the tachycardia. A rare alterna-
normal conduction system (AV node reentry or orthodromic tive possibility is that atrial tachycardia is present, and the
tachycardia), or an accessory pathway that is not responsible PAC is sufficiently early to decrement in the slow zone of the
for the tachycardia. Thus, the pathway that allows the PAC to macro-reentrant atrial tachycardia, and thus delay activation
reach the ventricle is a bystander. of the ventricle via a bystander accessory pathway. This is an
exceedingly unusual constellation of occurrences, and thus
Does the PAC Advance the Next V the response described is essentially diagnostic of antidromic
Only by Advancing the Antegrade His tachycardia.
Bundle Electrogram?
If this response is seen, the QRS morphology does not INTRODUCTION OF PVCS DURING WIDE
change, and the tachycardia is reset, an antegrade AV node COMPLEX TACHYCARDIA
conduction–dependent tachycardia can be diagnosed (exclud-
ing antidromic tachycardia, atrial tachycardia, and ventricu- The interpretation and utility of introducing PVCs dur-
lar tachycardia). The likely diagnoses are either AV node ing wide complex tachycardia are discussed in detail in
reentry or orthodromic reentrant tachycardia. Care must be Chapter 4. Here the specific differences in understanding the
taken, however, to ensure that the His bundle electrogram response with this maneuver in wide complex rhythms as
does in fact reflect antegrade conduction. If the His bundle opposed to narrow complex tachycardia are highlighted.
electrogram is retrograde and is advanced prior to advancing The preexcitation index distinguishes between retrograde
the ventricular electrogram, antidromic tachycardia with an activation of the atrium via the AV node (AV node reentry)
atriofascicular pathway is likely. and retrograde conduction via an accessory pathway (ortho-
dromic reciprocating tachycardia). The difference in ease of
Is the Next V Advanced Without preexcitablity is based on the fact that it is difficult to pen-
Advancing the His Bundle Electrogram but etrate the AV node in a retrograde fashion because with AV
Only When the Atrial Electrogram on the node reentry tachycardia, the AV node is being activated
Septum Near the AV Node Is Advanced? antegrade and the PVC has to be sufficiently early to activate
the atrium via the AV node. With orthodromic reciprocat-
If this rare response is seen repeatedly, the QRS morphology ing tachycardia, however, because of retrograde conducting
is unchanged, and the tachycardia is reset, then nodoven- accessory pathway, the atrium may be preexcited and the
tricular or nodofascicular tachycardia is diagnosed. An iden- tachycardia reset with a relatively late coupled PVC.
tical response may also be expected if a Mahaim-type fiber With antidromic tachycardia, including that associated
is located close to the septum or on the AV septum. This with a Mahaim fiber, whether retrograde activation of the
response would also be seen if an accessory (duplicate) AV atrium is via the AV node or another accessory pathway, fairly
node with a separate His bundle that is not being recorded late coupled PVCs can reset the tachycardia by advancing the
is present. Although all 3 possible responses are rare, it is next atrial electrogram. No antegrade activation of the AV
node occurs regardless of whether retrograde activation is via is, ventricular tachycardia is entrained from the V, with ret-
the AV node or another accessory pathway. Thus, in this situ- rograde conduction to the atrium. On cessation of pacing, the
ation, the preexcitation index is of little value. The distinc- last paced beat gets to the atrium, thus producing an atrial
tion can be made by seeing whether the PVCs preexcite the electrogram, and then the next beat is the resumption of
retrograde His prior to or to a greater extent than preexcit- ventricular tachycardia. A V-A-V response with ventricular
ing the atrial electrograms without changing the activation tachycardia is usually made apparent when more rapid ven-
sequence. Thus, during wide QRS tachycardia, if a PVC pre- tricular pacing is done. A V-A decrement or V-A block may
excites the atrium without changing the activation sequence be seen transiently without affecting the tachycardia. If such
and does not affect the retrograde His bundle electrogram, V-A decrement or block has not been observed, ventricular
then retrograde activation occurs via an accessory pathway, tachycardia remains a diagnostic possibility when a V-A-V
and orthodromic reciprocating tachycardia with aberrancy, response is seen with a Morady maneuver in wide complex
orthodromic reciprocating tachycardia with an antegrade tachycardia.
bystander accessory pathway, or pathway-to-pathway tachy-
cardia with antegrade conduction via 1 accessory pathway
and retrograde conduction via another is present. It is impor- SUMMARY
tant to determine if the tachycardia is reset in each of these
instances because a PVC may advance the next beat of ven- Students of electrophysiology know, either from their first
tricular tachycardia and thus advance the next A via the AV encounter with an unusual wide complex tachycardia or by
node or a bystander retrograde accessory pathway that does reading the preceding portions of this chapter, that the rea-
not participate in tachycardia. soning behind execution of the maneuvers and interpretation
of the responses of wide QRS tachycardia can be complex.
However, with careful study and repeated practice perform-
Morady Maneuver
ing and interpreting these maneuvers, clarity emerges. It is
When ventricular pacing is performed at a rate slightly faster important to perform these maneuvers (atrial pacing, placing
than wide QRS tachycardia and the tachycardia has been PACs, placing PVCs, ventricular pacing, etc) in all patients
entrained, the electrogram response on cessation of pacing with wide QRS tachycardia (or narrow complex tachycardia),
is observed (Morady maneuver). As described in Chapter 4 even when the diagnosis is apparent. For example, during
for SVT (narrow complex tachycardia), if a V-A-V response is ventricular tachycardia ablation when the diagnosis is clear
observed without a change in the atrial activation sequence, on the basis of the site of origin in the ventricle, experience
then AV node reentry or orthodromic reciprocating tachy- placing PACs, PVCs, or atrial pacing and ventricular pacing,
cardia is diagnosed. In the context of wide QRS tachycardia, when performed in all such cases with critical review of the
additional possibilities that produce a V-A-V pattern on ces- responses, the experience can aid the electrophysiologist when
sation of ventricular pacing include antidromic tachycardia he or she is confronted with a truly difficult or confusing case.
and pathway-to-pathway tachycardia. Although the distinc- To better emphasize and illustrate the principles described in
tion between these possibilities cannot be made with this the first part of this chapter, the discussion now turns to some
maneuver alone, the main utility is in excluding atrial tachy- case studies and electrograms that illustrate application of
cardia with bundle branch block or a bystander antegrade the above-mentioned principles and algorithms.
accessory pathway.
When the tachycardia has been entrained and a V-A-V CASE STUDIES
pattern is seen on cessation of pacing, the electrophysiolo-
gist should specifically see whether the last V of the V-A-V A wide complex tachycardia was the cause of recurrent
sequence has been advanced without advancing the antegrade palpitations in an otherwise healthy 24-year-old woman.
His bundle electrogram. That is, if the last paced beat reaches Symptoms of palpitations were present for several years.
the atrium either via a retrograde pathway or the AV node Previously documented arrhythmia had a QRS morphology
and gets back to the ventricle without activating the AV node, similar to that shown in Figure 6.10.
then antidromic tachycardia or pathway-to-pathway tachy-
cardia can be diagnosed. If the last V of the V-A-V sequence Which of the following diagnoses is least likely in this
is advanced only when the antegrade His bundle deflection is patient?
advanced, then AV node reentry or orthodromic reciprocat- A. Automatic left ventricular tachycardia
ing tachycardia with bundle branch block aberrancy is likely. B. Reentrant left ventricular tachycardia
If a V-A-V pattern is observed and the last V is advanced C. Preexcited AV node reentrant tachycardia
without advancing the antegrade His but without resetting D. Atrial tachycardia with right bundle branch block
tachycardia, then orthodromic reciprocating tachycardia or E. Antidromic tachycardia using a left-sided accessory
AV node reentry tachycardia can be diagnosed with an ante- pathway for antegrade conduction
grade conducting bystander accessory pathway. A V-A-V Answer: D—Atrial tachycardia with right bundle branch
response may also be seen with ventricular tachycardia. That block.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure 6.10 Wide complex tachycardia in an otherwise healthy 24-year-old woman. The arrow indicates the P wave.
As discussed in the preceding sections, the differential QS complexes in both aVR and aVL suggest an anterolateral
diagnosis for wide complex tachycardia includes all causes or anterior exit. Both ventricular tachycardias and accessory
of narrow complex tachycardia with bundle branch block, all pathways may occur in this location. More anterior at the
causes of narrow complex tachycardia with antegrade preex- base along the mitral annulus, however, accessory pathways
citation, ventricular tachycardia, and antidromic and other become less common. At the anteroseptal mitral annulus
preexcited reciprocating tachycardias. (aortic mitral continuity) accessory pathways are exceed-
The electrophysiologist should approach such cases in 2 ingly rare. Typically in these locations, lead I is biphasic with
segments: first asking a question about the mechanism for a clear initial positive deflection. In such left anteroseptal
the wide QRS complex and then asking a question about the locations, an accessory pathway can be excluded, and since
mechanism for the underlying tachycardia. Th is segmental or bundle branch block has been excluded, ventricular tachycar-
stepwise approach should be maintained in the electrophysi- dia from that region is the likely diagnosis. In this particular
ology laboratory, as detailed in the preceding discussion. ECG, however, in the anterior/anterolateral annular loca-
In terms of the mechanism for the wide QRS complex, the tion, both an antegrade conducting pathway and ventricular
main questions that have to be answered are whether this is tachycardia should be considered. As emphasized in several
ventricular tachycardia, preexcited tachycardia, or bundle places in this book, the mechanism of the tachycardia can-
branch block. The QRS morphology provides some important not be deduced from the morphology of the QRS complex or
clues. First, the lead V1 shows right bundle branch block mor- even with extensive invasive activation sequence mapping.
phology. This is consistent with a left ventricular tachycardia, Therefore, both anatomic and reentrant left ventricular tachy-
left-sided accessory pathway conducting in the antegrade cardia is possible. Thus, of all the possibilities given in the
direction, or right bundle branch block. However, the QRS question, the least likely is atrial tachycardia associated with
complex is positive in V1 to V6. In addition, both aVR and aVL right bundle branch block.
show QS complexes. This suggests a very basal early site of The arrow in Figure 6.10 indicates the P wave. If this
activation in the left ventricles (positive concordance). Such a arrhythmia is a ventricular tachycardia, then there is likely
basal site of activation would exclude bundle branch block as retrograde 1–1 conduction with a P-wave morphology (nar-
if the right bundle is blocked, then the exit to the ventricle is row and negative in the inferior leads) suggestive of retro-
through the left anterior or left posterior fascicle. Both these grade conduction via the AV node and the fast pathway. The
fascicles exit midway (somewhat closer to the apex) from base relatively long V-A interval could be from the early activa-
to apex. Thus, if bundle branch block can be excluded as the tion occurring at the base near the mitral annulus while the
cause of the wide QRS, ventricular tachycardia or an acces- entrance site for the left bundle is further toward the apex,
sory pathway remains as the explanation. Leads II, III, and and this transit time for conduction is responsible for the long
aVF all show a positive R wave. Lead I shows a predominantly RP interval. Another possibility is that there is retrograde
negative QRS deflection, and as noted above, both leads aVR left bundle branch block, and conduction to the AV node
and aVL show negative deflection. Simultaneously present occurs transseptally and then via the right bundle. If this is
an antidromic tachycardia, that is, the wide QRS complex is atrium being advanced near the AV node says that a pathway
caused by antegrade conduction via left anterolateral acces- is present. The fact that the QRS morphology is unchanged
sory pathway, then retrograde conduction proceeds similarly, suggests that this pathway has been used for antegrade acti-
either to the entrance of the left bundle or to the right bun- vation. Further, advancing the ventricular electrogram resets
dle to enter the AV node. A second septal bypass tract can- the tachycardia with a similar atrial activation sequence,
not be excluded as the mechanism for retrograde activation strongly suggesting that the tachycardia mechanism is anti-
of the atrium during a preexcited reciprocating tachycardia dromic tachycardia.
(pathway-to-pathway tachycardia). Answer B is the classic response for ventricular tachy-
cardia. PACs are able to advance the V but only by going
If premature sensed atrial beats are placed during tachy- through the AV node. And since they have preexcited the
cardia at electrophysiologic study, which of the following V via the AV node, the ventricular activation is fused and
responses is most consistent with a diagnosis of antidromic greatly changed. The tachycardia is not reset, all features sug-
tachycardia? gesting ventricular tachycardia as the primary cause of wide
A. A PAC placed from the distal coronary sinus advances QRS tachycardia.
the ventricular electrogram without changing the QRS The response described in answer C is consistent with a
morphology and without advancing the atrial electro- diagnosis of typical AV node reentrant tachycardia with
gram on the His bundle catheter. The advanced ven- right bundle branch block. Here, as in answer B, the V can
tricular electrogram in turn advances the retrograde be preexcited but only by going through the AV node and His
His and atrial electrogram without changing the atrial bundle. Thus, a pathway is not responsible for wide QRS. The
activation sequence. proximal to distal His bundle activation is consistent with
B. A PAC placed from the distal coronary sinus advances antegrade activation via the AV conduction system. When the
the ventricular electrogram when the atrial electro- His bundle and V are advanced, for the same beat the atrial
gram on the His bundle catheter and the His bundle electrogram near the fast pathway region is also advanced.
electrogram are advanced. When the ventricular elec- This strongly suggests AV node reentry because the ventricle
trograms are advanced, the QRS morphology changes does not need to be advanced first to advance the next A.
markedly. The tachycardia is not reset. The response discussed in answer D is consistent with a
C. A PAC placed from the distal coronary sinus advances preexcited reciprocating tachycardia that uses 1 pathway
the next ventricular electrogram without a change in (possibly a Mahaim fiber) to get to the ventricle and then
QRS morphology. Both the atrial electrogram and His uses another accessory pathway for retrograde activation.
bundle electrogram on the His bundle catheter are The key finding in this option is that the ventricle is preex-
advanced. A multipolar catheter placed on the His bun- cited by a PAC without activating the region of the AV node,
dle shows that both during tachycardia and on placing diagnostic of antegrade accessory pathway conduction. This
the PAC there is proximal to distal activation of the His activation advances the retrograde His, yet the retrograde
bundle. When the ventricular electrogram is advanced, A is advanced at about the same time. Thus, once the ven-
the next atrial electrogram (earliest site on the proxi- tricular myocardium is advanced, to get back to the atrium
mal His bundle catheter) is also advanced. another accessory pathway must be present. This is a form of
D. A PAC placed at the right atrial free wall advances the pathway-to-pathway tachycardia response.
next ventricular electrogram without a change in the Figure 6.11 illustrates some of the terminology used with
QRS morphology. A retrograde His bundle deflection regard to accessory pathways and wide complex tachycar-
is also advanced. On advancing the ventricular electro- dia in patients with Wolff-Parkinson-White syndrome.
gram, the atria are also preexcited, and it is consistently Wolff-Parkinson-White syndrome refers to a syndrome of
noted that the atrial preexcitation occurs simultane- antegrade preexcitation on a 12-lead ECG along with clinical
ously with advancement of the retrograde His. or electrocardiographic evidence of a reciprocating tachycar-
dia. A preexcited tachycardia simply refers to any tachycardia
Answer: A—A PAC placed from the distal coronary sinus
mechanism where the QRS complex is wide because of ante-
advances the ventricular electrogram without changing the
grade preexcitation. With preexcited tachycardias, the acces-
QRS morphology and without advancing the atrial electro-
sory pathway may be a bystander or may be part of the circuit
gram on the His bundle catheter. The advanced ventricular
of the tachycardia. Preexcited reciprocating tachycardias refer
electrogram in turn advances the retrograde His and atrial
specifically to preexcited tachycardias where the pathway is
electrogram without changing the atrial activation sequence.
in fact part of the circuit. Preexcited tachycardias include
PACs (like PVCs placed during narrow QRS tachycar- antidromic tachycardia, where the pathway constitutes the
dia) are essentially probes placed by the electrophysiologist antegrade limb and the AV conduction system the retrograde
to study the perturbations caused and to help diagnose the limb. Preexcited reciprocating tachycardia also includes a
tachycardia mechanisms. situation when the accessory pathway constitutes the ante-
Answer A is the classic response to a PAC for antidromic grade limb of the circuit, but another accessory pathway is
tachycardia. The fact that the V is advanced even without the the retrograde limb (pathway-to-pathway tachycardia).
The retrograde right bundle is blocked so transseptal conduc-

tion has to occur to enter the left bundle and from there the
Preexcited His bundle and AV node. This results in a relatively long V-H
interval during tachycardia. The extra time taken to reach
the AV node is often necessary for antidromic tachycardia to
occur (temporal delay).
Preexcited The antegrade accessory pathway in Figure 6.12B is respon-
reciprocating sible for activation of the ventricle from the atrium. The ret-
rograde limb of the circuit, however, is through another
accessory pathway. It is important in wide QRS tachycardia
to identify accurately the retrograde limb of the circuit, often
requiring placement of PVCs (in addition to PACs to define
the antegrade limb) during the tachycardia.
Sometimes during a preexcited reciprocating tachycardia,
Antidromic atrial activation is nearly simultaneously early in the region of
the fast pathway of the AV node, as well as a second annular
site (Figure 6.12C). Other maneuvers may identify retrograde
activation via the AV node or an accessory pathway (para-
hisian pacing). The tachycardia circuit itself may be antidro-
mic, with the second accessory pathway being a bystander or
a pathway-to-pathway tachycardia with the AV node being a
Figure 6.11 Tachycardias in patients with Wolff-Parkinson-White
syndrome.
bystander. When the retrograde right bundle is not blocked,
particularly right from the initiation of the tachycardia (V-H
interval not long), the basic mechanism is likely to be a
Figure 6.12 shows various mechanisms of tachycardia pathway-to-pathway tachycardia. The prerequisite spatial and
with antegrade conducting accessory pathway conduction. temporal delay is present to maintain a preexcited reciprocat-
Figure 6.12A shows a common tachycardia circuit seen ing tachycardia circuit.
particularly following initiation of antidromic tachycardia. The circuit shown in Figure 6.12D is consistent with ortho-
Antegrade conduction occurs via the accessory pathway. dromic reciprocating tachycardia, that is, conduction down
A B C
A AP AVN A AP AVN AP A AP AVN AP

V V V
H H H
BB BB BB
D E F
A AP AVN AP A AP AVN AP A AP AVN

V V V
H H H
BB BB BB
Figure 6.12 Mechanisms of tachycardia with antegrade accessory pathway conduction. A, Antidromic tachycardia with retrograde right
bundle branch block, a common tachycardia circuit seen particularly following initiation of antidromic tachycardia. B, Pathway-to-pathway
tachycardia with retrograde right and left bundle branch block. An antegrade accessory pathway is responsible for activation of the ventricle
from the atrium. C, Antidromic tachycardias with retrograde bystander accessory pathway or pathway-to-pathway tachycardia with bystander
AV nodal conduction. D, Pathway-to-pathway tachycardia with antegrade AV nodal bystander or orthodromic reciprocating tachycardia
with a bystander accessory pathway. E, Figure-of-8 antidromic tachycardia. F, Atriofascicular pathway with antidromic tachycardia (Mahaim
antidromic reciprocating tachycardia). AP indicates anteroposterior; AVN, atrioventricular node; BB, bundle branch; H, His bundle.
the AV node and up a left-sided accessory pathway. However, patient is very high because the QRS morphology excludes
another right-sided accessory pathway is present that may be bundle branch block as the cause of the wide QRS and the
responsible for preexcitation but is a bystander to the circuit. atrial pacing reproducing the QRS morphology excludes ven-
Rarely, pathway-to-pathway tachycardia (down a right-sided tricular tachycardia. These findings, along with analysis of
pathway and up a left-sided pathway) may be the primary cir- the likely retrograde P wave, make antidromic tachycardia by
cuit, but bystander antegrade AV node conduction, including far the leading diagnostic consideration in this patient.
down the left bundle, may be present. In this latter situation, a In another patient with wide QRS tachycardia and subtle
PAC placed during tachycardia preexcites the V with an iden- preexcitation on the surface 12-lead ECG, differential site
tical ventricular activation sequence and resets the tachycar- atrial pacing shows the following results. In Figure 6.14, pac-
dia without advancing the A near the AV node. ing is from the proximal coronary sinus catheter. Left bundle
In the rare situation shown in Figure 6.12E, there is ante- branch–like morphology is seen on the surface QRS in lead
grade activation via 2 accessory pathways. Both pathways V1. The QRS morphology in leads II and III is neither strongly
may be responsible for tachycardia, with the AV node con- positive nor negative, suggesting an exit somewhere between
stituting the retrograde limb of the circuit. This is extremely the anterior wall and the inferior wall, while there is a late pre-
rare, as are all figure-of-8 tachycardias (ventricular tachy- cordial QRS transition with QS complexes in leads V1 and V2
cardia, scar-related tachycardia, etc), because both circuit (V3, V4, and V5 not shown) and positive in lead VI, suggesting
lengths and time must be nearly identical to allow for simul- neither a very basal nor very apical exit. This morphology is
taneous retrograde activation of the AV node. Much more consistent with an exit through the right bundle, but as noted
commonly, particularly in ventricular tachycardia and atrial in the discussion above, atriofascicular pathways typically
tachycardia, what is referred to as figure-of-8 tachycardia is in insert to the right bundle and result in nearly identical QRS
fact an orthodromic reciprocating tachycardia–type circuit morphology to right bundle exit from AV nodal conduction
with another limb as a bystander. Analyzing the activation and left bundle branch block.
responses of a PAC placed in the right and left atrium sequen- The H-V interval is short at this pacing rate at 25 ms, with
tially can be used to identify whether one of these circuits is a the A-H interval at 127 ms. The S-V interval (stimulus to V) is
bystander or a true figure-of-8 reentry is present. a measure of earliest conduction to the ventricle. This interval
With a Mahaim fiber, an antegrade-only conducting dec- is fi xed during decremental atrial pacing when conduction
remental pathway may connect directly to the right bundle, via an accessory pathway would be expected to be shorter and
as shown in Figure 6.12F, close to the junction of the His when pacing the atrium at similar cycle lengths is progres-
bundle and right bundle. Retrograde activation is via the AV sively closer to the atrial insertion of the pathway.
node. Thus, this is a form of antidromic tachycardia. The dis- In Figure 6.14, the atrial pacing site at the same cycle length
tinguishing feature is the retrograde His bundle electrogram, is from the proximal coronary sinus to the high lateral right
which may in fact be earlier than the ventricular electrogram atrium (Figure 6.15). The S-V interval is shorter by about
during tachycardia. PACs placed from the lateral wall of 10 ms. The A-H interval is longer and the H-V interval, mea-
the right atrium can preexcite the tachycardia and reset the sured from the His bundle electrogram to the earliest ventricu-
tachycardia with a similar ventricular activation sequence lar activation recorded, is negative, –15 ms. The negative value
even without advancing the septal atrial electrogram (exclud- suggests that pacing closer to the atrial insertion of the acces-
ing antegrade AV nodal conduction). sory pathway gives rise to a greater degree of preexcitation.
Figure 6.13, top panel, shows atrial pacing from the high In Figure 6.16, atrial pacing at a similar rate is from the
right atrium at a rate similar to that in the patient’s tachy- anterolateral right atrium close to the tricuspid annulus. The
cardia shown in Figure 6.13, bottom panel. Atrial pacing S-V interval is essentially unchanged, but there is a dramatic
reproduces the wide QRS morphology seen during tachy- change in the A-H interval, now lengthened from 145 ms to
cardia. Careful analysis of all 12 leads shows that there is no 330 ms. The H-V interval, measured from the recorded His to
fusion, and the morphology match is exact. Even the small R the next ventricular activation, is 205 ms. There are 2 possible
wave seen in lead V1 and the notching of the QRS complex in explanations for the long A-H interval:
lead III and V1 is exactly reproduced. This maneuver alone
excludes ventricular tachycardia as the mechanism of tachy- 1. AV conduction has been blocked, and the His bundle
cardia in this patient. The rare exception is if the ventricular is being activated retrograde. There is an antegrade
tachycardia exit is exactly at the exit of the left bundle or a accessory pathway to the ventricle or to the conduction
bystander accessory pathway. Further analysis of Figure 6.13, system, and from there retrograde activation of the His
bottom panel, shows also that the P-wave morphology during bundle occurs.
pacing is different from the P wave seen during tachycardia. 2. There is antegrade conduction via the AV node, which
Notably, during atrial pacing, the P wave is wider and is posi- is very long (possible antegrade slow pathway activa-
tive in lead II. The width of the P wave can be well appreciated tion), and in addition there is infrahisian block possi-
in lead V5. The narrow P wave suggests that during tachy- bly because of antegrade conduction via the accessory
cardia, atrial activation is septal (narrow P wave) and likely pathway and retrograde penetration of the distal
retrograde. The likelihood of antidromic tachycardia in this His-Purkinje system.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure 6.13 The top panel shows atrial pacing from the high right atrium at a rate similar to that in the tachycardia shown in the bottom panel.
The arrow in the bottom panel indicates the retrograde P wave.
Distinguishing between an antegrade His and the retro- increase in the A-H interval (125, 130, 155, 170, 180, 255 ms),
grade His is critical in the interpretation of pacing maneuvers and then a plateau is reached with no further increase beyond
or complex cases involving wide QRS tachycardia. When a 255 ms. This characteristic plateauing of the A-H interval
multielectrode catheter is placed, the His bundle activation suggests that conduction of the His bundle has changed from
sequence, which is proximal to distal or distal to proximal, occurring via a decrementally conducting structure (AV
can be useful. The most telling evidence, however, is with node) to a nondecremental structure (accessory pathway and
analysis of progressive changes in the A-H interval during retrograde activation) and signifies that the His bundle acti-
decremental atrial pacing (Figure 6.17). vation is retrograde.
Figure 6.17 shows that as the atrial pacing cycle length Figure 6.18 shows the surface ECG and intracardiac elec-
decreases from 500 ms to 450 ms, there is first a progressive trogram during wide complex tachycardia in this patient. The
I
I
II II
III
III
V1
V1
V2
V2
V6
V6 CL=450
CL=450 RV
RV
SV=205 SV=190
RA AH=330
RA AH=127
HBE
HBE
HV=205
HV=25 PCS
PCS
DCS
DCS
200 ms
200 ms
Figure 6.14 Pacing from the proximal coronary sinus catheter in Figure 6.16 Atrial pacing at a rate similar to that shown
a patient with wide QRS tachycardia and subtle preexcitation on in Figure 6.15 from the anterolateral right atrium close to
a surface 12-lead electrocardiogram. AH indicates A-H interval; the tricuspid annulus. CL indicates cycle length. All other
CL, cycle length; DCS, distal coronary sinus; HBE, His bundle abbreviations are as defined for Figure 6.14.
electrogram; HV, H-V interval; PCS, proximal coronary sinus; RA,
right atrium; RV, right ventricle; SV, stimulus artifact to ventricular
activation time.
V-H interval is long at 215 ms, and in addition, the V-A and
the H-A intervals are also long, giving rise to long RP tachy-
cardia with a wide QRS complex.
Which of the following possible reasons explains the long
I H-A interval shown in Figure 6.18?
II A. Retrograde slow pathway activation
B. Retrograde delay in the compact AV node
III C. Retrograde accessory pathway conduction
D. Primary mechanism of tachycardia is atrial tachycardia
V1
with the V-A and H-A intervals not representing retro-
V2 grade conduction (pseudointerval)
V6 E. All of the above
CL=450 Answer: E—All of the above.
RV
SV=195 In patients with antidromic tachycardia, particularly
RA
AH=145 when an atriofascicular tract (Mahaim fiber) is being used
as the antegrade limb of the circuit, the V-A (RP) interval is
HBE expected to be very short because these fibers typically insert
HV=-15 into the right bundle and are expected to show nearly imme-
PCS
diate or simultaneous activation of the V and H and fairly
DCS quick ascent to the atrium via the AV node. In Figure 6.18, the
V-A interval is long.
200 ms One component of this long V-A interval is the long H-A
interval. Several possibilities exist for why the H-A interval
Figure 6.15 The atrial pacing site is the same as that shown in
Figure 6.14, from the proximal coronary sinus to the high lateral is long. There may be considerable delays in the compact AV
right atrium. Pacing appears to be closer to the atrial insertion node between the His and the atrial electrogram. Retrograde
of the accessory pathway, giving rise to greater preexcitation. CL slow pathway conduction is a possibility. The exact position
indicates cycle length. All other abbreviations are as defi ned for of the proximal coronary sinus electrode is not known. If in
Figure 6.14. fact the His bundle catheter is placed close to the fast pathway
II
III
V1
V2
V6
RV
500 500 500 500 500 500 450 450 450 450
RA AH=125 125 130 130 155 170 180 255 255 255
HBE
80 85 90 100 115 130 150 220 220 220
PCS
DCS
200 ms
Figure 6.17 The atrial pacing cycle length decreases, and the A-H interval increases to a plateau. All abbreviations are as defi ned for Figure
6.14.
and the proximal coronary sinus catheter is at the ostium in this situation occurs via the slow-conducting pathway, giv-
of the coronary sinus, retrograde slow pathway conduction ing rise to a long V-A interval. It is highly unusual, however,
can be excluded because anatomically the proximal coronary for decrementally conducting pathways to be located in the
sinus has to be activated earlier than the proximal His–fast anteroseptal region (early on His bundle catheter). Because
pathway region. However, this possibility cannot be excluded this interval does not represent true conduction, another pos-
on the basis of the electrograms, without fluoroscopy and the sible cause for a long V-A interval might be atrial tachycar-
exact catheter location. Another possibility is that retrograde dia as the primary mechanism. As seen in Figure 6.16 and
activation to the atrium is occurring via a decrementally con- Figure 6.18, during atrial pacing in patients with an ante-
ducting or slow-conducting accessory pathway (PJRT type). grade conducting accessory pathway, block in the AV node
In this situation, the H-A interval is a pseudointerval, with may occur with retrograde conduction of the His via the
retrograde ventriculohisian conduction occurring but no accessory pathway and ventricular myocardium. A similar
conduction via the AV node to the atrium. Atrial activation situation can arise with atrial tachycardia in patients with
II
III
V1
V2
V6
CL=560
RV
A A A A A A A
RA
A A A HA=170 A A A A
H H H H H H H
HBE
A A A VH=215 A A A A
PCS
A A A A A A A
DCS
200 ms
Figure 6.18 Wide complex tachycardia in the same patient. CL indicates cycle length. All other abbreviations are as defi ned for Figure 6.14.
a bystander accessory pathway. Thus, the A-H interval is long, and appropriate analysis of the results of these changes are
but the H-A interval (which also applies to the V-A, RP, and required to exclude some of the existing possibilities.
other intervals) represents a pseudointerval, and its duration Figure 6.19 shows that when atrial pacing is performed
depends on the cycle length of the atrial tachycardia. at about the cycle length of the tachycardia, the V-H inter-
Atrial tachycardia cannot be excluded as a mechanism for val (earliest ventricular activation to the retrograde His
this tachycardia on the basis of the electrograms shown so bundle electrogram) is identical to that seen in tachycardia.
far, but once the maneuvers described in the preceding text Further, the QRS morphology is also identical to that seen
are performed or when spontaneous cycle length changes are in tachycardia. The simple maneuver of atrial pacing at the
noted (see below), this diagnosis can be excluded. rate of tachycardia gives strong evidence that the mechanism
of the wide QRS complex is in fact the accessory pathway
In Figure 6.18, the His bundle electrogram is seen clearly and excludes ventricular tachycardia as a mechanism for the
to come after the ventricular electrogram and much after arrhythmia. It remains to be determined, however, what the
the initial portion of the QRS complex (long V-H interval = retrograde limb of the circuit is. The limbs of the circuit can
215 ms). Which of the following is the least likely cause for be determined individually, with pacing maneuvers in sinus
the long V-H interval? rhythm (atrial pacing, ventricular pacing, parahisian pac-
A. Right-sided accessory pathway conducting antegrade ing), but to define the circuit itself, dynamic maneuvers are
with retrograde right bundle branch block required during tachycardia, such as placing PACs, placing
B. Atriofascicular accessory pathway conducting ante- PVCs, or analyzing “wobbles” (spontaneous, apparently ran-
grade with retrograde right bundle branch block dom changes in tachycardia cycle length and intracardiac
C. Left-sided antegrade conducting accessory pathway intervals).
with retrograde right bundle branch block Figure 6.20 shows a long V-H interval of 104 ms during
D. Free wall accessory pathway inserting near the annu- wide complex tachycardia.
lus (not atriofascicular) with normal retrograde bundle Figure 6.21 from the same patient shows an abrupt change
branch and His conducting system in the V-H interval with continued observation and without
Answer: C–Left-sided antegrade conducting accessory change in the QRS morphology with the V-H interval mea-
pathway with retrograde right bundle branch block. suring approximately 36 ms. As discussed in the preceding
text, many reasons for a change in the V-H interval may be
As stated above, with atrial fascicular pathways, a very present. However, the most likely and most common are the
short V-A interval is expected, and when this occurs, there development and subsequent loss of retrograde right bundle
may be an appearance of AV nodal reentrant tachycardia branch block.
based on the retrograde conduction sequence. Often, how- Figure 6.22 is a diagrammatic representation of the change
ever, particularly at initiation of tachycardia, the V-H inter- shown in Figure 6.21. When the right bundle is blocked ret-
val is long. One potential reason for this is retrograde right rograde, the cycle length increases (for right-sided antegrade
bundle branch block at a level proximal to the insertion of the pathways) because transseptal conduction and retrograde
atriofascicular tract. Thus, to activate the His bundle, con- activation of the left bundle are required before the His
duction proceeds transseptally up the left bundle and then to bundle and AV node can be activated and allow retrograde
the His, giving rise to a long V-H interval. Antidromic tachy- activation of the atrium. Thus, 2 changes are expected to
cardia from pathways that insert near the annulus traverse occur if this is the mechanism. First, the time from earliest
the ventricular myocardium and the entrance site for the ventricular activation to activation of the His bundle (V-H
right bundle closer to the apex. The conduction then travels interval) increases. Second, the cycle length of the tachycar-
up the right bundle to the His bundle region and inscribes dia also increases because of the increased circuit length. In
the His electrogram, again giving rise to a relatively long V-H Figures 6.20 and 6.21 there is no change in the atrial acti-
interval. If a left-sided antegrade bypass tract is present and vation sequence, and perhaps more importantly, there is no
responsible for the antegrade limb of the antidromic tachy- change in the retrograde H-A interval. These findings suggest
cardia, retrograde right bundle branch block does not affect that retrograde activation of the atrium depends on activa-
the V-H interval because retrograde activation of the His is tion of the His bundle (retrograde limb is the A-V node).
expected to occur via the left bundle. If retrograde left bundle Figure 6.23 shows in a single tracing the effect of chang-
branch block occurs, then the V-A interval is in fact long. ing V-H intervals on the tachycardia cycle length. The initial
On the basis of the tracing shown in Figure 6.18, can cycle length of the tachycardia is 290 ms when the V-H inter-
ventricular tachycardia be excluded? The patient may still val is 95 ms, with a clearly defined His bundle electrogram.
have ventricular tachycardia as the primary mechanism, With loss of retrograde right bundle branch block, the V-H
with retrograde delayed activation of the His bundle from interval is shorter on the right side of this tracing (240 ms).
any of the mechanisms explained in the preceding text and With the V-H decreasing by 50 to 60 ms, a similar decrease
delayed activation from the His to the atrium, again with in the cycle length of the tachycardia is also noted (30 ms).
any of the mechanisms explained above. Dynamic changes, Further, the H-A interval is not changed, and the atrial acti-
either induced with extrastimuli or occurring spontaneously, vation sequence based on the electrogram shown in this
II
III
V1
V2
V6
RV
500 500 500 500 500 500
RA
AH=255 255 255 255 255 255
HBE
H H H H H H
VH=1 215 215 215 215 215 215
PCS
DCS
200 ms
Figure 6.19 When atrial pacing is performed at about the cycle length of the tachycardia, the V-H interval is identical to that seen in
tachycardia. All abbreviations are as defined for Figure 6.14.
II
V1
RVA
A A A
HRA
H H H
A A A
HBE2 V V V
PCS
A A A
DCS
104 ms
Figure 6.20 A long V-H interval of 104 ms during wide complex tachycardia. DCS indicates distal coronary sinus; HBE2, His bundle
electrogram; HRA, high right atrium; PCS, proximal coronary sinus; RVA, right ventricular apex.
II
V1
280
RVA
A A A A
HRA
V V V V
HBE2
A A A A
H H H H
PCS
A A A A
MCS
A A A A
DCS
36 ms
Figure 6.21 An abrupt change in the V-H interval with continued observation and without change in the QRS morphology. The number
280 refers to the cycle length of the tachycardia. DCS indicates distal coronary sinus; HBE2, His bundle electrogram; HRA, high right
atrium; MCS, mid coronary sinus; PCS, proximal coronary sinus; RVA, right ventricular apex.
tracing is also not changed. The fact that changes in the V-H retrograde right bundle branch block is present, ventricular
interval drive changes in the tachycardia cycle length is diag- myocardium activated by the right-sided AP must activate
nostic of the antegrade conducting accessory pathway as part the left ventricular myocardium and left bundle branch to
of the tachycardia circuit. Changes in His bundle activation reach the His and AV node.
time are reflected exactly in changes in the atrial activation Figure 6.24 shows diagrammatically why retrograde left
time, which is diagnostic of the retrograde limb of the circuit bundle branch block in a right-sided accessory pathway does
as His bundle activation dependent, ie, the AV node. The rea- not affect the V-H interval or the cycle length of the tachycar-
son the V-H interval abruptly changes (as discussed above) dia because the entire circuit is on the right side of the heart
is intermittent retrograde right bundle branch block. When independent of left bundle activation.
As shown in Figure 6.25, this concept is essentially the
inverse of the familiar observation that during orthodromic
reciprocating tachycardia when antegrade left bundle branch
block occurs, the cycle length (V-A interval) increases when
the retrograde accessory pathway is located on the left side. In
the context of wide QRS tachycardia when an antegrade con-
A AP AVN
ducting accessory pathway during antidromic reciprocating
V tachycardia is associated with retrograde left bundle branch
block, there is an increase in the cycle length of the tachycar-
dia for an increase in the V-H interval.
H
How does the occurrence of retrograde right bundle
BB branch block (which helps define the antegrade limb of the
circuit) help define the retrograde limb of the circuit? The
key is understanding that only retrograde AV nodal conduc-
tion changes on the basis of the time of activation of the His
bundle. This concept is used in various electrophysiologic
Figure 6.22 Diagrammatic representation of the change shown in maneuvers, including parahisian pacing (high-output and
Figure 6.21. AP indicates accessory pathway; AVN, atrioventricular low-output pacing to capture the His and analyze the time
node; BB, bundle branch; H, His bundle. taken to activate the atrium).
II
V1
290 240
RVA
HRA
H H
H H
HBE2
VH=95 30
PCS
DCS
Figure 6.23 The effect of changing V-H intervals on the tachycardia cycle length. The number 290 indicates the initial cycle length, 240 is
the changed cycle length, and 30 is the V-H interval with a changed cycle length. DCS indicates distal coronary sinus; HBE2, His bundle
electrogram; HRA, high right atrium; PCS, proximal coronary sinus; RVA, right ventricular apex.
Figure 6.26 shows diagrammatically the effect on ret- an accessory pathway is responsible for retrograde conduc-
rograde conduction when retrograde right bundle branch tion to the atrium, regardless of whether the V-H interval is
block is present with pacing close to the RV apex. Because short or long, the V-A interval is fi xed. With the development
of retrograde right bundle branch block, His bundle activa- of retrograde right bundle branch block, the retrograde H-A
tion occurs only after transseptal conduction and retrograde interval may be negative. However, if changes occurring dur-
activation of the left bundle; thus, the V-H interval is long. If ing either ventricular pacing or antidromic tachycardia in the
retrograde V-H interval predict changes in the retrograde
V-A conduction, then the retrograde limb of the circuit is
via the AV node. If during ventricular pacing or during anti-
dromic reciprocating tachycardia, clear changes in the V-H
interval are seen during tachycardia but the V-A interval
remains fi xed, then retrograde conduction in the circuit is via
A AP AVN an accessory pathway (pathway-to-pathway tachycardia or
during ventricular pacing).
V
Figure 6.27 shows the opposite transition where tachy-
cardia goes from a short V-H interval to a long V-H inter-
H val with development of retrograde right bundle branch
BB block. There is no change in the retrograde atrial activation
sequence or the H-A interval, yet the cycle length of tachy-
cardia increases. Thus, with relatively straightforward analy-
sis (after the concept is fully understood), both the antegrade
and retrograde limbs of the circuit can be deduced from a
Figure 6.24 Diagrammatic representation of retrograde left
single tracing.
bundle branch block in a right-sided accessory pathway not Figure 6.28 demonstrates the use of the concept of retro-
affecting the V-H interval or the tachycardia cycle length. AP grade right bundle branch block induction during ventricular
indicates accessory pathway; AVN, atrioventricular node; BB, pacing. A highly unusual coronary sinus activation sequence
bundle branch; H, His bundle. may be consistent with a left-sided accessory pathway.
LBBB
Accessory Accessory
pathway pathway
CL=310 ms CL=290 ms
Figure 6.25 Accessory pathway and ipsilateral bundle branch block in orthodromic reciprocating tachycardia. Yellow arrows indicate
primary conduction wave fronts; the blue arrow indicates intramyocardial transeptal conduction. CL indicates cycle length; LBBB,
left bundle branch block.
However, the placed ventricular extrastimulus induces retro- pathways. Often, for initiation and sometimes maintenance
grade right bundle branch block with an increase in the V-H of the tachycardia, retrograde ipsilateral bundle branch block
interval. The atrial activation sequence is unchanged, and the is necessary, creating the extra time resulting from activation
V-A interval increases by an amount equivalent to an increase to cross the intraventricular septum and climb up the con-
in the V-H interval. Thus, this unusual coronary sinus activa- tralateral bundle to reach the AV node. Other causes of delay,
tion sequence depends on retrograde conduction via the AV including decremental properties of the accessory pathway or
node (retrograde fast pathway with activation of the coronary intraventricular conduction delay, may also help perpetuate
sinus via the left atrium). the circuit.
The diagram in Figure 6.29 illustrates 2 important features The second issue illustrated in Figure 6.29 concerns
of antidromic reciprocating tachycardia. Often for antidro- techniques to imitate antidromic tachycardia during pro-
mic tachycardia to occur there must be significant spatial grammed stimulation. For example, in an attempt to initiate
or temporal delay between the 2 limbs of the circuit (acces- antidromic tachycardia from the atrium, causing unilateral
sory pathway and AV conduction system), which explains block in the proximal portion of the AV conduction system
why antidromic tachycardia is rare with septal accessory (compact AV node) is ideal because this site of block produces
the maximum amount of time for the antidromic wave front
to reach the site of unilateral block, thus maximizing the
Ventricular pacing chance that the tissue required to complete the circuit has
at apex with RBBB recovered from its refractoriness. If block during atrial pac-
V H A
ing is infrahisian, then conduction via the accessory pathway
and ventricle to the intrahisian conduction tissue is likely to
V-A 110 ms find refractory tissue and the inability to perpetuate antidro-
mic tachycardia. Thus, rapid atrial pacing or use of a short
cycle length drive train during extrastimulation is more
likely to initiate antidromic tachycardia. Similarly, to maxi-
mize the chance of initiating antidromic tachycardia during
ventricular pacing, it is ideal for the premature ventricular
Figure 6.26 The effect on retrograde conduction when retrograde beat to induce retrograde bundle branch block on the side
right bundle branch block (RBBB) is present with pacing from site of the accessory pathway (retrograde right bundle block for
C close to the right ventricular apex. Yellow arrows indicate the right-sided pathways and retrograde left bundle branch block
conduction wavefront. for left-sided pathways).
II
V1
240 280
RVA
HRA
H H H H H H
HBE2
VH=30 100
PCS
DCS
Figure 6.27 Tachycardia proceeds from a short V-H interval to a long V-H interval after development of retrograde right bundle branch
block. The number 240 indicates the initial cycle length, 280 is the changed cycle length, and 100 is the V-H interval with changed cycle
length. DCS indicates distal coronary sinus; HBE2, His bundle electrogram; HRA, high right atrium; PCS, proximal coronary sinus; RVA,
right ventricular apex.
Figure 6.28 Retrograde right bundle branch block induction during ventricular pacing.
Distance Figure 6.32 shows initiation of a left bundle branch block

* tachycardia during ventricular pacing. The extrastimulus
coupled at 340 ms initiates tachycardia if the tachycardia is
associated with a clearly seen His bundle electrogram and a
long H-A interval. The clearly seen His bundle electrogram
results from a long V-H interval from retrograde right bundle
branch block. This allows the greater transit time to the His,
and from the His there is additional delay via the compact AV
node to the atrium, all factors that enhance the likelihood of
completing the antidromic circuit.
HPS To summarize an approach to wide QRS tachycardia
as discussed in this section, analysis of the 12-lead ECG
(Figure 6.33) determines that the likely exit site is basal in the
left ventricle, somewhat anterolaterally. This is not a known
exit for any fascicle of the left bundle branch, and therefore
Transseptal right bundle branch block can be excluded as the mechanism
of the wide QRS complex during tachycardia. Further analy-
Figure 6.29 Site of critical delay in the initiation of antidromic
reciprocating tachycardia. The asterisk indicates a progressing
sis includes the following:
conduction wave front. HPS indicates His-Purkinje system.
1. Atrial pacing at the cycle length of the tachycardia
gives rise to an identical QRS morphology making ven-
Figure 6.30 shows the initiation of antidromic tachycardia tricular tachycardia unlikely as the mechanism of the
in a patient with a left-sided accessory pathway (right bundle wide QRS.
branch block pattern is seen during tachycardia). 2. Analysis of the intracardiac electrogram shows that
Figure 6.31 shows a close-up of the intracardiac electrogram the V-H interval predicts changes in the tachycar-
and relevant intervals. When the second extrastimulus (S3) is dia cycle length. A finding diagnostic of antegrade
placed, the A-H interval and consequently the V-H interval are conduction via the accessory pathway is part of the
very long (115 ms). Thus, it is likely that block in the compact circuit. Distinguishing antidromic reentrant tachycar-
AV node has occurred, and a retrograde His bundle potential dia from another preexcited reciprocating tachycardia
is seen. Because of the recent penetration into the AV node, (pathway-to-pathway tachycardia) remains important.
the H-A interval is also very long. This delay maximizes the When the changes in the V-H interval are noted and
chance for antegrade conduction via the accessory pathway the His is earlier retrograde (absence of retrograde
and the start of tachycardia. There is marked oscillation in the bundle branch block) without a change in the atrial
V-H interval (115 ms, 25 ms, 110 ms, 15 ms). As explained in activation sequence, the H-A interval is constant, and
the preceding text, this oscillation results from occurrence as a result, the atrial electrograms occur earlier. Th is is
and loss of retrograde bundle branch block. The V-H changes diagnostic of retrograde conduction occurring via the
cause changes in the cycle length of tachycardia without AV node. With these relatively simple maneuvers, the
changing the retrograde atrial activation sequence or the H-A circuit of antidromic reentrant tachycardia is defi ned
interval features diagnostic of antidromic tachycardia. (Box 6.3).
I
II
III
V1
V6
HRA AH AH A H A H A HA H A H A H A H A H A H A H AH AH AH
HBE
V-V 415 300 375 305 325 315 335 325 325 325 325 325
RV
320 260 V-H 115 25 110 15 25 25 35 25 25 25 25 25 25
PCS S1 S2 S3
200 ms
Figure 6.30 The initiation of antidromic tachycardia in a patient with a left-sided accessory pathway. Right bundle branch block pattern
is seen during tachycardia. AH indicates A-H interval; HA, His-atrium activation time; HBE, His bundle electrogram; HRA, high right
atrium; PCS, proximal coronary sinus; RV, right ventricle; V-H, ventricle-His activation time; V-V, ventricle-ventricle activation time.
HRA
A H A H A
H A H A H A H A
HBE
V-V 415 300 378 305

RV
320 260 V-H 115 25 110 15

PCS
S1 S2 S3
200 ms
Figure 6.31 A close-up of the intracardiac electrogram and relevant intervals. The arrow indicates the His bundle electrogram. AH
indicates A-H interval; HA, His-atrium activation time; HBE, His bundle electrogram; HRA, high right atrium; PCS, proximal coronary
sinus; RV, right ventricle; V-H, ventricle-His activation time; V-V, ventricle-ventricle activation time.
In the surface ECG and electrograms shown in Figure 6.34, pathway-to-pathway tachycardia, preexcited atrial tachycar-
which of the following diagnoses can be excluded? dia, preexcited AV node reentrant tachycardia, or preexcited
A. Antidromic tachycardia orthodromic reciprocating tachycardia, as discussed earlier
B. AV node reentry in this chapter. The latter part of the tracing shows right bun-
C. Pathway-to-pathway tachycardia dle branch block aberrancy with continued tachycardia. The
D. Atrial tachycardia critical piece to interpret this tracing is the premature atrial
E. A and C beat placed from the proximal coronary sinus. When this
F. B and D beat is placed, atrial activation continues at the same cycle
Answer: E—A and C. length, but there is loss of conduction to the ventricle for 1
beat. The tachycardia resumes first with a fusion beat likely
In the tracing shown in Figure 6.34, the atrial cycle from incomplete right bundle branch block and then with
length remains unchanged despite extensive changes in the right bundle branch block type of aberrancy.
QRS morphology. The initial wide QRS during tachycardia Why does the PAC from the proximal coronary sinus
is consistent with a left-sided antegrade conducting acces- result in loss of preexcitation? The pathway QRS morphology
sory pathway. Possibilities include antidromic tachycardia, suggests a left-sided pathway. If the PAC occurs from the left,
I
II
III
V1
V2
V6
600 600 340 CL=520
RV
A A A A A
RA
A A A A
HBE H H H H
PCS A A A A A
DCS A A A A A
200 ms
Figure 6.32 Initiation of left bundle branch block tachycardia during ventricular pacing. Ventricular pacing drive train is 600 ms, and the
coupling interval for ventricular extrastimulus is 340 ms. AH indicates A-H interval; CL, cycle length; DCS, distal coronary sinus; HBE,
His bundle electrogram; PCS, proximal coronary sinus; RA, right atrium; RV, right ventricle.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure 6.33 A 12-lead electrocardiogram showing antidromic reentrant tachycardia (as illustrated in the inset). Yellow arrow shows
conduction wavefront.
it is likely that this PAC penetrates the accessory pathway and

causes it to be refractory for the next beat of tachycardia, and Box 6.3
thus, pathway conduction is blocked. Characteristic Features of Antidromic Reciprocating
Tachycardia
Why then is there no AV conduction for that beat? It is
likely that with pathway conduction from the previous beats, Maximal preexcitation of the QRS during tachycardia
there is concealed penetration to the AV node. Since the beat QRS morphology replicated exactly by atrial pacing at the
tachycardia cycle length
that penetrates retrograde to the AV node is from the previ-
Concentric sequence of retrograde atrial activation
ous beat that conducted antegrade via the accessory pathway The V-H during tachycardia replicated during atrial pacing at
(beat prior to the PAC), the AV node is still refractory, and the tachycardia cycle length
the PAC prevents conduction via the pathway. Thus, there Persistent 1:1 atrial-ventricular relationship
is no AV conduction for the beat after the PAC. Since the Changes in the retrograde V-H interval predict changes in the
tachycardia cycle length
refractoriness of the AV conduction system induced by the
Changes in the V-H interval result in changes in the V-A interval
concealed penetration via the accessory pathway is absent, with a constant H-A interval and atrial activation sequence
subsequent beats of tachycardia conduct via the AV conduc- (retrograde AV node conduction)
tion system and, in this patient, with antegrade right bundle PVCs placed during the tachycardia preexcite the atrium only
branch block. by preexciting the His bundle and reset the tachycardia
PVCs that do not conduct to the atrium via the pathway or His
The loss of the mandatory 1:1 AV relationship during the
bundle may interrupt tachycardia
tachycardia excludes any reciprocating tachycardia involv- PACs placed during tachycardia preexcite the ventricle and the
ing an accessory pathway. Thus, antidromic tachycardia, retrograde His bundle electrograms without advancing the
pathway-to-pathway tachycardia, orthodromic reciprocat- septal atrial electrogram or an antegrade His bundle electro-
ing tachycardia with bystander antegrade accessory pathway gram and reset the tachycardia with an identical QRS mor-
phology and subsequent retrograde atrial activation sequence
conduction, or orthodromic reciprocating tachycardia with
antegrade bundle branch block can all be excluded. The most Abbreviations: AV, atrioventricular; PAC, premature atrial contrac-
likely diagnosis is atrial tachycardia that conducts initially via tion; PVC, premature ventricular contraction.
a left-sided accessory pathway and then via the AV node with
II
V1
RVA
HRA
HBE
PCS
*
Figure 6.34 The atrial cycle length remains unchanged despite significant changes in the QRS morphology. The asterisk indicates a pacing
stimulus artifact. HBE indicates His bundle electrogram; HRA, high right atrium; PCS, proximal coronary sinus; RVA, right ventricular apex.
right bundle branch block. AV node reentry cannot be com- bundle branch block is continued tachycardia with preexcita-
pletely excluded because AV node reentry may occur rarely tion via the right-sided accessory pathway. With the peeling
with infrahisian block or compact AV nodal block to the back of refractoriness, why is continued conduction via the
ventricle maintained by concealed penetration via an ante- AV node and through both bundles not seen? The PVC may
grade bystander pathway, as described above. However, this induce left bundle branch block in addition to the fi xed pre-
is considerably less likely than a preexcited atrial tachycardia existing right bundle branch block, and thus there is no AV
but still needs to be excluded with appropriate maneuvers, nodal conduction and the only conduction possible is via the
including the placement of PVCs and PACs to probe the cir- accessory pathway. Concealed retrograde penetration of the
cuit, as discussed earlier in this chapter. atrial fascicular pathway prevents accessory pathway conduc-
Figure 6.35 is from a patient with a wide complex tachy- tion from being seen. Such retrograde activation has not been
cardia and known Ebstein anomaly. Also known in this clearly demonstrated with atrial fascicular pathways. Another
patient from previous parts of the electrophysiologic study explanation is that the accessory pathway inserts into the
is that a right-sided accessory pathway with characteristics right bundle branch proximal to the site of the previous right
of an atrial fascicular pathway (Mahaim) is likely present. bundle branch block with the peeling back of the right bundle
Underlying right bundle branch block, an almost universal refractoriness, allowing conduction via the accessory path-
characteristic in patients with Ebstein anomaly, is also pres- way through the distal right bundle to its exit.
ent. The key feature in this tracing is that following placement What is the mechanism of the tachycardia? The elec-
of a PVC during tachycardia, there is a marked change in the trophysiologist should immediately realize that with such
QRS morphology with no change in the atrial cycle length. marked changes in the H-V and V-H intervals and QRS mor-
The primary observation is that the PVC is placed at a phology (all features of intrapathway and infranodal conduc-
time of retrograde His bundle refractoriness. The PVC does tion), there is no change in the tachycardia cycle length. Thus,
not preexcite the atrium and does not penetrate the His bun- antidromic tachycardia, pathway-to-pathway tachycardia, or
dle in a retrograde fashion (His bundle refractoriness). Yet other tachycardias where the infrahisian conduction system
this PVC causes a change in the QRS morphology, which is an integral part of the circuit can be excluded. Preexcited
suggests that the wide QRS is as a result of antegrade activa- atrial tachycardia and AV node reentry remain diagnostic
tion of the ventricle either by AV node with bundle branch possibilities. A very short V-A interval is suggestive of AV
block or an accessory pathway (not ventricular tachycardia). nodal reentry, although atrial tachycardia with a long conduc-
With the PVC, the captured beat shows a fused morphology tion time from the atrium to the ventricle cannot be excluded
between the paced PVC and antegrade conduction. There is on the basis of timing alone. With careful measurement, par-
then loss of antegrade right bundle branch block (peel-back ticularly in the beat following the PVC, the H-A interval is
refractoriness). Simultaneous with this loss of antegrade right longer than the H-A interval in the last 2 beats in the tracings
II
III
V1
A
Esophagus
RV
305 ms S 305 ms
Foramen
H H H H H
HBE
A
PCS
A
DCS
PVC
200 ms
Figure 6.35 Electrocardiogram and electrograms from a patient with wide complex tachycardia and Ebstein anomaly. The electrogram
marked “Esophagus” is an esophageal electrode reflecting atrial activation, and the electrogram marked “Foramen” is an intra-atrial
electrogram from the region of the fast pathway near the foramen ovale. DCS indicates distal coronary sinus; HBE, His bundle electrogram;
PCS, proximal coronary sinus; PVC, premature ventricular contraction; RV, right ventricle.
without a change in the cycle length of the tachycardia. If this application of findings on the 12-lead ECG and invasive elec-
measurement is confirmed and the phenomenon is reproduc- trograms and application of the maneuvers described in this
ible, a diagnosis of atrial tachycardia is more likely than AV chapter will lead to the correct diagnosis (or diagnoses) in
node reentry and preexcitation (H-A as a “driver” with AV most instances.
node reentry; see Chapter 4).
When an electrophysiologist is confronted with complex
wide QRS tachycardia, an opportunity exists to apply all the ABBREVIATIONS
diagnostic techniques involved with invasive management
of narrow complex tachycardia in addition to the unique AV, atrioventricular
maneuvers for wide QRS tachycardia. In some instances, ECG, electrocardiogram, electrocardiographic
the different interpretations of maneuvers used in narrow PAC, premature atrial contraction
complex tachycardia are required. Although these cases PVC, premature ventricular contraction
are challenging, a thorough understanding and systematic SVT, supraventricular tachycardia
7
Basic Cardiac Electrophysiology
Hon-Chi Lee , MD, PhD, and Arshad Jahangir, MD
INTRODUCTION 2. Voltage-gated K+ channels are proteins that have 6

transmembrane segments (S1 to S6) (Figure 7.1B),
The learning objectives of this chapter are to review some with cytoplasmic N and C termini. The voltage sensor
basic electrophysiologic concepts that are useful for the clini- is located in the fourth transmembrane segment (S4),
cian. These include 1) the structure and function of cardiac ion which contains a high density of positively charged
channels; 2) the role of ion channels in the generation of car- amino acids (lysine and arginine) that move accord-
diac action potentials; 3) the mechanisms of cardiac arrhyth- ing to changes in membrane potential. This move-
mias; and 4) inherited and acquired channelopathies. ment causes the ion channel to open and close through
allosteric and conformational changes in the channel
STRUCTURE AND FUNCTION OF ION CHANNELS structure. The fi ft h and sixth transmembrane seg-
ments (S5 and S6) sandwich a pore loop. Four of these
Ion channels are integral membrane proteins that regu- pore-forming channel protein subunits coassemble as
late the traffic of ions in heart cells (Dictionary of Cardiac a tetramer, forming a functional channel. Examples
Pacing, Defibrillation, Resynchronization, and Arrhythmias. include the transient outward K+ channels and the
2nd ed. cardiotext; c2007). By strictly controlling the flow of delayed rectifier K+ channels. Clinically, these chan-
electrically active ions in and out of myocytes, ion channels nels are important in regulation of cardiac excitability
regulate cardiac electrical activity. Their activity generates and refractoriness, and their abnormalities contribute
the cardiac action potential, which in turn underlies cardiac to the development of AF and various inherited and
automaticity, impulse conduction, excitation-contraction acquired channelopathies.
coupling, triggered automaticity, and arrhythmogenesis. 3. Voltage-gated Na+ and Ca2+ channel proteins are the
In the heart, most of the important ion channels assume most structurally complex. Each channel is a single
one of the following structural motifs, presented in increas- peptide consisting of 4 homologous domains, each of
ing order of complexity: which has 6 transmembrane segments that include a
voltage sensing S4 and a pore loop between S5 and S6
1. The inwardly rectifying K+ (Kir) channels are proteins
(Figure 7.1C).
with 2 transmembrane segments that sandwich a chan-
nel pore loop (Figure 7.1A). Four of these subunits coas- In summary, ion channels in the heart have a 4-fold struc-
semble to form a functional channel. These channels tural symmetry, the ion channel pore is lined by 4 pore loops,
are frequently gated by binding of ligands to the chan- and voltage-gated channels contain the voltage-sensing S4.
nel protein subunits. Examples include the adenosine The function of the pore-forming subunit (α subunit) of most
triphosphate (ATP)–sensitive K+ (K ATP) channel and ion channels is modulated by accessory proteins forming the
the inwardly rectifying G-protein gated K+ (GIRK) β, γ, and δ regulatory subunits.
channel. Abnormalities of these channels are associ-
ated with atrial fibrillation (AF), long QT syndrome, Conductance and Gating
and short QT syndrome.
The function of ion channels is defined by 2 basic properties:
Abbreviations are expanded at the end of this chapter. conductance and gating.
171
A Inward rectifier K+ channels

Extracellular
Intracellular
NH2
COOH
B Voltage-gated K+ channels
Extracellular
+
+
+
+
+
Intracellular
NH2
COOH
C Voltage-gated Na+ and Ca2+ channels

Extracellular
+ + + +
+ + + +
+ + + +
+ + + +
+ + + +
NH2
Intracellular COOH
Figure 7.1 Structure of cardiac ion channels. A, Inward rectifier K+ channels have 2 transmembrane segments and an intervening pore
loop. Four of these subunits coassemble to form a functional channel. B, Voltage-gated K+ channels have 6 transmembrane segments,
including the voltage sensor S4 and the pore loop between S5 and S6. Four of these subunits coassemble to form a functional channel.
C, Voltage-gated Na+ and Ca 2+ channels are channel proteins that consist of a single polypeptide containing 4 repeats of 6 transmembrane
segments.
Conductance is an equilibrium potential (Ex) at which there is no net driv-

ing force for the ion to move across the membrane. Ex can be
Conductance describes which ions are allowed to pass through calculated by applying the Nernst equation, 61/z log [x]o/[x]i,
the channel pore and the rate at which they do so. Ion channel where [x]o is the extracellular, [x]i is the intracellular concen-
conductance is determined by the selectivity fi lter in the pore tration of the ion, and z is the charge of the ion. The calcu-
loop that lines the narrowest portion of the channel pore. Na+ lated equilibrium potential for K+ (EK) for [K]o = 4 mmol and
channels preferentially conduct Na+ over K+ (12:1 ratio) and [K]i = 140 mmol is –94 mV. Thus, at a transmembrane poten-
Ca2+ (10:1 ratio), whereas K+ channels are selective for K+ over tial of −94 mV (ie, the inside of the cell has a negative potential
Na+ (1,000:1 ratio). relative to the outside of the cell), there is no net movement
The driving force for each ion into or from the cell is deter- of K+ into or from a cell because the negative potential inside
mined by the electrical and chemical gradient created by the the cell (which tends to draw the positively charged K+ ions
membrane potential and differences in concentration of the into the cell) is exactly offset by the concentration gradient
ion across the cell membrane. For each individual ion x, there generated by the higher K+ concentration in the cell, which, if
unopposed, promotes K+ extrusion. The typical intracellular 1,500

and extracellular concentrations of the important ions and
their equilibrium potentials are listed in Table 7.1.
1,000
Taking into account the permeabilities and activities of
the multiple ions simultaneously, the membrane potential Linear (ohmic)
Current, pA
(Em) can be calculated using the Goldman-Hodgkin-Katz 500 Outward
equation, rectifier
0
Em = RT/zF ln [(PKaKo + PNaaNao + PCaaCao + PClaCli)/
(PKaKi + PNaaNai + PCaaCai + PClaClo)],
−500
Inward rectifier
where P is the permeability, i is the intracellular component,
and o is the extracellular component of the ionic activity, a. −1,000
In normal resting cardiac cells at negative transmembrane −150 −100 −50 0 50
potential (−80 to −90 mV), the major channel that is open is
IK1, which maintains the resting membrane potential around Membrane potential, mV
the equilibrium potential of K+. During conditions such as Figure 7.2 Cardiac ionic current rectification. The current-voltage
myocardial ischemia or renal failure, when [K]o is elevated, (IV) relationships of ion channels show a linear or ohmic
EK rises to less negative potentials and the resting membrane relationship (blue line). Most ion channels in the heart exhibit
potential becomes depolarized, that is, less negative relative nonlinear IV relationships. The Kir family of channels show
to the extracellular space. inward rectification (orange line) in which large currents are
Most cardiac ion channels show rectification, which refers conducted at potentials negative to EK (the calculated equilibrium
potential for K+) but conduct very little current at positive
to the preferential conduction of ions in a single direction,
potentials. Key examples include IK1 and K ATP channels. In
either outward or inward (Figure 7.2). Ion channel rectifica-
contrast, outwardly rectifying channels (green line) conduct
tion can be influenced by unequal ion concentration across mainly repolarizing currents with little inward current at negative
the membrane, the range of voltages that open voltage-gated potentials. Key examples include IKr and IKs.
ion channels (eg, Ito and If ), or blockade of the channel by
intracellular Mg2+ or positively charged polyamines such as
spermine, spermidine, and putrescine at depolarized voltages Some channels may remain open as long as the stimulus
(eg, Kir channels). (eg, depolarization) persists. On removal of the activating
stimulus, the activity decays (deactivation of the channel).
Gating The delayed rectifier K+ channels are noninactivating. In
these channels, K+ conduction stops when membrane poten-
Gating describes how the opening and closing of ion channels tials are hyperpolarized, resulting in channel deactivation
is governed. Voltage-gated channels open and close according (Figure 7.3). Other channels do not display such simple
to changes in membrane potential. INa, ICaL , ICa,T, Ito, IKr, and behavior but instead undergo inactivation. In other words,
IKs are all activated by membrane depolarization, whereas If despite persistence of the activation stimulus, the channel
is activated by membrane hyperpolarization. Voltage-gated enters into a nonconducting state and cannot be activated
ion channels all contain a voltage-sensing S4 in which every unless recovery from inactivation occurs. Open channels can
third amino acid is a positively charged lysine or arginine. be inactivated by different mechanisms, including 1) physical
Ligand-gated channels are activated or inactivated by the occlusion of the channel pore by cytoplasmic portions of the
binding of chemical ligands; for example, If is activated by channel (eg, “ball-and-chain” mechanism in Ito or a “hinge
cyclic adenosine monophosphate, whereas IKATP is inhibited lid” mechanism in INa); 2) conformational changes in chan-
by ATP. nel structure (eg, C-type inactivation in Ito); 3) increase in
intracellular Ca 2+, which promotes Ca2+-calmodulin binding
Table 7.1 to the C terminus of the channel (eg, ICaL); and 4) chemical
Concentrations and Equilibrium Potentials of Important ligand binding (eg, IKATP).
Ions in Heart Cells
Ion Extracellular Intracellular Gradient Across Ex, mV Cardiac Ionic Currents
Concentration Concentration Membrane,
[x]o, mmol [x]i, mmol [x]o/ [x]i INa
Na 140 15 9.3 60
Atrial myocytes, ventricular myocytes, and Purkinje fibers are
K 4 140 0.028 −94
densely populated with Na+ channels. These channels open
Ca 2 0.0001 20,000 130
very briefly (≤1 ms) when the membrane is depolarized above
Cl 120 30 4 –36
a threshold potential of –50 mV, producing conformational
A impaired inactivation, leading to excessive action potential

+100 mV duration) and Brugada syndrome. Sinus and atrioventricular
(AV) nodal cells have little functional INa because of reduced
expression of the channel protein and channel inactiva-
−40 mV
tion due to depolarized resting potentials of −50 to −70 mV.
Therefore, their action potential upstrokes are slow and
Deactivation depend on calcium currents.
Activation K+ currents ICaL
L-type Ca2+ channels are present in all cell types in the heart.
ICa,L is activated by membrane depolarization but has a much
slower inactivation than INa. In nodal cells, ICaL is respon-
sible for impulse generation and conduction. In atrial and
B ventricular myocytes, ICaL is a critical determinant of the
−30 mV action potential plateau and plays a crucial role in cardiac
excitation-contraction coupling, since calcium influx during
−80 mV the plateau is essential in the regulation of mechanical con-
traction. ICaL is enhanced severalfold by sympathetic stimu-
Na+ currents lation. It is inactivated by membrane repolarization and by
increases in intracellular Ca 2+ concentration, which promote
Ca2+-calmodulin binding to the C terminus of the channel,
Inactivation inducing channel inactivation by conformational changes.
Activation ICa,T
Figure 7.3 Current activation, inactivation, and deactivation.
A, In response to a voltage step, the channel is activated, and the T-type Ca2+ channels are more highly expressed in atrial
current is noninactivating and sustained. The current is reduced myocardium, the conduction system, and nodal cells than
or deactivated only on voltage return to negative potentials. A key in ventricular myocytes. ICa,T is activated at hyperpolarized
example is IKs. B, In response to a voltage step, the channel is potentials (positive to −70 mV) and is rapidly inactivated. ICa,T
activated, but the current undergoes time-dependent inactivation, is small compared to ICaL and negligible in ventricular cells.
returning to baseline even when the voltage stimulus is sustained. ICa,T is thought to be responsible for impulse generation in
A key example is the voltage-gated Na+ channel. nodal cells, automaticity in atrial myocytes, and pulmonary
vein potentials.
changes that move the channel from a closed (resting) state to Ito
an open (conducting) state. This allows the influx of Na+ into
the cell and produces rapid phase 0 (100-200 V/s) upstrokes The transient outward K+ current Ito is produced by the
of the action potential, depolarizing the transmembrane voltage-gated K+ channels Kv1.4, Kv4.2, and Kv4.3, with Kv4.3
potential toward ENa (+60 mV). With membrane depolariza- being the dominant contributor. Ito is present in atrial, ven-
tion, the channel proteins undergo further conformational tricular, and conduction system cells. The rapid activation and
changes, causing occlusion of the channel pore by the cyto- inactivation of Ito contributes to phase 1 of the cardiac action
plasmic linker between domains III and IV of the chan- potential. In the ventricular myocardium, Ito is differentially
nel protein in the hinge lid mechanism. The pore occlusion expressed: it is robust in the epicardium and modest in the
brings the channel into an inactivated, nonconducting state. endocardial layers, leading to a transmural gradient that is
The inactivated channel requires repolarization to the rest- responsible for the J or Osborn wave on an electrocardiogram
ing potential (−90 mV) to reenter the closed (resting) state (ECG), seen during hypothermia. Ito is mainly inactivated by
for recovery. The relationship between Na+ channel availabil- the physical occlusion of the channel pore by the N-terminal
ity and membrane potential is an important determinant of portion of the channel in a ball-and-chain mechanism.
conduction and refractoriness. Injured or ischemic myocar-
dium has depolarized resting membrane potentials that pre- IK
vent complete recovery of Na+ channels, resulting in reduced
INa, action potential upstroke, and conduction velocity. This Three components of the delayed rectifier K+ channels are
may be one of the mechanisms of arrhythmia associated with identified: IKur, IKr, and IKs. The rapidly activating and slowly
ischemia. Genetic disorders affecting the Na+ channel have inactivating IKur is prominent in atrial myocytes, account-
been implicated in long QT syndrome (where the channel has ing for their shortened action potential duration. IKr and IKs
are activated very slowly during the cardiac action potential negative chronotropic and dromotropic response and short-
and are responsible for phase 3 repolarization. IKr inactivates ening the action potential in the atria, which may increase the
at depolarized potentials, whereas IKs is noninactivating; K+ propensity for development of AF.
conduction stops when membrane potentials are hyperpolar-
ized, resulting in channel deactivation. The slow deactivation If
of IKs contributes to short action potential durations at high
heart rates. The “funny” current If is activated by membrane hyperpolar-
ization. A nonselective cationic channel, If is responsible for
IK1 pacemaker activity and diastolic depolarization during phase
4 in the sinus node, the AV node, and the Purkinje fibers. The
The strong inward rectifier K+ current IK1 is robust in ven- activity of If is tightly regulated by sympathetic activation and
tricular myocytes, weak in atrial myocytes, and absent in by parasympathetic inhibition.
nodal cells. IK1 conducts inward currents at hyperpolar-
ized membrane potentials with very little outward cur- Electrogenic Membrane Pumps
rent at depolarized membrane potentials. IK1 is crucial and Exchangers
for maintaining the resting potential near the K+ reversal
potential at around −90 mV and is responsible for rapid ter- The Na+/K+ pump is ubiquitous and is inhibited by digitalis.
minal repolarization in phase 3. Diseased myocardium with The pump extrudes 3 Na+ ions in exchange for the entry of
weakened IK1 is susceptible to the development of abnormal 2 K+ ions, with hydrolysis of ATP, resulting in net excretion
automaticity. of a positive charge; hence, the pump is electrogenic and con-
tributes a repolarizing outward current to the cardiac action
IKATP potential.
The Na+/Ca2+ exchange facilitates the exchange of 1 Ca 2+
IKATP, a member of the inward rectifier K+ channel family, is ion for 3 Na+ ions. The direction of exchange depends on the
formed in the myocardium as a heteromultimeric complex membrane potential. At the resting potential, Ca 2+ is extruded,
composed of 4 K+ conducting subunits (Kir6.2) and 4 sulfonyl- allowing the cell to maintain low intracellular Ca 2+ concentra-
urea receptor subunits (SUR2A). K ATP channels are normally tion. At the action potential plateau, the exchanger facilitates
inhibited by intracellular ATP. They couple cellular metab- Ca2+ entry and contributes to cardiac excitation-contraction
olism with membrane excitability and are activated during coupling. The exchanger is electrogenic and is thought to
ischemia when a decrease in the ATP/adenosine diphosphate mediate the development of delayed afterdepolarizations
(ADP) ratio occurs with depletion of ATP and a rise in ADP (DADs) and triggered activity.
concentration. Ventricular myocytes are endowed with high In addition to the sarcolemmal voltage-gated ion channels
densities of these channels and their activation accounts for mentioned above, 2 other ion channels are worth noting for
the ST-segment elevation seen on an ECG during myocardial their important roles in cardiac electrophysiology and in the
infarction and for mediation of the cardioprotective response development of cardiac arrhythmias.
by ischemic preconditioning. The opening of K ATP channels Gap junction channels are hexomeric complexes of con-
leads to the shortening of the action potential and membrane nexin (connexin 40 and connexin 43) that form hemichan-
hyperpolarization, which in turn reduces Ca 2+ influx through nels on the cell surface. Two hemichannels from 2 different
ICa. The reduced Ca2+ influx in turn results in a decrease in cel- cells are united to form a functional gap junction. The open-
lular excitability and protection of the heart under metabolic ing and closing of gap junction channels that allow intercel-
stress and ischemia-reperfusion injury. lular communications is regulated by a number of metabolic
parameters, including pH, intracellular Ca 2+ concentration,
IKACh or IKAdo and channel phosphorylation. Each cell is connected by
gap junctions to many adjacent cells predominantly at their
The inwardly rectifying G-protein–gated K+ channel is ends, with little lateral connections, so more gap junctions
formed by association of 2 K+-channel proteins GIRK1 are present between cells in the longitudinal direction than
(Kir2.1) and GIRK4 (Kir2.4) in the heart. These channels, in the transverse direction. This uneven distribution results
mainly expressed in pacemaker tissues (sinoatrial and AV in preference of electrical signal propagation in the longitu-
node and Purkinje fibers) and in the atria, are involved in the dinal direction rather than the transverse direction, a phe-
parasympathetic modulation of heart rate and are targets of nomenon termed anisotropy, which in some situations may
modulation by the autonomic nervous system and adenosine. promote arrhythmia. Impulse propagation between cells is
The channel is activated by the binding of the βγ subunits of rapid, because of gap junctions between cells. The current
the inhibitory G protein (Gi), which in turn is activated by generated by an action potential is quickly injected into a
binding of acetylcholine to the muscarinic (M2) receptor or neighboring cell, leading to its depolarization and trigger-
adenosine to the adenosine (A1) receptor. There is now hyper- ing of an action potential. Because of these gap junctions, the
polarization of the sinoatrial and AV nodal cells, causing a heart acts like a syncytium. Intercellular transfer of currents
can occur only where cells share gap junctions, and activities the delayed rectifier K+ currents and inactivation of the Ca 2+
and distribution of the gap junction channels can profoundly currents. Toward the terminal portion of phase 3, the strong
affect electrical impulse conduction, especially under condi- inward rectifier K+ currents, IK1, are activated, leading to rapid
tions of ischemia. repolarization. During diastole or phase 4, atrial and ventric-
Ryanodine receptors are intracellular ion channels located ular myocytes are normally quiescent electrically. However,
in the sarcoplasmic reticulum. They are responsible for releas- pacemaker tissues such as the sinus node, AV node, and
ing Ca2+ from the sarcoplasmic reticulum and are crucial ele- His-Purkinje fibers show slow diastolic depolarization, indi-
ments in the regulation of intracellular Ca2+ homeostasis. The cating the presence of pacemaker activity caused by the acti-
opening of ryanodine receptors is triggered by Ca 2+ entry vation of If and Ca2+ currents and inactivation of K+ currents.
through sarcolemmal Ca2+ channels, ie, Ca 2+-induced Ca 2+ The rate of phase 4 depolarization and spontaneous action
release, and is critical in regulating excitation-contraction potential generation is fastest in sinus node cells, which form
coupling of the heart. In the normal heart, ryanodine recep- the dominant pacemaker of the heart. Activities of the dif-
tors are closed during diastole. In disease states, however, ferent ionic currents during the cardiac action potential are
these channels become “leaky,” resulting in intracellular Ca 2+ shown in Figure 7.4.
overload and the development of arrhythmias. To summarize, the major currents activated at different
Many ion channels in the heart contain auxiliary sub- phases of the cardiac action potential are as follows:
units, which modulate the expression and function of the
• Phase 0: Na+ currents (atria, ventricles, and His-
pore-forming channel subunits that allow exchange of ions
Purkinje) and Ca 2+ currents (sinus and AV nodes)
across the cell membrane. Some notable examples are the
• Phase 1: Transient outward K+ currents, Ito
following:
• Phase 2: Ca2+ currents, Na+/Ca2+ exchange currents,
• The function and expression of Na+ channels are regu- and delayed rectifier K+ currents
lated by β subunits. • Phase 3: Delayed rectifier K+ currents (IKr and IKs) and
• The L-type Ca2+ channels in the heart contain α2, β, IK1 (late phase 3)
and δ subunits. • Phase 4: Pacemaker currents, If and ICa,T
• Kv1.4 and Kv4.3, which form Ito, are modulated by the
Differential expression of ion channels in various regions
K+ channel interacting protein, which may be respon-
of the heart gives rise to differences in configurations of
sible for channel trafficking and the transmural gradi-
action potentials (Figure 7.5). The sinus node is character-
ent of Ito.
ized by its phase 4 depolarization, which gives rise to pace-
• K ATP channels contain Kir6.2 and the sulfonylurea
maker activities. Phase 4 depolarization is attributable to
receptor SUR2A subunits. SUR2A confers channel
the high density of pacemaker currents and the lack of IK1,
sensitivity to sulfonylurea and potassium channel
which also accounts for the relatively depolarized state of
openers.
the tissue (resting membrane potential −50 to −70 mV). Na +
• KvLQT1, which forms the pore-forming subunit of IKs,
channels are sparse and the action potential upstroke is slow
is profoundly modulated by MinK.
since it is mediated mainly by ICa,L . No phase 1 is discern-
• HERG, which forms the pore-forming subunit of IKr,
ible because of the lack of Ito. Action potential durations are
is profoundly modulated by MiRP. Mutations in genes
short, and the frequency of depolarization is determined
coding for KvLQT1 (KCNQ1), HERG (KCNH2), MinK
by the sympathetic and parasympathetic modulation of
(KCNE1), and MiRP (KCNE2) are known to cause long
If and ICa,L .
QT syndromes.
The atrial action potential has rapid upstrokes, allowing
rapid electrical impulse conduction across the atria and from
ION CHANNELS AND THE CARDIAC ACTION the sinus node to the AV node. It has a discernible phase 1 fol-
POTENTIALS lowed by a short plateau phase and rapid repolarization, prob-
ably attributable to larger Ito and other repolarizing currents
The cardiac action potential is determined by the sum of ionic such as IKur and IKACh. The short plateau may partially explain
current activities at any given time point during the cardiac why an antiarrhythmic drug like lidocaine, which exerts its
cycle. Upstroke of the action potential, phase 0, is associated effects during the plateau phase (binding to the inactivated
with the opening of the Na+ channels. Inactivation of the Na+ Na+ channel), is ineffective in the treatment of atrial arrhyth-
currents and activation of the transient outward K+ currents mias. Normal atrial tissue has no phase 4 activity because of
give rise to early rapid partial repolarization of the action the presence of IK1.
potential (phase 1). The balance between inactivation of tran- The AV node is similar to the sinus node in its lack of INa
sient outward K+ currents, activation of L-type Ca 2+ currents, and IK1. Conduction through the AV node is mediated by
delayed rectifier K+ currents, and the Na+/Ca2+ exchange cur- ICaL and propagation is slow, accounting for its decremental
rents constitutes phase 2, which is the plateau of the action conduction properties. Activities of the ICaL are activated by
potential. Phase 3 represents the fi nal rapid repolarization of sympathetic stimulation and inhibited by parasympathetic
the action potential and is the result of further activation of influences; these are important determinants of impulse
A Depolarizing currents
INa Zero
ICa,T
ICaL ICaL
If
INa/Ca Ex INa/Ca Ex
Ito Ito
ICaL IKur
ICaL ICaL
IKr,IKs
IKr,IKs IK (IKr,IKs)
INa INa ICa,T
If
IK1 IK1
Ventricle Atrium Nodal tissue
B Repolarizing currents
IK1 Zero
Ito
IKr IK
IKs
IKur
Figure 7.4 Ionic currents that contribute to cardiac action potentials. Depolarizing currents (A, red) and repolarizing currents (B, blue)
contribute to the action potentials in the ventricle (left panels), atrium (middle panels), and nodal tissue (right panels).
conduction through the AV node. Phase 4 depolarization is thought to be the basis for development of U waves and trig-
present but at a slower rate than and not as prominent as that gered activities.
in the sinus node.
His-Purkinje fibers have high densities of INa that facilitate Cardiac Refractoriness, Excitability, and
rapid conduction of impulses so that ventricular myocytes Impulse Propagation
can be activated synchronously. In addition, the His-Purkinje
fibers have strong IK1 and weak pacemaker currents. Thus, When an activated cardiac cell is stimulated by an electri-
His-Purkinje tissue is characterized by a resting potential cal current (such as a pacemaker impulse) during the plateau
of –90 mV, close to the reversal potential of K+, and slow dia- phase of action potential, the majority of Na+ channels are in
stolic depolarization that can form a subsidiary pacemaker if the inactivated state and are unavailable for excitation, so no
AV nodal conduction is blocked. action potential can be generated and the cell is considered
Ventricular myocytes have densities of INa and IK1 higher refractory. Recovery from refractoriness of the atrial, ventric-
than those in atrial myocytes; hence, these cells rest near –90 ular, and His-Purkinje systems depends on the voltage- and
mV and are electrically quiescent. Configuration of the time-dependent recovery of Na+ channels. With repolariza-
action potential varies according to location in the left ven- tion, the Na+ channels fully recover from inactivation to the
tricle. Myocytes in the epicardial layer have a very strong Ito. closed state and are available for generating a rapid action
This leads to marked repolarization in phase 1 followed by potential upstroke, thus restoring excitability of the cardiac
depolarization as Ca 2+ currents are activated, generating the tissue. Interestingly, in Purkinje fibers and under some con-
characteristic “spike-and-dome” configuration (Figure 7.5). ditions in the working myocardium, supernormal excitabil-
In contrast, the endocardial layer has a much lower Ito den- ity is noted at the end of repolarization. This phenomenon
sity, with reduced phase 1 amplitude and no spike-and-dome. refers to the ability to elicit an action potential by a stimulus
The mid-myocardial layer is endowed with the so-called M that is normally subthreshold. There may now be enough Na+
cells, ie, mid-myocardial cells, which have strong Ito but weak channels that are reactivated during repolarization and when
delayed rectifier K+ currents and enhanced slow component the membrane potential is closer to the threshold for action
of the voltage-gated Na+ currents. Thus, the M-cell action potential generation than when the cell is completely repolar-
potential is characterized by a spike-and-dome configuration ized at rest. Supernormal excitability underlies the vulnerable
and a lengthened action potential duration exceeding those period of the cardiac cycle and may contribute to susceptibil-
of epicardial and endocardial myocytes (Figure 7.5). This ity for development of reentrant arrhythmias. Supernormal
regional heterogeneity in the electrophysiology of the heart is excitability has been demonstrated in the Bachmann bundle
Sinus node
Atria
AV node
His-Purkinje tissue
Endocardium
Mid-myocardium Ventricles
Epicardium
ECG
Figure 7.5 Action potential waveforms in different tissues in the heart. Action potential configurations from various tissues of the heart
are different according to their specific roles in impulse generation, conduction, and contraction. The sinoatrial and atrioventricular (AV)
nodes are important in impulse generation and have pacemaker activity. Atrial and ventricular myocardium is important for contraction.
His-Purkinje tissue has the fastest upstroke velocity for rapid conduction of electrical impulse to activate the ventricles synchronously. The
ventricular epicardium, endocardium, and mid-myocardium have distinct action potential configurations. The contributions of the action
potentials from various tissues to the surface electrocardiographic (ECG) signals are displayed.
and in Purkinje fibers. However, true supernormal excit- using premature stimuli that cause propagated responses.
ability is difficult to confirm, and its existence in ventricular The effective refractory period is the longest interval at which
myocardium and AV nodal tissue is controversial. a premature stimulus fails to propagate.
In partially depolarized ischemic atrial and ventricular tis- Following the generation of a cardiac impulse in a cell,
sue with inactivated Na+ channels, as well as in the sinus and activation propagates to adjacent cells. Two essential factors
AV nodes, activation depends on ICaL, and the restoration of determine cell-to-cell impulse conduction: the strength of
excitability depends on recovery of Ca2+ channels from inac- the source or depolarizing current and the cell-to-cell elec-
tivation. This is a slower process, and excitability may not be trical connections through gap junctions. Gap junctions are
fully restored even after repolarization. Therefore, a prema- normally distributed more at longitudinal end-to-end cell
ture stimulus may find some channels recovered and produce connections than at transverse side-to-side cell connections.
a reduced ICaL that may propagate slowly with a decrement in Therefore, the propagation velocity is much faster along the
conduction as the prematurity of impulses increases. A clini- cell than across the cell. This direction-dependent or aniso-
cal example of this phenomenon is the observation that, as tropic conduction is important since factors that affect the
premature atrial complexes are placed progressively earlier, strength of the depolarizing currents, such as ischemia that
the time through the AV node (reflected in the PR interval) causes Na+ channel inactivation or inhibition of the gap junc-
becomes progressively longer. In the cardiac electrophysiology tions, can slow propagation of impulses more in 1 direction
laboratory, refractoriness or excitability can be determined than the other, creating a milieu that promotes reentrant
arrhythmias. Excitability or refractoriness of the cardiac arrhythmias but are important because they are frequently
tissue and conduction velocity are important parameters associated with life-threatening conditions. Unless a proper
that determine the propensity toward arrhythmias and are diagnosis is made and the underlying conditions that set up
targeted by antiarrhythmic agents to prevent or terminate the triggered activities are removed, the ensuing arrhythmias
arrhythmias. are potentially lethal. There are 2 types of triggered activity:
DADs and early afterdepolarizations (EADs).
EADs occur during phase 2 or 3 of the cardiac action
MECHANISMS OF CARDIAC ARRHYTHMIA potential before complete repolarization (Figure 7.6) and are
therefore seen more frequently with prolonged repolariza-
Coordinated activation and inactivation of several voltage- tion. EADs are induced more easily in the Purkinje and M
and ligand-gated ion channels, transporters, and pumps cells than in epicardial or endocardial cells. Conditions asso-
within the myocardium are required to achieve normal acti- ciated with marked prolongation of action potential durations
vation of the heart. Abnormality in any of these may result (Table 7.2) and, hence, prolonged QT intervals promote the
in the development of arrhythmias. Cardiac arrhythmias development of EADs, which in the setting of increased dis-
occur as a result of abnormalities in either impulse initiation persion of refractoriness are thought to be the mechanism
or impulse propagation (Figure 7.6). Failures of impulse ini- that underlies torsades de pointes, the polymorphic VT in the
tiation or conduction are responsible for bradyarrhythmias setting of prolonged QT intervals.
and heart block. Tachyarrhythmias are caused by enhanced Torsades de pointes is characterized by the following:
impulse generation due to altered automaticity, triggered
activity, or abnormal impulse propagation with reentry. • prolonged QT intervals
• polymorphic VT with characteristic “twisting around
the axis” morphology
Arrhythmias Due to Abnormalities • exacerbation by bradycardia (which prolongs QT and
of Impulse Initiation increases dispersion of refractoriness)
• long-short coupling intervals
Automaticity is the ability of an excitable cell to undergo
• recurrent bursts or salvos of nonsustained polymor-
spontaneous diastolic depolarization and to initiate an electri-
phic VT before degeneration into sustained polymor-
cal impulse in the absence of external stimulation. In tissues
phic VT and ventricular fibrillation (VF)
such as the sinus node, the AV node, and the His-Purkinje
system that display normal automaticity with spontaneous DADs occur after the action potential has completely repo-
diastolic depolarization, an increase in the slope of phase 4 larized (Figure 7.6) in the setting of intracellular Ca2+ over-
depolarization due to enhanced automaticity can result in load, after ischemia-reperfusion or with adrenergic stress,
increased heart rate. The underlying ionic currents (If, ICa,T, digitalis intoxication, or intracellular Ca2+ release channel
ICaL) are the same involved in impulse initiation during physi- (ryanodine receptor) dysfunction. Arrhythmias involving
ologic conditions. Examples of enhanced automaticity include DADs are characterized by the following conditions:
inappropriate sinus tachycardia, junctional rhythm, and idio-
• intracellular Ca2+ overload
ventricular rhythm from Purkinje fibers. These arrhythmias
• exacerbation by tachycardia (which increases intracel-
are influenced by neurohormones and drugs affecting the
lular Ca2+)
sympathetic or parasympathetic system.
• enhancement by sympathomimetics
Abnormal automaticity refers to the spontaneous devel-
opment of impulses independent of preceding impulses in Triggered activity is usually not inducible with pro-
tissues, such as atria or ventricles that normally do not dis- grammed electrical stimulation. Burst pacing may induce
play spontaneous depolarization. The underlying mechanism DADs and triggered activity since pacing at rapid rates
involves ionic currents not normally active in these cells promotes calcium buildup in cells. Current facilities in the
and is usually observed following tissue injury. Examples electrophysiology laboratory cannot reliably record or differ-
of abnormal automaticity include ectopic atrial tachycardia, entiate between EADs and DADs.
accelerated idioventricular rhythm, and ventricular tachycar-
dia (VT) following ischemia-reperfusion injury. Automatic Arrhythmias Due to Abnormalities
tachycardias are usually not inducible by programmed elec- of Impulse Propagation
trical stimulation during electrophysiologic studies. They
are characterized by rate acceleration at the onset (warm- Reentry is the most common mechanism involved in many
ing up) and deceleration before termination (cooling down) clinically important cardiac arrhythmias, including AV
and responsiveness to sympathomimetics and autonomic nodal reentry tachycardia, AV reentry tachycardia using an
modulation (Figure 7.6). AV accessory connection, atrial flutter, AF, and VT in scarred
Triggered activity is the development of abnormal impulses myocardium. Reentry arises as a result of altered conduction
as a result of the preceding impulse or impulses. Triggered when impulses propagate by more than 1 pathway, each dif-
activities are involved in only a small portion of clinically seen fering in its electrophysiologic properties. With a premature
A Reentry
Area of slow Unidirectional
conduction block Reentry
B Automaticity
↑ Sympathetic
Normal stimulation
myocardial
action
potential
↑ Diastolic Diastolic
depolarization depolarization
C Triggered activity–EAD
Normal AP ↑ APD EAD
↑ QT
ECG
D Triggered activity–DAD
Rapid pacing 1s
1s
0 mV 0 mV
Sustained
DADs triggered
activity
−50 mV
−100 mV
Normal
Figure 7.6 Mechanisms of cardiac arrhythmias. A, For reentry arrhythmia to occur, it requires the presence of a substrate and an area
of slow conduction (left panel). Reentry is initiated by unidirectional block (middle panel). The electrical impulse conducts from the
opposite direction to the area of block when the area of block recovers, allowing reentry to occur (right panel). B, Automaticity is normally
absent in atrial and ventricular myocardium (left panel). In injured or depolarized tissue, abnormal automaticity can occur with diastolic
depolarization (right panel, red). Automaticity usually is augmented by sympathetic or adrenergic stimulation, which enhances the rate of
diastolic depolarization (green). C, In triggered activity after early afterdepolarization (EAD) (upper tracings), a normal action potential
(AP) is associated with a normal QT interval (left panel). With an increase in action potential duration (APD) (for causes see Table 7.1),
QT is prolonged (middle panel). With further prolongation of the AP, a depolarization occurs in late phase 2 as an EAD (right panel).
Depolarization occurs before complete repolarization of the AP. D, Delayed afterdepolarization (DAD) in cardiac tissue is induced by rapid
pacing. Normal tissue shows no afterdepolarizations (left panel). Under conditions of intracellular Ca 2+ overload, the same conditions with
rapid pacing induce DADs (red, middle panel). Depolarizations occur after complete repolarization of the AP. Further Ca 2+ overload results
in sustained triggered activity (red, right panel).
beat, conduction may fail in 1 pathway (with a longer refrac- can proceed in the retrograde direction along the first path-
tory period), creating a unidirectional block while continuing way to create a reentry circuit (Figure 7.6).
in the other at a slower rate (Figure 7.6). Consequently, by the Reentry may occur in anatomically defined pathways
time the impulse reaches the other end of the first pathway, such as AV accessory connections in Wolff-Parkinson-White
the tissue has recovered from refractoriness, and activation syndrome or around scarred myocardium after myocardial
Table 7.2 circuit collides with the tail of refractory tissue, extinguish-
Conditions Known to Promote Prolonged Action ing reentry. These properties are important in determining
Potential Duration and Triggered Activity Due to Early the effectiveness of antiarrhythmic drugs and overdrive pac-
Afterdepolarization
ing in the termination of reentry arrhythmias.
Condition Mechanism During electrophysiologic study, reentrant arrhythmias
usually 1) are inducible by programmed electrical stimula-
Hypokalemia ↓ K+ channel activity
tion; 2) exhibit abrupt onset and offset; 3) exhibit regular R-R
Hypomagnesemia ? ↑ Ca 2+ channel activity
intervals during the tachycardia with minimum oscillation
Antiarrhythmic drugs
in rate (particularly in the absence of antiarrhythmic drugs);
Class 1A antiarrhythmics K+ channel blockade
Class 3 antiarrhythmics and 4) can be reset or entrained by pacing. Resetting or
Sotalol, dofetilide K+ channel blockade entrainment occurs when a pacing impulse enters the circuit
Ibutilide Na+ channel activation, K+ to advance it. It is an important diagnostic tool, discussed in
channel blockade detail in Chapter 5.
Antihistamines K+ channel blockade
Macrolide antibiotics, ie, K+ channel blockade
erythromycin INHERITED CARDIAC CHANNELOPATHIES
Congenital long QT syndrome Channelopathies (INa, IKr, IKs, IK1)
With advances in molecular biology approaches, more infor-
mation is available on primary ion channel abnormalities,
infarction. Reentry can also occur due to the development of termed channelopathies, that constitute the molecular basis
functional block that does not involve an anatomically defined of familial cardiac rhythm disturbances. The key features of
conduction discontinuity such as an infarct scar but occurs these channelopathies are highlighted below (Table 7.3).
in tissues exhibiting heterogeneity in refractoriness or con-
duction velocities, giving rise to leading-circle, spiral wave, Long QT Syndrome
or figure-of-8 reentry. Reentry may also develop as a result of
changes in cell-to-cell coupling or an increase in anisotropy • Long QT syndrome has been shown to be associated
in longitudinal vs transverse direction (anisotropic reentry). with mutations in membrane proteins that affect K+
Critical portions of anatomically defined reentrant path- channels (loss of function, with reduced IKr, IKs, and
ways can be identified during electrophysiologic study and IK1), Na+ channels (gain of channel function with
ablated, eliminating reentry and curing the patient. These incomplete inactivation during phase 2), Ca 2+ channels
circuits usually have a long excitable gap (Figure 7.7). (gain of function), and nonchannel proteins (ankyrin B
Anatomically determined reentry requires the presence of and caveolin 3).
anatomically distinct pathways, heterogeneity in refractori- • A number of mutations involving different ion chan-
ness within regions in the circuit, and slow conduction in 1 nels and proteins underlie long QT syndrome, and all
part of the circuit. Examples of anatomic reentry include AV lead to action potential prolongation, because either
nodal reentry tachycardia, reciprocating tachycardia utilizing depolarizing currents are incompletely inactivated or
an accessory connection, typical atrial flutter, and VT around repolarizing currents are weakened.
scarred tissue after myocardial infarction or involving dis- • In long QT syndrome type 3, defects due to mutations
eased His-Purkinje branches. in the SCN5A gene lead to alterations in the structural
In contrast to anatomic reentry circuits, functional reen- regions of the Na+ channel protein responsible for
trant circuits do not have fi xed pathways. The propagating channel inactivation. Repolarization is prolonged by
wave front turns on itself with the rate of turning limited the inappropriate continuous influx of Na+ ions (gain of
only by conduction velocity or by encountering of relatively function) during the plateau phase of action potential.
refractory tissues. Functional reentry circuits are dynamic as • Loss of channel function (IKr and IKs) can be attribut-
cells are reexcited as soon as they recover from refractoriness. able to reduced channel expression, increased channel
These circuits possess no or a short excitable gap, may ana- turnover, impaired channel maturation, or impaired
tomically wander, and thus are hard to define and difficult to channel trafficking.
ablate. Examples included AF and VF. • Mutations can occur at many different sites on the same
An important concept to remember for reentrant arrhyth- channel protein, resulting in the gain or loss of channel
mias is that the wavelength of the reentry impulse is defined function and manifesting as the same phenotype.
by the product of conduction velocity and refractoriness. • Ankyrin B mutations affect the function of the Na+/K+
Conditions that shorten the wavelength by decreasing the pump, the Na+/Ca2+ exchange, and other mechanisms,
conduction velocity and/or decreasing refractoriness pro- resulting in abnormal Ca2+ homeostasis and Ca2+ overload,
mote reentry by increasing the excitable gap. Conversely, thereby promoting the development of DADs and EADs.
if wavelength properties are altered so that the wavelength • Mutations in caveolin 3, which is the principal protein
exceeds the available circuit, the leading edge of the reentrant of caveolae membrane microdomains where cardiac
Short EG Long EG
EG AF, atypical AFI, AFI, ORT, ART, VT (Na+)

PVT, VF AVNRT, ORT, ART (Ca2+)
Wavelength
(λ = R • V)
↑ Refractoriness Convert unidirectional

Class III, I block to bidirectional block
Class I, II, IV (AV node)
Figure 7.7 Reentry circuit showing propagating wave front of tachycardia, refractory period, and excitable gap (EG). The reentry circuit
shows propagating wave front (curved arrow), refractory tissue (shaded area), and EG (white area). Wavelength (λ) of the reentrant circuit
is defined by the product of refractoriness (R) of cardiac tissue and conduction velocity (V). Examples of arrhythmias with short and
long EGs and antiarrhythmic drugs that can terminate or prevent arrhythmias by prolonging refractoriness or promoting conduction
block are shown. AF indicates atrial fibrillation; AFl, atrial flutter; ART, antidromic reciprocating tachycardia; AV, atrioventricular;
AVNRT, atrioventricular node recovery time; ORT, orthodromic reciprocating tachycardia; PVT, polymorphic ventricular tachycardia;
VF, ventricular fibrillation; VT, ventricular tachycardia.
Na+ channels are localized, have been shown to increase Brugada Syndrome
the late sodium currents, resulting in long QT type 3.
• Figure 7.8 shows the typical ECG features associated • Brugada syndrome is an autosomal dominant primary
with long QT syndrome type 1 (broad-based T waves), arrhythmia syndrome with male predilection (75%).
long QT type 2 (low-amplitude T waves), and long QT • It is characterized by reduced peak INa due to
type 3 (long ST segments). Although these features are loss-of-function mutations of INa in 20% of patients.
suggestive, they are not diagnostic of specific subtypes • Abnormal ST-segment elevations are seen in the right
of long QT syndrome. precordial leads V1 to V3.
• Class I antiarrhythmic drugs may be used to unmask
Short QT Syndrome
and bring out ST abnormalities.
• A high-risk group of patients developed highly lethal
• Short QT syndrome is characterized by corrected QT idiopathic VF with a 5-year survival of only 40%.
intervals of less than 320 ms, high incidence of sudden • Brugada syndrome is the same disease referred to as
cardiac death, syncope, AF, and frequently inducible sudden unexplained death syndrome in Southeast Asia.
VF in a structurally normal heart. • Figure 7.10 shows ECGs of patients with Brugada syn-
• It is caused by gain-of-function mutations in K+ chan- drome demonstrating the typical coved or saddleback
nels (IKr, IKs, and IK1). features in the precordial leads.
• Treatment with an implantable cardioverter- • Fever is known to unmask the ECG patterns in patients
defibrillator is indicated in sudden death survivors and with Brugada syndrome (Figure 7.11).
those with a history of syncope or a strong family his-
tory of sudden death.
• The use of QT-prolonging drugs such as sotalol, quini- Catecholaminergic Polymorphic VT
dine, and hydroquinidine has been tried, but long-term
effectiveness has not been established. • Catecholaminergic polymorphic VT is characterized
• Figure 7.9 shows the ECG of a patient with short QT by exercise- or stress-induced polymorphic VT, syn-
syndrome. cope, and sudden death.
Table 7.3
Inherited Cardiac Channelopathies
Condition Mutated Gene Channel/ Protein Functional Effects Relative Frequency
Affected of Mutations
Long QT syndrome
LQT1 KCNQ1 KvLQT1 ↓ IKs +++
LQT2 KCNH2 HERG ↓ IKr ++
LQT3 SCN5A Nav1.5 ↑ INa with noninactivating +
CAV3 Caveolin 3 Na+ currents Rare
LQT4 ANK2 Ankyrin B ↓ IKs Rare
LQT5 KCNE1 MinK ↓ IKr Rare
LQT6 KCNE2 MiRP1 ↓ IK1 Rare
LQT7 (Anderson syndrome) KCNJ2 Kir2.1 ↑ ICaL Rare
LQT8 (Timothy syndrome) CACNA1C Cav1.2 Rare
Short QT syndrome
SQT1 KCNH2 HERG ↑ IKr Rare
SQT2 KCNQ1 KvLQT1 ↑ IKs Rare
SQT3 KCNJ2 Kir2.1 ↑ IK1 Rare
Brugada syndrome SCN5A Nav1.5 ↓ INa +
Catecholaminergic RYR2 Ryanodine receptor ↑ Abnormal Ca 2+ release from Rare
polymorphic VT CASQ2 Calsequestrin sarcoplasmic reticulum Rare
Familial AF KCNQ1 KvLQT1 ↑ IKs Rare
KCNE2 MiRP1 ↑ IKs Rare
KCNH2 HERG ↑ IKr Rare
KCNA5 Kv1.5 ↓ IKur Rare
KCNJ2 Kir2.1 ↑ IK1 Rare
SCN5A Nav1.5 ↓ INa Rare
ABCC9 SUR2A ↓ IKATP Rare
Conduction disease SCN5A Nav1.5 ↓ INa Rare
Sinus node dysfunction SCN5A Nav1.5 ↓ INa Rare
HCN4 hHCN4 ↓ If Rare
Abbreviations: AF, atrial fibrillation; LQT, long QT syndrome (followed by type number); SQT, short QT syndrome (followed by type number);
VT, ventricular tachycardia.
Chromosome 11 Chromosome 7 Chromosome 3
II
aVF
V5
LQT1 LQT2 LQT3

Figure 7.8 Typical electrocardiographic (ECG) features associated with long QT syndrome type 1, type 2, and type 3 (LQT1, LQT2, and
LQT3). Shown are ECG recordings from leads II, aVF, and V5 in 3 patients from families with long QT syndrome linked to genetic markers
on chromosomes 11 (LQT1), 7 (LQT2), and 3 (LQT3). (Adapted from Moss AJ, Zaregba W, Benhorin J, Locati E, Hall WJ, Robinson JL,
et al. ECG T-wave patterns in genetically distinct forms of the hereditary long QT syndrome. Circulation. 1995;92[10]:2929–34. Used with
permission.)
Figure 7.9 Short QT syndrome. Twelve-lead electrocardiogram from a patient with short QT syndrome. The QT interval is 240 ms with
tall and narrow T waves. (Adapted from Bjerregaard P, Gussak I. Short QT syndrome: mechanisms, diagnosis and treatment. Nat Clin Pract
Cardiovasc Med. 2005;2[2]:84–7. Used with permission.)
Type 1 Type 2 Type 3
V1
V2
V3
V4
V5
V6
Figure 7.10 Brugada syndrome with different characteristic ST–segment abnormalities. Type 1 or coved–type ST-segment elevation of
2 mm or more is followed by a negative T wave with little isoelectric separation. Type 2 or saddleback appearance with a high takeoff
ST-segment elevation of 2 mm or more is followed by gradually descending ST-segment elevation remaining 1 mm or more above baseline
and a positive or biphasic T wave. Type 3 has either a coved or saddleback appearance with an ST-segment elevation less than 1 mm.
(Adapted from Rossenbacker T, Priori SG. The Brugada syndrome. Curr Opin Cardiol. 2007;22:163–70. Used with permission.)
A Fever (42°C)
B Normal temperature (36.5°C)
Figure 7.11 Fever and Brugada syndrome. The febrile state is known to unmask the ECG patterns of Brugada syndrome. The ECGs are
obtained from a 43-year-old man who presented with fever (A, 42°C) and after recovery (B, 36.5°C).
• Catecholamine infusion produces bidirectional VT, catecholaminergic polymorphic VT show decreased

polymorphic VT, and VF. binding to calstabin2. Catecholamine stimulation
• It is caused by mutations in the cardiac ryanodine significantly disrupts RyR2-calstabin2 interaction by
receptor (RyR2, autosomal dominant) and calseques- increasing Ca2+ release and by producing polymorphic
trin (CASQ2, autosomal recessive), which are critical VT, possibly through triggered activity and DADs.
elements in intracellular Ca2+ homeostasis and in the • Figure 7.12 shows bidirectional VT in a patient with
regulation of excitation-contraction coupling. catecholaminergic polymorphic VT.
• RyR2 is regulated by binding to calstabin2, which keeps
the channel in a closed state and prevents Ca2+ leakage Familial AF
during diastole. RyR2 is activated by sympathetic stim-
ulation, which causes the dissociation of RyR2 from • Familial AF is caused by mutations that lead to an increase
calstabin2. The mutant RyR2 channels in patients with in IKs, IKr, and IK1 or a reduction in INa, IKur, and IKATP.
Figure 7.12 Electrocardiogram showing bidirectional ventricular tachycardia in a patient with ryanodine receptor 2–catecholaminergic
polymorphic ventricular tachycardia. (Adapted from Napolitano C, Priori SG. Diagnosis and treatment of catecholaminergic polymorphic
ventricular tachycardia. Heart Rhythm. 2007;4:675–8. Used with permission.)
• Atrial action potentials are altered with enhanced sus- Polymorphisms involving connexin 40 are associated with
ceptibility to development of reentry and increased dis- increased susceptibility to developing AF because of a slow-
persion of refractoriness. ing in impulse conduction. The overall net effect is a reduc-
tion in the AF wavelength, allowing more AF wavelets to exist
Other Arrhythmia Conditions simultaneously with more stable circuits. The increased spa-
tial heterogeneity in refractoriness and conduction provides
• Isolated cardiac conduction disease is a loss-of-function the substrate for reentry and fibrillation.
mutation in INa (G514C) manifested as cardiac impulse In addition to electrical remodeling, structural remodel-
conduction abnormalities, including broad P waves, ing occurs in the atria with the development of AF. Atrial
prolonged PR, and widened QRS. dilation with a decrease in atrial contractility results from
• Congenital sick sinus syndrome is caused by autosomal AF. The resulting atrial stunning is probably a form of
recessive inheritance of INa mutations that cause loss tachycardia-induced cardiomyopathy in the atria. These
of function or impairment in inactivation gating with structural and functional changes provide further accommo-
reduced cardiac excitability. dation to the fibrillation wavelets, resulting in a vicious cycle.
• Sinus node dysfunction is a truncation mutation of If
that causes sick sinus syndrome.
Heart Failure
ACQUIRED CARDIAC CHANNELOPATHIES Patients with New York Heart Association class III or IV
heart failure have a 2-year mortality rate of 50%, and many
Abnormal ion channel expression, regulation, and function of these patients die from arrhythmia. Electrical remodeling
are known to be associated with various cardiac pathologic occurs in heart failure, and the hallmark is prolongation of
conditions. These changes in cardiac electrophysiologic prop- ventricular action potential, resulting from downregulation
erties are thought to be the result of maladaptation to disease of repolarizing K+ currents, including Ito, IKr, IKs, and IK1, and
states, a process termed electrical remodeling. Some of the altered intracellular Ca 2+ homeostasis.
important examples are highlighted below (Table 7.4). Decrease in Ito, IKr, and IKs leads to prolongation of the
action potential duration with an increase in propensity for
Atrial Fibrillation developing EADs and triggered activity. Reduced IK1 leads to
enhanced automaticity and prolongation of the termination
Sustained AF has been shown to produce adaptive changes in portion of phase 3 of the action potential.
the electrical properties of the heart or electrical remodeling, An increase in intracellular Ca2+ may increase inactiva-
which in turn accommodate AF. The accommodation now tion of the L-type Ca 2+ currents, enhance Na+/Ca2+ exchange
allows AF to stabilize and perpetuate, a concept described as activities, and cause the development of DADs and triggered
“atrial fibrillation begets atrial fibrillation.” In the fibrillating activity.
atria, the action potential is shortened with loss of adaptation In addition, longstanding heart failure is associated with
to rate. Normal atrial tissues show an increase in refractori- structural remodeling, which includes interstitial fibrosis,
ness with slowing in the rate, which may protect against ini- cardiac chamber dilation, and connexin 43 redistribution.
tiation of AF by premature atrial complexes. The loss of this The structural modeling results in reduced impulse con-
physiologic adaptation to rate in hearts with AF makes them duction velocity and increased anisotropy and provides the
vulnerable to AF induction by premature beats and prevents substrate for reentry.
sustained restoration of sinus rhythm. Factors contributing
to the electrical remodeling in AF include reduced functional Cardiac Hypertrophy
expression of L-type Ca2+ channels, reduction in the transient
outward K+ currents, enhanced IK1, and persistent activation Cardiac hypertrophy occurs in many pathologic conditions,
of IKACh. including ischemic heart disease, hypertension, valvular
Table 7.4
Acquired Cardiac Channelopathies
Condition Change in Ion Currents Change in Electrophysiologic Mechanism of Arrhythmias
Properties
Atrial fibrillation ↓ ICaL ↓ AERP Overall net effect = ↓ wavelength

↓ Ito ↑ AERP of tachycardia and loss of rate
↑ IK1 ↓ AERP adaptation
↑ IKACh ↓ AERP
↓ Connexin 40 ↓ Conduction
Heart failure ↓ Ito ↑ VERP ↓ Rate adaptation
↓ IKr ↑ VERP ↑ APD
↓ IKs ↑ VERP ↑ EAD
↓ IK1 ↑ VERP ↑ Automaticity
↑ Na+/Ca 2+ exchange ↑ DAD
↑ ICaL inactivation ↓ APD
Connexin 43 redistribution ↓ Conduction ↑ Reentry
Cardiac hypertrophy ↑ ICaL ↑ APD ↑ EAD
↓ Na+/Ca 2+ exchange Ca 2+ overload ↑ DAD
Myocardial infarction ↓ Connexin 43 ↓ Conduction ↑ Reentry
↓ INa ↓ Conduction
↓ Ito ↑ VERP
↓ IKr ↑ VERP
↓ IKs ↑ VERP
↓ ICaL ↓ Plateau
Abbreviations: AERP, atrial effective refractory period; APD, action potential duration; DAD, delayed afterdepolarization; EAD, early
afterdepolarization; VERP, ventricular effective refractory period.
heart disease, and heart failure. Cardiac hypertrophy is an excitability with slowing of impulse conduction velocity,
independent predictor of morbidity and mortality and pre- which contributes to reentry arrhythmias. In addition, the
disposes the heart to the development of arrhythmia, isch- densities of ICaL , Ito, IKr, and IKs have all been found to be
emia, and congestive failure. Ventricular action potential reduced in the infarct border zone. The remodeling of ion
of the hypertrophied heart is prolonged. Unlike heart fail- channels alters action potential configuration and creates
ure, the increased action potential duration is caused by ICaL heterogeneity in repolarization, contributing to the devel-
upregulation, no change in Ito and IK1, and reduced Na+/Ca2+ opment of arrhythmias.
exchange activity with intracellular Ca 2+ overload.
In addition, prolongation of the action potential dura-
tion is more pronounced in the endocardial layers where Ito APPENDIX: PASSIVE MEMBRANE
is weak. The hypertrophied heart is susceptible to develop- PROPERTIES, CABLE THEORY, CURRENT
ing arrhythmia from triggered activity. EADs may result SOURCES, AND SINKS
from prolonged action potential durations, and DADs may
result from an increase in intracellular Ca2+ overload. Cardiac In addition to the active membrane properties that are
hypertrophy is also associated with interstitial fibrosis with defi ned by the activities of ion channels, electrogenic pumps,
myofibrillar disarray, leading to altered impulse conduction and action potential generation, the passive membrane
and dispersion of refractoriness. properties, determined by the dielectric nonconducting
lipid bilayer, also contribute to electrical impulse propa-
Myocardial Infarction gation. A resistor-capacitor electronic circuit can be used
to model cardiac membrane properties (Figure 7.13). The
Patients with previous myocardial infarctions are known to various conductances of ion channels can be represented
have an increased risk for the development of life-threatening by variable resistors, while the membrane lipid bilayer
VT and VF. The peri-infarct zone appears to be the major can be represented by a capacitor in parallel. As currents
site where extensive electrical remodeling takes place. In flow through the ion channels, the membrane capacitor is
the human infarct border zone, connexin 43 is displaced charged and discharged, resulting in changes in membrane
from its usual location in intercalated disks to random potential.
locations over the cell surface. Also, I Na density is reduced Electrical impulse propagation in cardiac muscle can be
with altered channel kinetics, including enhanced cur- modeled using the cable theory. The cable equations were
rent inactivation. These changes underlie reduced cardiac developed 150 years ago to characterize the changes in
Direction of impulse
Extracellular propagation
Extracellular
- - - - + + + +
+ + + + - - - -
gNa gK gCa gCl VM
Intracellular
+ + + + - - - -
ENa EK ECa ECl CM
- - - - + + + +
Extracellular
Figure 7.14 Cable properties of impulse propagation in cardiac
muscle fibers. Arrows show current flow between depolarized
Intracellular tissue (left side) and resting tissue (right side).
Figure 7.13 Equivalent circuit of cardiac membrane represented

by resistor-capacitor components. The membrane is represented by
The electrotonic currents on cells far away from the advanc-
the capacitor (CM). The major ion channels (Na+, K+, Ca 2+, and Cl–)
are represented by the equilibrium potential (E, driving force) and
ing wave front are subthreshold. However, for cells imme-
channel conductance (g). VM represents the membrane potential. diately adjacent to the activated myocytes, if the strength of
this stimulus exceeds the thresholds of Na+ or Ca 2+ channels,
action potentials are generated. The activated cell becomes the
source of excitatory currents, which in turn activate the cells
voltage and current in trans-Atlantic telegraphic cables. The immediately downstream, allowing regenerative propagation
idealized cable in its simplest form is a continuous uniform of action potentials.
1–dimensional structure of infinite length. The cable theory The currents generated by the action potential serve as
has some notable limitations. First, cardiac muscle is neither a a source of excitatory currents for downstream cells in the
uniform nor a continuous structure, and cardiac cells are not resting state (sink). As the electrical impulse travels through
passive conducting cables but can generate action potentials cardiac muscle fibers, there is a voltage gradient along the
when stimulated. In addition, the heart is not a 1-dimensional path of conduction, with current flowing from source to
tissue. Indeed, conduction properties in the myocardium are sink. Conduction velocity along the cable is determined by
anisotropic, with membrane resistance greater in the trans- the properties of both source and sink. These include the
verse direction, perpendicular to the longitudinal axis of the amplitude and the rate of the upstroke of action potential, ie,
muscle fibers. Furthermore, during conditions of ischemia, magnitude and rate of depolarizing currents (source prop-
there is an abrupt loss of cell-to-cell coupling as gap junctions erties), as well as membrane resistance and the difference
are closed or uncoupled, and the basic assumptions of the between resting and threshold potentials (sink properties).
cable theory become untenable. Despite these limitations, the Conduction failure may occur when these properties are
cable theory still provides a conceptual foundation for elec- altered, such as by Na + and Ca 2+ channel-blocking antiar-
trical impulse propagation in the heart. rhythmic drugs, membrane depolarization, cell-cell uncou-
The cable theory predicts that the voltage change along pling, and activation of K ATP channels during hypoxia and
the cable from a point source of stimulus diminishes expo- ischemia.
nentially with a space constant that is the distance from the For impulse propagation to occur, the magnitude of the
source at which the voltage has declined by 1/e. The space source current must exceed that required to activate the cur-
constant is directly proportional to the cable diameter. rent sink. The safety factor is a measure of the source current
Hence, electrotonic influence reaches a greater distance in in excess of the sink needs. The AV node has a low safety
a thick cable than a thin one. Impulse propagation is illus- factor, and impulse propagation frequently fails. Conduction
trated in Figure 7.14. Propagation of depolarization along of impulse may also fail if there is a mismatch between
cardiac muscle fibers depends on the spread of depolarizing source and sink that reduces the safety factor. Figure 7.15
electrotonic currents from the activated and depolarized area depicts situations described by the funnel theory in which
to reach ahead to the downstream areas that are in resting a current source has to activate a much greater mass of tis-
state. In mammalian Purkinje fibers, the space constant is sue (Figure 7.15A). The safety factor is reduced, and conduc-
around 2 mm, and that for working myocardium is only a tion velocity is slowed. In contrast, for conditions in which
fraction of this value, but the electrotonic spread of currents the source is large and the sink is small, conduction veloc-
is adequate to influence many cells ahead of the wave front. ity is fast, and the safety factor is enhanced (Figure 7.15B).
A A Linear interface
Source Sink Source Sink
B Convex interface
Source Sink
Sink Source
C Concave interface
Figure 7.15 Source-sink mismatch. A, Depiction of a condition

in which the current source has to activate a much greater mass
of tissue. B, Depiction of a condition in which the current source Source Sink
from a larger mass of tissue is activating a smaller mass of tissue.
This condition of structural heterogeneity occurs at the Purkinje
fiber–ventricular myocardium junction. Conduction velocity is
slower with a lower safety margin when conduction occurs in the Figure 7.16 Source-sink interface. Source-sink mismatch occurs
antegrade direction (A), whereas conduction velocity is faster with as the curvature of the impulse conduction wave front changes.
a greater safety factor in the retrograde direction (B). Compared with a linear interface (A), a convex interface (B) is
accompanied by slower conduction velocity and lower safety
margin, whereas conduction velocity is faster with a greater safety
Hence, impulse conduction may occur in 1 direction but not margin at a concave interface (C).
the other across structural boundaries. Such structural mis-
match occurs at the Purkinje-ventricular myocardium junc- hence frequently deviates from that predicted in an idealized
tion. Retrograde conduction is more favorable than antegrade cable.
conduction across this anatomic transition. Another clinical
example in which this type of principle may apply is the ret-
rograde conduction in AV accessory connections in patients ABBREVIATIONS
with concealed bypass tracts. Similarly, in a 2–dimensional
propagation model (Figure 7.16), for situations in which a ADP, adenosine diphosphate
small source has to activate a large sink, such as a convex and AF, atrial fibrillation
expanding propagation wave front (Figure 7.16B), the safety ATP, adenosine triphosphate
factor is reduced, and conduction velocity is slowed. When a AV, atrioventricular
large source is activating a small sink, such as a concave and DAD, delayed afterdepolarization
diminishing wave front, safety factor and conduction veloc- EAD, early afterdepolarization
ity are enhanced (Figure 7.16C). Relevant clinical examples ECG, electrocardiogram, electrocardiographic
include impulse propagation through anatomic isthmuses GIRK, G-protein gated K+
and the unidirectional exit block of impulses in pulmo- K ATP, ATP-sensitive K+
nary veins. Because the heart is a 3-dimensional structure Kir, inward rectifier K+
and the muscle fibers undergo 120° transmural rotation in VF, ventricular fibrillation
some areas, impulse propagation in the heart is complex and VT, ventricular tachycardia
8
Antiarrhythmic Drug Therapy: Understanding
Options for the Ablationist
Arshad Jahangir, MD
ANTIARRHYTHMIC DRUGS importance are Na+, Ca2+, and K+. The cellular mechanism
of cardiac excitability and refractoriness are discussed in
Antiarrhythmic agents play an important role in the man- more detail in Chapter 7. Important components of the car-
agement of cardiac arrhythmias as both primary and hybrid diac cell action potential (AP) include inward sodium cur-
therapy. The essential goals of antiarrhythmic therapy are ter- rent (INa), which is responsible for the rapid upstroke of AP;
mination of an ongoing arrhythmia, prevention of arrhyth- voltage-gated calcium current (ICaL), along with outward
mia recurrence, or both. Antiarrhythmic drugs help control delayed rectifier potassium currents (IKr, IKs), which maintain
arrhythmias but also may cause them. Therefore, selection of the plateau phase of AP and IKr; IKs and inward rectifier potas-
an effective yet safe medication may be challenging. sium channel (IK1), which are responsible for the repolariza-
The challenge arises from factors intrinsic to the patient, tion phase of the AP. The Singh Vaughan Williams system
the disease condition, or the drug itself. These factors include classifies antiarrhythmic drugs into 4 groups on the basis of
variability in the pathophysiologic substrate, arrhythmia their effects on AP configuration, conduction velocity, and
mechanisms, clinical presentation, prognostic implications, refractoriness (Figure 8.1 and Table 8.1).
drug disposition, and response. Patients with arrhythmia Several drugs that alter cardiac electrophysiology and
comprise a highly heterogeneous patient population, with exert antiarrhythmic effects, such as digoxin, adenosine,
variable comorbid conditions and concomitant drug use. atropine, or specific bradycardia agents, cannot be classified
Clinical trials such as the Cardiac Arrhythmia Suppression using the Singh Vaughan Williams classification system. The
Trial (CAST) and the Survival With Oral D-Sotalol (SWORD) actions of several other antiarrhythmic agents are much more
trial, demonstrated increased mortality in patients treated complex, exhibiting properties that can be classified in mul-
with class I and class III antiarrhythmic agents, respectively, tiple categories. For example, amiodarone displays effects of
compared with placebo. Such studies have increased aware- all 4 Singh Vaughan Williams classes, including blockade of
ness of the proarrhythmic potential of drugs and emphasize Na+ channels, β-adrenergic response, K+ channels, and Ca2+
the need for better understanding of mechanisms of arrhyth- channels. Moreover, not all drugs in the same class have iden-
mogenesis, drug actions, and the interactions of drugs with tical effects. Although sotalol, bretylium, amiodarone, and
the end target, other drugs, and disease conditions. The prac- azimilide are all class III agents, they target different ion chan-
tice of treating arrhythmias regardless of their prognostic nels to prolong the AP duration (APD). To overcome some of
importance or choosing an antiarrhythmic agent by trial and these limitations, other classification systems have been pro-
error is no longer acceptable. posed, such as “the Sicilian Gambit” by the Task Force of the
This chapter briefly discusses the principles of drug actions Working Group on Arrhythmias of the European Society of
and interactions that may help in the selection of drugs based Cardiology, in which antiarrhythmic drugs are considered in
on arrhythmia mechanism for use in an individual patient. the context of their targets of action and arrhythmia mecha-
nism, identifying 1 or more vulnerable parameters that can
DRUG CLASSIFICATION be altered with drugs.
The currently used antiarrhythmic drugs act by altering Points to Remember

refractoriness or conduction velocity of cardiac tissue mainly
by changing ion fluxes in the heart. The 3 ions of primary • Na+ channel blocking drugs act at phase 0 of the
ventricular AP, whereas class III agents act during
Abbreviations are expanded at the end of this chapter. repolarization.
191
Class I: Na+ channel blockers Class IA IK block

IA: Moderately depress phase 0 INa block
Slow conduction
Prolong repolarization
IB: Mildly depress phase 0 in normal tissue Class IB

Shorten repolarization
IC: Markedly depress phase 0 Class IC

Markedly slow conduction
Prolong repolarization slightly
Class II: β-Adrenergic receptor blockers

(indirect Ca2+ channel blockade) Class IV Ca2+ blockers
Class III: K+ channel blockers
Prolong repolarization Class III K+ blockers
Class IV: Ca2+ channel blockers

Class II β-blockers
Figure 8.1 Singh Vaughan Williams classification of antiarrhythmic drugs. Class I drugs reduce the upstroke velocity of phase 0 of action
potentials (APs) predominantly by block of inward sodium current (INa). Based on the effects on refractoriness and AP duration (APD)
(inhibition of K+ channels), class I drugs are further divided into 3 subgroups (Table 8.1). Class IA drugs reduce the upstroke velocity of
phase 0 of AP, slow conduction, and prolong APD and refractoriness by K+ channel inhibition (mainly block of outward delayed rectifier
potassium current). The kinetics of Na+ channel block onset and offset of these drugs is intermediate in speed, lasting 1 to 5 seconds. Class
IB drugs minimally reduce the upstroke velocity and slightly decrease refractoriness by shortening APD. The kinetics of Na+ channel block
onset and offset are fast, lasting for less than 1 second. Class IC drugs reduce the upstroke velocity and slow conduction to maximum but
prolong refractoriness minimally. The kinetics of Na+ channel block onset and offset are slow, lasting for up to 10 to 20 seconds. Class II
drugs block β -adrenergic receptors and counteract the effect of catecholamines. Class III drugs prolong repolarization predominantly by
blocking K+ channels. Class IV drugs predominantly block voltage-gated Ca 2+ current.
• Block of Na+ channels by class I agents decreases avail- channel transitions to resting, open, and inactivated states
able Na+ channels for cellular activation resulting in in response to changes in membrane potential (modulated
slowing of conduction that manifests as prolongation receptor hypothesis for antiarrhythmic action). For Na+
of the QRS width on the surface electrocardiogram channels, the affinity of drugs is higher for the open and
(ECG). inactivated states than it is for the resting state (Figure 8.2).
• Block of outward K+ current (class III agent) results in Channel state affinities of some of the Na+ channel blockers
prolongation of the APD and manifests as QT prolon- are summarized in Table 8.2.
gation on the surface ECG. The channel affinity for inactivated vs closed state has
important therapeutic implications. During pathologic states
SOME BASIC CONCEPTS OF (after infarction, during ischemia, or in hyperkalemia), the
ELECTROPHARMACOLOGY myocardial membrane is partially depolarized, and a frac-
tion of the Na+ channels exist in the inactivated state, so
Relationship of Antiarrhythmics and drugs like amiodarone or lidocaine that bind preferentially
Channel State to the inactivated state are more effective in slowing conduc-
tion than those that bind to the open state of the channel.
The affinity of a drug to its receptor site on an ion channel The same principle could be used to therapeutic advantage
changes with a change in the channel configuration as the by combining drugs that prolong APD (class IA or III) with
8. Antiarrhythmic Drug Therapy 193
Table 8.1 Table 8.2

Antiarrhythmic Drugs Channel State Affinities of Na + Channel Blockers
Class I (Na+ channel blockers reduce excitability and conduction Drug Preferential State for Activity
velocity)
Amiodarone Inactivated >> Open
IA
Lidocaine Inactivated >> Open
• Ajmaline
• Disopyramide Mexiletine Inactivated >> Open
• Procainamide Procainamide Inactivated > Open
• Quinidine Quinidine Open >> Inactivated
IB Disopyramide Open >> Inactivated
• Lidocaine Propafenone Open >> Inactivated
• Mexiletine Symbols: >, more affi nity; >>, much more specific affi nity.
• Phenytoin
IC
• Flecainide drugs that bind to the inactivated channel (class IB). Greater
• Propafenone channel inhibition can be achieved at a lower concentra-
Class II (β -adreneric receptor blockers reduce SAN automaticity tion of the drugs because channel blockade is increased with
and AVN conduction) higher affinity to the inactivated Na+ channels. This also
• Acebutolol explains the lack of efficacy of drugs like lidocaine and mexil-
• Atenolol etine for atrial arrhythmias because of the brief duration of
• Esmolol the atrial AP.
• Metoprolol
• Propranolol
Use Dependence
• Timolol
Class III (K+ channel blockers increase APD and refractoriness) The concept of use dependence is important and refers to the
• Amiodarone rate-related increase in the inhibitory effect of drugs on ion
• Bretylium channels (Figure 8.3). In general, drugs that bind preferen-
• Dofetilide tially to open or inactivated channels show greater effects at
• Ibutilide
faster heart rates. The block occurs during depolarization
• NAPA
and dissipates during repolarization (Figure 8.4). Based on
• Sotalol
the rate of block development or dissipation, drugs can be
Class IV (Ca 2+ channel blockers reduce SAN automaticity and grouped as having fast, intermediate, or slow dissociation
AVN conduction) kinetics (Figure 8.5). For drugs that have fast dissociation
• Diltiazem constants (such as lidocaine and mexiletine), the chan-
• Verapamil
nel block dissipates during diastole or before the next AP
Other occurs, so no slowing of conduction velocity or prolongation
• Digoxin (inhibits Na+/K+ ATPase, increases vagal tone) of QRS complexes is seen at normal heart rates, but during
• Adenosine, ATP tachycardia, substantial block may develop (Figure 8.6). For
• Atropine (muscarinic receptor antagonist antagonizes vagal effect) drugs with slower rates of dissociation from the Na+ chan-
Specific bradycardic agents (If channel blockers) nel (propafenone, flecainide), conduction slowing and QRS
• Ivabradine prolongation may be seen even during normal heart rates,
• Zatebradine which is further exaggerated at faster rates (eg, during exer-
Abbreviations: APD, action potential duration; ATP, adenosine triphosphate; AVN, cise) because of a progressive accumulation of channel block-
atrioventricular node; NAPA, N-acetyl procainamide; SAN, sinoatrial node. ade with a decrease in intervals between APs (Figure 8.6).
IB IC IA III
K+ channel block
Na+ channel block
Figure 8.2 Degree of Na + and K+ channel block by class IA, IB, IC, and III antiarrhythmic agents.
Points to Remember
• Drugs that show use-dependent block (class IC) are

monitored by increasing heart rate (treadmill exercise
50th pulse after the testing) to maximize drug-channel block and assess for
addition of lidocaine QRS widening when maximal channel block would be
occurring.
Use- Antiarrhythmic effect at • Agents that show reverse use dependency (class III)
dependent more rapid heart rate are most likely to have the greatest effect during rest or
block
with bradycardia. Therefore, QT-interval prolongation
is best observed at rest, and treadmill exercise testing is
* 1st pulse after the not indicated or useful.
addition of lidocaine
Tonic block DRUGS FOR ARRHYTHMIA SUPPRESSION

Control
Selection of drugs for termination or prevention of arrhyth-
Figure 8.3 Tonic and use-dependent block of inward sodium
mia requires understanding of the basic arrhythmia mech-
current. Tonic block (indicated by the asterisk) is present during
anism (see Chapter 7 and Table 8.4) and the properties of
a single or infrequent depolarization. Use-dependent block is the
additional block produced by more frequent depolarization. drugs that target vulnerable parameters of the arrhythmia.
Moreover, factors that alter cardiac electrophysiology and
precipitate arrhythmia, such as ischemia, electrolyte and pH
disturbances, or drugs, need to be controlled.
If substantial prolongation of the QRS interval (>20%) is
observed at rest with class IC Na+ channel blockers, the dose
needs to be reduced because marked conduction slowing DRUGS FOR ARRHYTHMIA DUE TO
may occur that can increase the risk of reentrant arrhythmia ENHANCED OR ABNORMAL AUTOMATICITY
which may become incessant.
Reverse use dependency refers to the rate-related decrease Enhanced or abnormal automaticity results from an increased
in the inhibitory effect of antiarrhythmic drugs on ion chan- rate of spontaneous depolarization in the automatic focus and
nels, with greater effects seen at slower rather than more can be altered by targeting 1 of the 4 determinants of auto-
rapid heart rates (Figure 8.7). This effect is particularly true maticity (Figure 8.8): maximum diastolic potential (MDP),
for most class III agents (dofetilide, sotalol, ibutilide), which phase 4 diastolic depolarization, threshold potential of AP
block the rapid component of the delayed rectifier potassium upstroke, or APD.
channel (IKr) and thus prolong repolarization and refracto- The MDP of the automatic focus in the sinoatrial node or
riness, manifesting as greater QT-interval prolongation at atrioventricular node can be increased by hyperpolarization
slower rather than more rapid heart rates. This limits the anti- of the cell membrane by activation of outward K+ current
arrhythmic efficacy of these drugs during tachycardia, while through the IKAch/IKAdo channel, achieved by administering
increasing the risk of proarrhythmia and torsades de pointes adenosine (Ado) or promoting acetylcholine (Ach) release
during bradycardia (Table 8.3). with vagal stimulation (carotid sinus massage or digoxin).
% Block
τd τr
τd τr τd
Figure 8.4 Development of drug block during the action potential and recovery from the block (blue line). Na + channel block develops
exponentially during depolarization and dissipates exponentially during repolarization. Class IB drugs have affi nity for the inactivated
(I) state, whereas class IC and IA for the open (O) state of the Na+ channel.
Recovery of the Na+ channel
Control
Lidocaine
τ
Phenytoin IB
Lidocaine IC
Tocainide
Mexiletine
IA
Aprindine
Procainamide
Propafenone
Chinicine
Flecainide
Ajmaline
Disopyramide
Prajmalium
0 0.5 12 5 10 15 20 50 150 250
Time Constant of the Recovery of the Na+ Channel

Figure 8.5 Kinetics of recovery from Na+ channel blockade. In general the kinetics of recovery are fast with class IB drugs, intermediate
speed with class IA drugs, and slow with class IC drugs.
The cardiac effects of adenosine and acetylcholine are medi- (Figure 8.8). β-Blockers and Ca2+ channel–blocking drugs,
ated by their interaction with specific G protein–coupled such as verapamil and diltiazem, can slow the rate of auto-
adenosine or muscarinic receptors. matic tachycardia by their inhibitory effects on activation of If
The slope of the spontaneous diastolic depolarization can and ICaL. Drugs with anticholinergic or vagolytic effects, such
be decreased by inhibiting the depolarizing currents (If, ICaT, as atropine, quinidine, or disopyramide, can increase the
or ICaL) or increasing the repolarizing current (IKAch/IKAdo) sinus discharge rate.
Normal Tachycardia Slowed recovery
Open (Activated)
Inactivated
Rest
100 100 100
% Na+
Channels
Blocked
0 0 0
Figure 8.6 Use-dependent Na + channel blockade. The Na + channel block with class IA, IB, and IC antiarrhythmics develops exponentially
during depolarization and dissipates during repolarization. If the heart rate increases, even for the normal binding of the drug, the
depolarization occurs earlier, before the channel fully recovers, and thus, block accumulates, manifesting as slowed conduction and an
increase in the QRS interval at faster rate. If the drug binds longer, as with class IC agents, recovery is prolonged, and the block is apparent
(QRS prolongation), even at slower rates, and further increases as the heart rate increases. Arrows indicate the points of inflection in the
slope of recovery, as explained in the text.
100 Table 8.4

NAPA, 20 µM Mechanisms of Arrhythmogenesis
APD Prolongation, ms
Quinidine, 1 µM
75 Sotalol, 10 µM Arrhythmias Due to Abnormal Impulse Initiation
Automaticity Normal
Abnormal
50 Triggered activity Early afterdepolarization
Delayed afterdepolarization
25 Arrhythmias Due to Abnormal Impulse Conduction
Reentry Anatomic
0 Functional
200 500 1,000 2,000 Anisotropic
Phase 2
Cycle Length, ms
Figure 8.7 Reverse rate-dependent effect of K+ channel blockers
on action potential duration (APD). The magnitude of APD result in triggered beats can be suppressed by Mg2+ through
prolongation caused by N-acetyl procainamide (NAPA), quinidine, mechanisms that are not fully understood. Electrolyte distur-
and sotalol decreases as the heart rate increases (cycle length bances such as hypokalemia and hypomagnesemia that pro-
shortening). (Adapted from Hondeghem LM, Snyders DJ. Class III
long APD should be corrected. In patients with familial long
antiarrhythmic agents have a lot of potential but a long way to
QT syndrome, torsades de pointes often occurs with adrener-
go: reduced effectiveness and dangers of reverse use dependence.
Circulation. 1990 Feb;81[2]:686–90. Used with permission.) gic stress; thus, β-adrenergic blockade can be used.
DAD-mediated arrhythmias occur in patients with intra-
cellular Ca 2+ overload, such as following ischemia-reperfusion
DRUGS FOR ARRHYTHMIA DUE TO or with adrenergic stress, digitalis intoxication, or dysfunc-
TRIGGERED ACTIVITY tional sarcoplasmic reticulum Ca2+ release channel (ryano-
dine receptor RYR2). Arrhythmias due to DAD-mediated
Arrhythmias caused by triggered activity develop under triggered activity can be suppressed by prevention of intra-
pathologic conditions when abnormal cellular depolarization cellular Ca 2+ overload and suppression of DADs by β-blockers
occurs either during (early afterdepolarization [EAD]) or or Ca2+ channel blockers (Figure 8.10). Newer drugs that
immediately following (delayed afterdepolarization [DAD]) increase the binding affinity of calstabin-2, a regulatory pro-
repolarization to generate AP that can propagate. tein that stabilizes RYR2 and thus inhibits the diastolic strain
EAD-mediated triggered activity is mainly observed in rate Ca2+ leak and DADs, are being developed to suppress
conditions associated with marked prolongation of APD, such triggered activity–mediated arrhythmias in patients with
as with the use of drugs that prolong APD (Table 8.5) or in catecholaminergic polymorphic ventricular tachycardia and
patients with excessively slow heart rate, low extracellular K+, heart failure.
or familial long QT syndrome (mutations in K+, Na+, or Ca2+
channels). Therefore, drugs that shorten APD may prevent
arrhythmias in these patients (Figure 8.9). Shortening the DRUGS FOR ARRHYTHMIA DUE TO REENTRY
APD can be accomplished by increasing the heart rate with
Reentry is the mechanism for most of the commonly observed
use of isoproterenol or pacing in those with bradycardia or
arrhythmias. Reentry arises as a result of altered conduction
by opening K+ channels with K+ channel openers. EADs that
when impulses propagate by more than 1 pathway, each dif-
fering in their electrophysiologic properties that result in uni-
Table 8.3
directional conduction block in 1 pathway with conduction
Differences Between Use Dependence and Reverse Use in the other, with retrograde reexcitation of the first pathway
Dependence as the pathway recovers from refractoriness. An important
concept to remember for reentrant arrhythmias is that the
Use Dependence Reverse Use Dependence
wavelength of the reentry (λ) impulse is defined by the prod-
Increased channel block at Increased channel block at uct of refractoriness (R) and conduction velocity (V) (λ=R·V).
faster heart rate slower rate Conditions that shorten the wavelength by a decrease in the
INa blockers IKr blockers conduction velocity and/or refractoriness promote reentry.
Increased conduction leading to Repolarization prolongation Thus, a drug may terminate an ongoing reentrant tachycar-
slowing at faster rate at slower rate; loses effect at dia or prevent its initiation by prolonging the wavelength of
faster rate the circuit by increasing refractoriness, slowing conduction
Increased risk of proarrhythmia Increased risk of proarrhythmia velocity, or promoting conduction block (Figure 8.11). In
at faster rate at slower rate arrhythmias due to reentry with a short excitable gap, such as
Abbreviations: I Na, inward sodium current; IKr, inward rectifier potassium current. atrial fibrillation, class III antiarrhythmic agents effectively
Mechanisms Vulnerable Parameter Ion Channel Targets

and Drugs
Enhanced Phase 4 depolarization
Normal (decrease)
Automaticity
IK
ST If SBA, β-blockers
Current, mV
Inappropriate ST ICaT Mibefradil
Idiopathic VT ICaL
ICaT ICaL Ca2+ channel blockers,
If Ib β-blockers
IKAch Ado, digoxin
0 200 400 600 800

Time, ms
MDP APD
Phase 4
Threshold
Figure 8.8 Cellular mechanisms and pharmacology of arrhythmias due to enhanced automaticity (see text). Ado indicates adenosine;
APD, action potential duration; Ib, baseline current; ICaL , voltage-gated calcium current; ICaT, calcium current referred to as T-type calcium
current; If, pacemaker current in Purkinje fibers; IK, K+ current; IKAch, acetylcholine-activated K+ current; MDP, maximum diastolic
potential; NAPA, N-acetyl procainamide; SBA, specific bradycardic agents; ST, sinus tachycardia; VT, ventricular tachycardia.
Table 8.5
QT-Prolonging Drugs That Increase the Risk of Torsades de Pointes
Categories of Drugs Specific Drugs
Antiarrhythmic
• IA Ajmaline, disopyramide, procainamide, quinidine
• III Amiodarone, azimilide, dofetilide, ibutilide, NAPA, sotalol
Antimicrobial
• Antibiotic Clarithromycin, erythromycin, sparfloxacin, trimethoprim-sulfamethoxazole
• Antifungal Itraconazole, ketoconazole
• Antimalarial Chloroquine
• Antiparasitic Pentamidine
Antiviral Amantadine
Antihistamine Terfenadine, astemizole
Antidepressant Tricyclics, tetracyclics
Anaglesic/sedative Droperidol, methadone
Psychotropic Droperidol, haloperidol, mesoridazine, pimozide, thioridazine, phenothiazines
Miscellaneous Cisapride, chloral hydrate overdose, ketanserin, probucol, vasopressin, organophosphate
poisoning
Abbreviation: NAPA, N-acetyl procainamide.
Mechanisms Vulnerable Parameter Antiarrhythmic Drugs
Triggered activity APD (shorten) β-agonist

Vagolytics, pacing (increase rate)
EAD or K+ channel openers
Torsades de pointes
EAD (suppress)
Mg, K
0
β-blockers
Current, mV
Ca2+ channel blockers
-80
200 ms
Figure 8.9 Cellular mechanisms and pharmacology of arrhythmias due to early afterdepolarization (EAD)–mediated triggered activity
(see text). APD indicates action potential duration.
prolong refractoriness so that the reentrant pathway may not drugs that block Na+ channels (class I) slow the velocity of the
recover excitability in time to be depolarized by the reenter- propagating wave front (ie, conduction velocity is decreased)
ing impulse, thus terminating reentry (Figures 8.11 and 8.12). or block conduction, whereas drugs that block outward K+
A drug that depresses conduction can transform the unidi- channels (most commonly IKr) increase tissue refractoriness
rectional block to a bidirectional block and thus can also ter- and thereby decrease the excitable gap. In reentrant arrhyth-
minate or prevent reentry (Figures 8.11 and 8.12). In general, mias with long excitable gaps, conduction slowing or block
Triggered activity Ca2+ overload β-blockers

(unload) Ca2+ channel blockers
DAD
or NCX inhibitors
Digitalis induced
DAD (suppress) Adenosine

Vagal
Catecholamine-sensitive VT 0
CPVT β-blockers
Current, mV
ARVC-2 Ca2+ channel blockers

DCM Calstabin-RYR2 stabilizers
-80
RVOT VT 200 ms
Figure 8.10 Cellular mechanisms and pharmacology of arrhythmias due to delayed afterdepolarization (DAD)–mediated triggered
activity (see text). ARVC-2 indicates arrhythmogenic right ventricular cardiomyopathy type 2; CPVT, catecholaminergic polymorphic
ventricular tachycardia; DCM, dilated cardiomyopathy; NCX, Na + -Ca 2+ exchange; RVOT VT, right ventricular outflow tract ventricular
tachycardia.
Short EG Long EG
EG
(λ = R • V)
↑ Refractoriness Conduction Block

Figure 8.11 Determinants of reentrant circuit. Left panel, Wavelength of a reentrant circuit (λ) is defi ned by the product of refractoriness
(R) and conduction velocity (V). Middle panel, In arrhythmias due to a short excitable gap (EG), increase in refractoriness can terminate
reentry by reducing the EG and decreasing the available myocardium for reexcitation by the advancing wave front. Right panel,
In arrhythmias due to a long EG, conduction slowing or block promotes abolition of the propagating wave front.
with Na+ channel blockers (class I drugs) can terminate or MONITORING OF ANTIARRHYTHMIC DRUGS
prevent arrhythmias (Figure 8.13). In reentrant arrhythmias,
which contain Ca2+ channel–dependent tissue as part of the Class I
circuit, such as atrioventricular node reentrant tachycardia or
atrioventricular reentrant tachycardia, Ca2+ channel blockers Since Na+ channel blocking agents slow conduction velocity,
may be effective in terminating or preventing recurrence of the drug tissue effect is best monitored with reference to the PR
arrhythmias (Figure 8.14). and QRS interval and duration. Class I drugs, especially class
Reentry Refractory period (prolong) K+ channel blockers

Short excitable gap Sotalol
Atrial fibrillation Dofetilide
Atypical atrial flutter Amiodarone
Polymorphic VT Class IA
Monomorphic VT
Ventricular fibrillation Na+ channel blockers
Class IC
Conduction (block)
Figure 8.12 Cellular mechanisms and pharmacology of reentrant arrhythmias due to a short excitable gap (see text). Left panel, The
mechanism for arrhythmia. Middle panel, The vulnerable parameter relevant to the arrhythmogenic mechanism. Right panel, Known
antagonists with antiarrhythmic activity related to a vulnerable parameter and described mechanism. VT indicates ventricular tachycardia.
Reentry Conduction and excitability Atrium

Long excitable gap (depress) Na+ channel blockers (except
(Na+ channel dependent) lidocaine, mexiletine)
Atrial flutter
AVRT Ventricle
ORT Na+ channel blockers
ART
VT
Figure 8.13 Cellular mechanisms and pharmacology of reentrant arrhythmias due to long excitable gap (see text). Examples of
a specific arrhythmogenic mechanism with the associated vulnerable parameter that may be manipulated for clinical benefit with
a mechanism-specific antiarrhythmic drug are explained. The panels are the same as described for Figure 8.12. The yellow dashed line
indicates the direction of propagation of the reentrant circuit. ART indicates antidromic reciprocating tachycardia; AVRT, atrioventricular
tachycardia; ORT, orthodromic reciprocating tachycardia; VT, ventricular tachycardia.
Reentry Conduction and excitability Ca2+ channel blockers

Long excitable gap (depress) β-blockers
(Ca2+ channel dependent)
AVNRT Adenosine
AVRT
ORT
Na+ channel blockers
ART
ILVT
Figure 8.14 Cellular mechanisms and pharmacology of reentrant arrhythmias due to a long excitable gap involving Ca 2+ channel–
dependent tissue (see text), as described in the legend for Figure 8.13. ART indicates antidromic reciprocating tachycardia; AVNRT,
atrioventricular node reentry tachycardia; AVRT, atrioventricular tachycardia; ILVT, idiopathic left ventricular tachycardia; ORT,
orthodromic reciprocating tachycardia.
SAN/AVN
IA, IC IA, III
INa IK
ICa
Phase 0 Phase 3
II, IV
Cholinergic
Refractory period adenosine
IKAch/Ado
I IA, III
II, IV
PR QT
QRS
Figure 8.15 Effect of antiarrhythmic agents on action potential (top panels) and electrocardiogram (bottom panel). Class I agents
(Na+ channel blockers) reduce upstroke of atrial and ventricular action potential and slow conduction velocity, thus manifesting as
QRS prolongation. Class II and class IV agents (β-blockers and Ca 2+ channel blockers, respectively) affect sinoatrial node (SAN) and
atrioventricular node (AVN) automaticity and phase 4 depolarization, resulting in slowing of sinus rate and AVN conduction, manifesting
as sinus bradycardia and PR prolongation. Class III agents (K+ channel blockers) prolong repolarization and refractoriness, manifesting
as QT-interval prolongation. ICa indicates inward calcium current; IK, inward potassium current; IKAch/Ado, adenosine-sensitive potassium
channel; INa, inward sodium current.
IC agents (flecainide and propafenone), exhibit use depen- agents, the efficacy with which class III drugs block K+ chan-
dence in that the degree of Na+ channel blocking increases nels increases with slower heart rates (reverse use depen-
as the heart rate increases. Thus, increasing heart rate using a dence), increasing the likelihood of torsades de pointes at
predismissal treadmill exercise test is a useful screening tool slower heart rates.
for proarrhythmic effect. In general, widening of the QRS
should not exceed 150% of pretreatment interval.
ABBREVIATIONS
Class III
AP, action potential
Increased cardiac repolarization manifests as QT prolonga- APD, action potential duration
tion on the surface ECG (Figure 8.15). In most cases, the cor- DAD, delayed afterdepolarization
rected QT interval should not exceed 520 ms during therapy EAD, early afterdepolarization
with class III agents. The incidence of torsades de pointes ECG, electrocardiogram
with use of class III agents is about 1% to 3%. Unlike class I MDP, maximum diastolic potential
9
Catheter Ablation and Device Therapy
in Congenital Heart Disease
Chenni S. Sriram , MBBS , Malini Madhavan , MBBS ,
Peter A. Brady, MB, ChB, MD, Bryan C. Cannon , MD,
Christopher J. McLeod , MB, ChB, PhD, and Samuel J. Asirvatham , MD
INTRODUCTION Prior to any invasive procedure, a basic understanding of

the expected arrhythmia, surgical substrate, and anatomic
As a result of the sustained and incremental success in man- variance in individual patients is essential. Noninvasive car-
aging patients with congenital heart disease (CHD), an esti- diac imaging, including preprocedural magnetic resonance
mated 85% of CHD patients reach adulthood. Arrhythmias imaging (MRI) or computed tomography (CT), in conjunc-
in adult CHD patients represent the leading cause of morbid- tion with use of fluoroscopic and intracardiac ultrasound
ity and hospitalization, resulting in a major increase in abla- visualization, helps delineate the complex anatomy and
tion and device-related procedures in these patients. These allows correlation between the electrogram and prevalent
procedures are often complex, not only because of underly- pathology.
ing congenital anatomic variations but also because of the
effects of prior surgical repair that can modify the arrhyth-
mic substrate leading to an increased likelihood of multiple COMMON ARRHYTHMIAS AND SUBSTRATES
types of arrhythmias, even in the same patient. To optimize IN CHD
both success and safety with these procedures, the electro-
physiologist must be thoroughly familiar with the underlying The arrhythmogenic substrate in CHD can be grouped
cardiac anatomy, prior cardiac surgical history, and known as either a congenital substrate (eg, accessory pathway in
variants of both the pathology and surgical techniques. The Ebstein anomaly) or an acquired substrate such as chamber
purpose of this chapter is to outline the salient concepts and enlargement, fibrosis, myocardial dysfunction, conduction
principles pertinent to arrhythmia and device management tissue injury, and surgically created patches, suture lines, and
in patients with CHD. Subsequent case studies in this text- scars. Table 9.1 identifies common congenital lesions with
book further illustrate applications of the principles covered their associated arrhythmias and conduction system disor-
in this chapter. ders encountered in patients with CHD.
The primary considerations in the approach to invasive
electrophysiologic procedures in patients with CHD are Atrial Tachycardias
numerous:
Patients with atrial scars, surgical or otherwise, have a high
• Is cardiac access adequate? Is there a path for catheters incidence of atrial arrhythmias. These are most often mac-
to reach the arrhythmia site? roreentrant tachycardias involving scars and anatomic obsta-
• Where is the coronary sinus (CS), and can it be cles and are termed intra-atrial reentrant tachycardia (IART).
accessed? IARTs are particularly common after Mustard or Senning
• Where is the conduction system likely to be located in procedures and Fontan operations. Coexistent sinus node
this anomaly? dysfunction and older age at operation are additional risk fac-
• Where are the surgical scars likely to be? tors. Less commonly, CHD patients may develop atrial fibril-
• In the standard fluoroscopic views, where is each lation related to marked left atrial dilation and focal atrial
chamber? tachycardia (FAT).
Prevention of recurrence of IART with antiarrhythmic
drugs has been disappointing, and interventional procedures
Abbreviations are expanded at the end of this chapter. are the mainstay of treatment. Patients with normal chamber
203
Table 9.1
Arrhythmias and Conduction System Disorders in Patients With Congenital Heart Disease
Lesion Common Arrhythmias Less Common Arrhythmias Conduction System Disorders
Atrial septal defect (after repair) Intra-atrial reentrant Focal atrial tachycardia, atrial
tachycardia, atrial flutter fibrillation
Ventricular septal defect Intra-atrial reentrant Acquired AV block
tachycardia, ventricular
tachycardia
AV septal defect (after repair) Intra-atrial reentrant AV reentrant tachycardia, AV Spontaneous and acquired AV
tachycardia, atrial flutter nodal reentrant tachycardia block
Tetralogy of Fallot (after repair) Ventricular tachycardia Intra-atrial reentrant
tachycardia, atrial flutter
Ebstein anomaly (before and after AV reentrant tachycardia, AV Intra-atrial reentrant Accessory pathway
repair) nodal reentrant tachycardia tachycardia, atrial flutter,
ventricular tachycardia
D-TGA (after Mustard or Senning Intra-atrial reentrant AV nodal reentrant tachycardia, Sinus node dysfunction
repair) tachycardia, atrial flutter focal atrial tachycardia
L-TGA (before and after repair) AV reentrant tachycardia Ventricular tachycardia Spontaneous and acquired AV
block, accessory pathway
Single-ventricle physiology patients Intra-atrial reentrant Focal atrial tachycardia, atrial Sinus node dysfunction
after Fontan operation tachycardia, atrial flutter fibrillation (particularly with
atriopulmonary type of Fontan
operation)
Heterotaxy AV reentrant tachycardia Twin AV node, accessory
pathway
Abbreviations: AV, atrioventricular; D-TGA, dextrotransposition of the great arteries; L-TGA, levotransposition of the great arteries.
Data from Kanter RJ. Pearls for ablation in congenital heart disease. J Cardiovasc Electrophysiol. 2010 Feb;21(2):223–30 and Walsh EP. Interventional electrophysiology in
patients with congenital heart disease. Circulation. 2007 Jun 26;115(25):3224–34.
orientation, such as those with tetralogy of Fallot (TOF) and Sinus Node Dysfunction
atrial septal defect, tend to have circuits limited to the right
atrium (RA), often involving the cavotricuspid isthmus (CTI) Sinus node dysfunction may follow injury to the node due to
and a lateral atriotomy scar. Circuits are more complex in surgical incisions and suturing in the high RA as in Mustard,
patients with abnormal atrial situs or atresia of the atrioven- Senning, Glenn, and atriopulmonary Fontan operations. It
tricular (AV) valve and the corresponding ventricle. Acute can also be congenital in patients with heterotaxy with left
success rates for IART ablation have substantially improved atrial isomerism and left-juxtaposed atrial appendage.
from 60% a decade ago to 90% in the current era. However,
IART recurs in 20% of 4-chambered hearts and 40% of AV Block
patients at 3 years after a Fontan operation. Even when not
fully successful, catheter ablation can provide effective pallia- In patients with levotransposition of the great arteries (L-TGA)
tion by decreasing IART frequency and eliminating the need and AV septal defect (AVSD), the AV node is developmen-
for drug therapy. tally displaced outside the Koch triangle and often exhibits
impaired conduction, predisposing to both spontaneous AV
Ventricular Tachycardia and Sudden block and iatrogenic injury. AV block may complicate proce-
Cardiac Death dures such as left ventricular (LV) outflow tract surgery, atrial
reduction surgery, ventricular septal defect (VSD) closure,
Patients who have a ventricular scar, particularly those with and AV valve replacement because of iatrogenic injury to an
TOF who underwent ventriculotomy and placement of a ven- anatomically normal conduction system.
tricular patch, are at high risk for ventricular tachycardia
(VT). VT may also occur in patients with global ventricular AV Accessory Pathways
dysfunction and adverse remodeling following long-standing
hemodynamic stress. Our current approach to the treatment AV accessory pathways occur commonly in patients with
of VT and the prevention of sudden death involves implant- Ebstein anomaly (frequently multiple accessory pathways) or
able cardioverter-defibrillator (ICD) placement and catheter L-TGA. Catheter ablation, when feasible, is the treatment of
ablation. choice.
9. Catheter Ablation and Device Therapy in Congenital Heart Disease 205
ANATOMY OF THE CONDUCTION bundle and its branches are usually deviated toward the left
SYSTEM IN CHD side of the conal septal malalignment VSD.
Sinus Node
Atrioventricular Septal Defect
The morphologically normal arrangement of atrial chambers
is referred to as atrial situs solitus. In atrial situs solitus, the The AV node is displaced outside the Koch triangle. It is pos-
crescentic sinus node is located epicardially along the lateral terior and inferior to its usual location and is in proximity to
aspect of the superior cavoatrial junction. Most patients with the junction of the posterior rims of the atrial and ventricular
CHD have atrial situs solitus and normally positioned sinus septa. In the right anterior oblique projection, the AV node
node, but the position of the sinus node may vary with abnor- is located anterior to the CS ostium (ie, below the base of the
mally positioned atrial chambers and appendages. hypothetical Koch triangle). Thus, the CS ostium forms the
In atrial situs inversus, the atria are positioned in a upper border of a new nodal triangle containing the displaced
mirror-image fashion, with the RA and sinus node on the AV node. The remaining borders are formed by the posterior
left side. attachment of the posterior bridging leaflet and the posterior
insertion of the bridging tendon (ie, the leading edge of the
atrial septum) to the posterior fibrous area.
Juxtaposition of the Atrial Appendages
The His bundle penetrates the apex of this nodal triangle
In normal hearts, each atrial appendage is ipsilateral to its and runs along the lower rim of the ventricular septum. This
respective atrium. In juxtaposition, both atrial appendages results in a posteriorly displaced conduction network. The left
are on the same side of the arterial pedicle. In left juxtaposi- anterior hemifascicle is relatively hypoplastic. In a heart with
tion with left-sided atrial appendages, the sinus node is anteri- AVSD, unlike the normal heart, the posteriorly displaced con-
orly and inferiorly displaced (below the crista terminalis). Left duction tissue and the anterocephalad deviated aortic outflow
juxtaposition is often associated with tricuspid atresia and tract are unrelated to each other. The His electrograms are
abnormal ventriculoarterial connections (eg, discordant or best recorded by directing the catheter tip to a low position
double-outlet right ventricle [RV]). Right juxtaposition is less on the septum and rotating the catheter medially and slightly
common and is not associated with a displaced sinus node. left ward.
Heterotaxy Syndromes Ebstein’s Anomaly
In heterotaxy, the abdominal and thoracic visceral situs are The AV node is normally located in the Ebstein’s anomaly.
indeterminate or ambiguous and therefore cannot be later- However, compared with normal hearts, the Koch triangle is
alized into situs solitus or situs inversus. Right heterotaxy usually smaller and the AV node is positioned closer to the
(asplenia syndrome) is characterized by RA isomerism and CS ostium. An ablation procedure performed near the base of
bilateral right-sidedness of thoracoabdominal viscera. There the Koch triangle may result in AV block, because of its close
are often 2 distinct sinus nodes, one each at the right and left proximity to the AV node.
sides of the superior cavoatrial junction. In left heterotaxy AV node localization is also challenging because of dis-
(polysplenia syndrome) with left atrial isomerism, sinus nodes placement of the septal and posterior tricuspid valve leaflets
may be hypoplastic and displaced posteroinferiorly from the as well as RA enlargement. A right coronary angiogram or
superior vena cava (SVC) orifice or completely absent. fine-diameter catheter in this vessel can be used to defi ne the
true AV groove that marks the edge of the tricuspid annulus.
AV Node and His-Purkinje System
Dextrotransposition of the Great Arteries
The AV conduction system can be displaced when there are
discordant AV chamber connections, malalignment between In native dextrotransposition of the great arteries (D-TGA),
atrial and ventricular septa, or a univentricular heart. The the conduction tissue is normally positioned. Electro-
following section discusses the common anatomic variants physiologic study can be challenging, however, in patients who
in different CHDs. It must be noted, however, that marked have undergone a previous atrial switch (Mustard or Senning)
individual variation can be noted in these patients. procedure because of distortion of the atrial anatomy. It is
possible to record discrete His potentials from the proxi-
Perimembranous VSD and TOF mal left bundle by passing the catheter through the systemic
venous atrial baffle and positioning it at the medial aspect of
The AV node and proximal His bundle are located normally the mitral valve along the LV septum. For a more precise His
when the VSD is distant from the AV septum. However, the recording, a retrograde aortic approach is usually necessary.
His bundle is more elongated and runs distally along the The catheter can be positioned near the central fibrous body
posterior-inferior rim of the VSD. Specifically in TOF, the His close to the tricuspid valve by entering the systemic subaortic
RV. In addition, a His signal may be obtained from the non- ventriculoarterial discordance. In L-TGA, a small or absent
coronary cusp of the aortic valve. pulmonary trunk is associated with good AV septal align-
ment while a larger pulmonary trunk usually results in septal
Tricuspid Atresia
malalignment.
In L-TGA with septal malalignment at the cardiac crux,
A small dimple lined with endocardium anterior to the CS functional anterosuperiorly positioned conduction tissue
ostium marks the site of the imperforate fibrous AV connec- is often noted (Figure 9.1A). This occurs because the septal
tion denoting the absent tricuspid valve. The AV node is usu- malalignment usually results in a gap that is filled by a large
ally located on the RA floor, close to the central fibrous body. membranous septum or may be open due to a VSD. This gap
Its hypothetical boundaries are formed by the RA dimple, may prevent the normally located AV node (at the apex of
CS, and tendon of Todaro. However, the main body of the the Koch triangle) from connecting with the distal conduc-
AV node is posterior to the insertion of the tendon of Todaro tion system (Figure 9.1A). There is another AV node antero-
and in direct contact with the right AV sulcus. The AV node superiorly and slightly laterally outside the Koch triangle,
then pierces the abnormally formed central fibrous body and between the right-sided mitral annulus and the ostium of the
courses as a very short His bundle along the left side of the RA appendage. An elongated His bundle extends from this
septum. It then divides early into the left bundle. displaced AV node and penetrates the AV junction laterally
The course of the His-Purkinje system is determined at the region of the mitral–pulmonary valve fibrous continu-
partly by presence and location of any associated VSD. In ity. It courses along the anterior rim of the subpulmonary
general, the His bundle is further left ward and away from the outflow tract and then across the anterosuperior wall of the
more anteriorly positioned VSDs. The elongated right bun- morphologic LV to the upper part of the ventricular septum
dle travels along the lower rim of the VSD on the LV side of (Figure 9.1A). Instead, if there is an associated perimembra-
the septum and subsequently crosses into the RV. Thus, His nous VSD, the conduction tissue passes along its anterosu-
electrograms can be recorded from the LV side of the septum perior rim. From there the conduction system descends and
through the retrograde arterial approach or by the transatrial branches into right and left bundles. The conduction system
septal approach through the atrial septal defect. is prone to spontaneous or procedure-induced AV block. The
His electrogram can usually be recorded at the anterior and
Single-Ventricle Physiology Other Than medial aspect of the right AV (mitral) valve.
Tricuspid Atresia L-TGA with pulmonary valve hypoplasia or atresia is
associated with good AV septal alignment. The AV nodal
Typically in single-ventricle patients, one ventricle is dominant, tissue lies in its usual posteroinferior location at the apex of
while the other ventricle is hypoplastic. The type of ventricu- the Koch triangle. In addition, there is also AV nodal tissue
lar looping, the morphologically dominant ventricle, and the positioned anterosuperiorly, as described above. The anterior
degree of AV septal alignment determine the conduction axis. and posterior AV nodes (twin AV nodes) may form a sling of
In patients with normal atrial situs, normal rightward (or D) conduction tissue termed a Mönckeberg sling.
ventricular looping, and a dominant RV (eg, hypoplastic left cc-TGA with situs inversus and a D-looped ventricle is
heart syndrome), the AV node lies within the Koch triangle. often associated with coexistent pulmonary valve atresia or
The His bundle then directly enters the ventricular septum. In hypoplasia. The connecting AV node is posteriorly situated at
left atrial isomerism with a common AV junction (AVSD) and the apex of a left-sided Koch triangle, in a mirror-image posi-
D-looped ventricle, the solitary AV node is located posteroinfe- tion compared to the regular AV node. An anterior AV node
riorly where the ventricular septum meets the AV junction. The may be present but usually does not connect to the His bundle.
conduction axis is often discontinuous, resulting in AV block. The His bundle follows a standard course along the ventricu-
A double-inlet LV is associated with malalignment of the lar septum. In the case of a coexistent VSD, the His bundle
AV septum. The functional AV node lies in an anterior and traverses along its lower rim. The His electrogram is recorded
right superolateral position and connects with an antero- at the anterior and medial aspect of the left AV (mitral) valve.
superior conduction pathway. The conduction axis runs
proximally to the right of the VSD, while the distal bundle Twin AV Nodes and Mönckeberg Sling
branches are oriented apically and left ward. The presence of
twin AV nodes and a displaced conduction system in hearts The original description of twin AV nodes with a Mönckeberg
with a single ventricle is discussed below. sling spanning the 2 penetrating bundles was in a heart with
a double-outlet RV and ventricular inversion. As summa-
Congenitally Corrected Transposition of the rized above, twin AV nodes in L-TGA are more likely to form
Great Arteries a sling of conduction tissue when there is good AV septal
alignment. However, AV septal malalignment is more com-
In the left ward or levo (or L) type of congenitally cor- mon in L-TGA, in which case one of the twin AV nodes is
rected transposition of the great arteries (cc-TGA or, in this usually disconnected.
case, L-TGA), there is normal atrial situs with L-looped Twin AV nodes are also reported in other conditions,
ventricles and transposed great arteries leading to AV and including certain types of single ventricles. In general, twin
Anterior AV node
Aorta
Pulm
Tr
Morphologically
right ventricle
Morphologically
left ventricle
Posterior AV node
Figure 9.1 Left panel, Atrioventricular (AV) node and His bundle anatomy in a congenitally corrected transposition of the great arteries.
Right panel, AV septal defect with twin AV nodes and Mönckeberg sling. The anterior and posterior AV nodes connect to form the
Mönckeberg sling. Pulm Tr indicates pulmonary trunk.
AV nodes are expected in heterotaxy (right or left isomer- a Fontan operation. Tables 9.2 and 9.3 and Figure 9.2 describe
ism), with L-looped ventricular topology (L-TGA if there is the anatomy of these palliative approaches, of interest to the
an associated transposition of the great arteries). An endo- electrophysiologist trying to establish access for various cath-
cardial cushion defect is usual in this setting, particularly in eters. The purpose of these surgical procedures is to connect
left isomerism. The endocardial cushion defect may be rep- pulmonary and systemic circulation in series in which the
resented by an ostium primum AVSD (2 separate AV valve single ventricle (morphologic RV or LV) functions as the sys-
orifices) or by a complete AVSD (single common AV valve temic pump, and systemic venous return drains passively into
orifice). The AVSD is typically unbalanced, with one domi- the pulmonary circulation.
nant and another hypoplastic ventricle resulting in a single-
ventricle physiology. The twin AV nodes may be connected
Common Arrhythmias and
by a Mönckeberg sling (Figure 9.1B) but can also show dis-
Arrhythmogenic Substrate
continuity in the His bundle. The His bundle is usually elon-
gated and is susceptible to fibrous degeneration and complete Patients who have undergone palliative treatment with
AV block. Two separate His electrograms may be recorded if the Fontan operation have a highly proarrhythmic milieu
there is a connecting sling of tissue. When there is discon- in the atria due to hypertrophy and dilation from chronic
tinuity, either the inferior AV node or both nodes may be pressure overload, fibrosis, suture lines, and natural con-
disconnected from the His bundle. duction barriers. IART is the most common arrhythmia in
these patients, occurring in 28% to 41% of patients within a
decade of surgery. Older age at surgical repair and surgical
INDIVIDUAL CHD LESIONS: PRACTICAL
technique (with an atriopulmonary Fontan procedure hav-
ISSUES FOR THE ELECTROPHYSIOLOGIST
ing a higher risk than the lateral tunnel Fontan approach)
Single-Ventricle Patients With are risk factors for IART. Complex and multiple circuits may
Fontan Palliation be present, and these circuits vary in each patient, depending
on the anatomic defect and surgical correction. The circuit
Anatomy of the Fontan Connection may include the CTI, lateral wall atrial scars, natural ana-
tomic obstacles such as the crista terminalis and eustachian
Patients with single-ventricle physiology are typically palli- ridge, atrial septal patches, and a region of atriopulmonary
ated through a staged surgical approach. This usually includes anastomosis. Tricuspid atresia patients with atriopulmonary
superior cavopulmonary anastomosis, followed later by Fontan palliation are challenging because of an indistinct or
Table 9.2
Types of Superior Cavopulmonary Anastomosis
General principles Establishes SVC drainage into pulmonary circulation; venous blood from IVC still mixes with oxygenated
blood from the pulmonary atrium in the single systemic ventricle
Classic Glenn Procedure is obsolete and of historical interest only; end-to-side anastomosis of distal end of RPA to SVC;
ligation of superior cavoatrial (SVC-RA) junction; SVC drains exclusively into the RPA resulting in
unidirectional flow into the right pulmonary circulation
Bidirectional Glenn End-to-side anastomosis of SVC to RPA; ligation of superior cavoatrial (SVC-RA) junction; surgical division
of proximal MPA; RPA and LPA remain in continuity through distal MPA; SVC drains into both RPA
and LPA, resulting in bidirectional flow into both lungs; with 2 similar-sized SVCs (right and left), each is
anastomosed to its respective ipsilateral PA (bilateral bidirectional Glenn)
Hemi-Fontan Continuity of the SVC and RA is maintained when SVC is connected to RPA; a dam of homograft tissue
sewn across the superior cavoatrial junction prohibits blood flow into the right atrium from the SVC;
surgical division of proximal MPA; SVC drains into both RPA and LPA, which remain in continuity
through distal MPA
Abbreviations: IVC, inferior vena cava; LPA, left pulmonary artery; MPA, main pulmonary artery; PA, pulmonary artery; RA, right atrium; RPA, right pulmonary artery;
SVC, superior vena cava.
absent CTI, massive systemic atrial dilation, and multiple In the modern total cavopulmonary Fontan anastomoses
circuits. (extracardiac, lateral tunnel, and intra-atrial conduits), the
Other atrial arrhythmias such as FAT, supraventricu- CTI and CS are surgically excluded from the systemic venous
lar tachycardia, and atrial fibrillation may also occur. Sinus pathway. They become part of the remaining portion of the
node dysfunction is present in about 10% of atriopulmonary RA (called the neopulmonary atrium), which usually freely
Fontan patients. Ventricular arrhythmia can occur in about communicates with the original pulmonary atrium through
13% of Fontan patients. an atrial septectomy opening or defect. In such patients, the
neopulmonary and pulmonary atrium cannot be accessed
Implications of Clinical Anatomy for from the systemic venous side unless there is a fenestration.
Electrophysiologist In the case of lateral tunnel and intra-atrial Fontan pathways,
the fenestration is created either at the time of Fontan surgery
The anatomy of different Fontan palliation procedures has or by transcatheter perforation. For transvenous access to an
important implications for the electrophysiologist implanting existing fenestration or to create a new one, the site can be
device leads or placing electrodes for ablation. In the modi- approached from either the IVC or SVC. Transcatheter per-
fied atriopulmonary Fontan connection, the RA, including foration is not attempted in an extracardiac Fontan conduit,
the CTI and CS, is part of the systemic venous pathway and because it is outside the heart.
is amenable to venous access via the inferior vena cava (IVC) The systemic venous return is diverted to the pulmonary
or SVC. The CTI cannot be accessed from within the systemic artery, which precludes direct transvenous access to the ven-
venous atrium when the tricuspid valve is surgically excluded tricle with some exceptions. In general, placement of endo-
with a patch. cardial leads should be avoided in patients who have cyanosis
Table 9.3
Types of Fontan Operation
General principle Venous and arterial circulation are in series without any mixing
Classic atriopulmonary Fontan Consists of a classic Glenn (SVC to RPA) shunt, RA to LPA anastomosis (IVC drains
into LPA), and closure of interatrial communication; no longer performed
Modified atriopulmonary Fontan Includes a bidirectional Glenn, atriopulmonary Fontan connection, and closure of
interatrial communication; IVC and SVC drain into the pulmonary circulation;
supplanted by modern “total cavopulmonary” Fontan procedures described below
Extracardiac total cavopulmonary Fontan Follows bidirectional Glenn operation; extracardiac conduit is connected to IVC
and RPA; inferior cavoatrial junction is ligated; IVC drains into the pulmonary
circulation through the conduit
Lateral tunnel total cavopulmonary Fontan Typically follows hemi-Fontan operation; homograft dam in the RA across the
superior cavoatrial junction is excised; an intra-atrial lateral tunnel (using
pericardial or prosthetic material) is sewn in place to baffle IVC flow into the
superior cavopulmonary junction
Abbreviations: IVC, inferior vena cava; LPA, left pulmonary artery; MPA, main pulmonary artery; RA, right atrium; RPA, right pulmonary artery; SVC, superior vena cava.
Figure 9.2 Surgical techniques used for palliation in univentricular physiology. Left, Atriopulmonary Fontan procedure. Middle,
Extracardiac total cavopulmonary Fontan procedure. Right, Lateral tunnel total cavopulmonary Fontan procedure.
and intracardiac shunts, and an epicardial approach should juxta-annular tissue may only be accessed from the aortic or
be undertaken in these patients. Thus, we do not recommend ventricular side.
endocardial lead placement for patients with total cavopul- In patients with lateral tunnel and extracardiac total
monary Fontan connections. cavopulmonary Fontan, the atrial tachycardia substrate may
Some case reports have described endocardial lead place- not be accessible percutaneously. In such cases, hybrid pro-
ment in patients who previously underwent a Fontan opera- cedures with surgical placement of atrial sheaths may be an
tion. This is very challenging, and such patients should option. Both retrograde aortic and transseptal approaches in
receive long-term anticoagulation because of the high risk select Fontan patients have been described to access the sur-
for thrombus formation on the lead. In total cavopulmo- gically excluded CTI (Table 9.4). Catheter ablation of atrial
nary Fontan connections with a preexistent or newly created arrhythmias in Fontan patients has a high acute success rate
transcatheter fenestration, the catheter or lead can be passed (>80%) but also a relatively high rate of late recurrence (20%).
via fenestration into neopulmonary atrium or pulmonary
atrium to reach the ventricle through the systemic AV valve. Complete Transposition of the Great Arteries
In a modified atriopulmonary Fontan connection, the CS can (D-TGA) After Intra-atrial Baffle (Mustard or
be accessed to pace the systemic ventricle. Alternatively, an Senning Operations)
entirely epicardial approach can be used for endocardial lead
placement. An atrial stab incision is performed through a Anatomy of the Lesion
sternotomy, and endocardial leads are advanced into the pul-
monary atrium for atrial pacing and from the atrium through In complete D-TGA, the AV relationship is preserved, the
the systemic AV valve for systemic ventricular pacing. ventricles are D-looped (normal looping with morphologic
RV to the right of morphologic LV), and there is ventriculoar-
Ablation of Atrial Tachycardias Following terial discordance (aorta arises from RV, while pulmonary
Atriopulmonary Fontan Operations artery arises from LV). Thus, the systemic and pulmonary
circulations are in parallel and cyanosis ensues. Atrial and
IART is the predominant tachycardia in atriopulmonary ventricular septal defects and LV (pulmonary) outflow tract
Fontan patients, although FAT and AV nodal reentry may obstruction may be associated.
occur. Electroanatomic mapping of the atriotomy site (low
anterolateral atrium), CTI, the caval orifices, crista termi- Surgical Correction
nalis, and the proximal anterior RA appendage (edge of the
roof of the atriopulmonary conduit) should be done. In atrio- Anatomic and physiologic correction with the arterial switch
pulmonary Fontan patients with an underlying double-inlet operation is the procedure of choice for D-TGA patients. In
LV, a surgical patch is sutured above the systemic venous the past, physiologic correction with an atrial switch opera-
(or right) atrium–associated AV valve annulus. This rim of tion using complex intra-atrial baffles (Mustard or Senning
Table 9.4
Catheter-Based Approach to Access the Surgically Excluded Cavotricuspid Isthmus
Original Lesion Type Type of Fontan Surgery Vascular Approach to Brief Description of Procedure
Surgically Excluded CTI
Double-inlet left ventricle with L-TGA Lateral tunnel Fontan Retrograde aortic Ao → RV → VSD → LV → CTI
Double-inlet left ventricle with Lateral tunnel Fontan Retrograde aortic Ao → LV → Left AV valve → LA
normally related great arteries → neo LA → CTI
Unbalanced complete AV septal defect Intra-atrial Fontan conduit Retrograde aortic Ao → RV → CTI
with double-outlet right ventricle
TA with D-TGA and VSD Atriopulmonary Fontan Transseptal RA → Transseptal puncture →
with patch exclusion of LA → LV → VSD → RV → RV
tricuspid valve side of CTI
Abbreviations: Ao, aorta; AV, atrioventricular; CTI, cavotricuspid isthmus; D-TGA, dextrotransposition of the great arteries; LA, left atrium; L-TGA, levotransposition of
the great arteries; LV, left ventricle; RA, right atrium; RV, right ventricle; TA, tricuspid atresia; VSD, ventricular septal defect.
procedures) was used (Table 9.5). The systemic venous blood refractoriness and intra-atrial conduction delays. Sinus node
is redirected through the left AV (mitral) valve into the LV dysfunction and IART occur in 60% and 24% of patients,
and pulmonary artery. Pulmonary venous blood is redirected respectively, at 20 years. Sinus node dysfunction necessitates
through the right AV (tricuspid) valve into the RV and aorta. permanent pacemaker implantation in more than 50% of
Thus, the RV is the systemic ventricle in patients who have adults. The most common IART circuit is CTI dependent.
had Mustard or Senning procedures. D-TGA patients with IART with slow conduction zones between a suture line and
previous Mustard or Senning repairs constitute an important the SVC orifice, mitral valve annulus, and pulmonary vein
subset of adult CHD arrhythmia patients. orifice is less common. FAT adjacent to suture lines is also
described. Sinus node dysfunction, perioperative bradyar-
Disposition of CTI With the Mustard Procedure rhythmias, and reoperation were noted to increase the risk
of IART in 1 study. Atrial tachycardias may also be related
The CTI and the area between the CS orifice and tricuspid to sudden death as supraventricular tachycardia preceded or
annulus are critical components in the intra-atrial reentry coexisted with VT in 50% of patients with an atrial baffle and
circuit. With the Mustard operation, the location of the baf- an appropriate ICD shock.
fle suture line within the CTI may vary. The CS and most of
the CTI are commonly delegated to the pulmonary venous Implications of Clinical Anatomy for the
atrium, although less commonly, they can be delegated to the Electrophysiologist
systemic venous atrium, depending on whether the inferior
baffle suture line is anterior or posterior in relation to the CS The systemic venous atrium can be accessed through the sys-
ostium. A suture line anterior to the CS ostium can also be temic veins for placement of atrial lead or catheters. When
destructive to the slow inputs to the AV node. placing an atrial lead, lead fi xation should be done in the few
areas of the atrial muscle away from patches, scars, and left
Common Arrhythmias and Arrhythmogenic phrenic nerve. Access to the subpulmonary LV is through the
Substrate Following Atrial Switch Operation systemic venous atrium and the left AV (mitral) valve.
Placement of endocardial leads in the setting of cyano-
The extensive atrial incisions and suture lines created during sis or any residual shunts or into the systemic ventricle
Mustard and Senning procedures result in abnormal atrial (RV) is not recommended because the risk of stroke despite
Table 9.5
Atrial Switch Operations for D-TGA
Atrial switch operation through Systemic venous atrium opening into LV and a pulmonary venous atrium opening
intra-atrial baffle procedures into the RV are created.
Senning operation An atrial septal flap is sewn to the posterior wall of LA, isolating the pulmonary
veins behind it. The walls of the RA are then wrapped around one another to
create a systemic venous atrium and a pulmonary venous atrium.
Mustard operation Complete atrial septectomy is performed. An intra-atrial prosthetic or pericardial
baffle acts as a divider to redirect systemic blood flow into LV and pulmonary
blood flow into RV.
Abbreviations: D-TGA, dextrotransposition of the great arteries; LV, left ventricle; RA, right atrium; RV, right ventricle.
Data from Gaca AM, Jaggers JJ, Dudley LT, Bisset GS 3rd. Repair of congenital heart disease: a primer-part 1. Radiology. 2008 Jun;247(3):617–31.
Epub 2008 Mar 28.
anticoagulation is prohibitive. Pacing the systemic RV for is irrespective of the presence of atrial or ventricular lead or
cardiac resynchronization therapy (CRT) can be done epi- documented right-to-left shunting, and aspirin and warfarin
cardially. Transvenous epicardial RV lead placement may be may not be protective. Thus, it is preferable to avoid endocar-
possible through a patent CS in the systemic venous atrium, dial lead placement even in the case of smaller residual leaks
which drains smaller veins from the RV. This approach is after attempted baffle closure. Smaller leaks mandate lifelong
an option only when such veins are big enough to accom- anticoagulation if endovascular leads are placed.
modate the lead. Contrast-enhanced MRI may be use-
ful to delineate the CS venous drainage. In patients with a Congenitally Corrected Transposition
malformed or underdeveloped CS, a hybrid approach may of the Great Arteries
be used. The atrial and subpulmonary LV leads are placed
transvenously, while an epicardial RV lead is implanted via a Anatomy of the Lesion
minithoracotomy.
In general, the peculiar anatomy and surgically placed In the most common type of cc-TGA (levo or L-TGA), there is
obstacles in D-TGA patients who have had Mustard or atrial situs solitus (normal arrangement of atria), AV discor-
Senning procedures may limit access to ablation targets. For a dance due to L–looped ventricles (ventricular inversion) with
stable atrial reference site for 3-dimensional mapping, a cath- left-sided morphologic RV and right-sided morphologic LV,
eter is placed in the CS when it is in the systemic venous side and ventriculoarterial discordance. The circulation is physi-
or in a retrocardiac esophageal location when the CS is in the ologically corrected but anatomically uncorrected (morpho-
pulmonary venous side or alternatively by an active fi xation logic RV is the systemic ventricle). Because of ventricular
temporary pacing lead. His bundle electrogram recording inversion, associated bundle branches are reversed, but the
and tachycardia substrate mapping in the pulmonary venous sinus node is in its normal location.
atrium are usually necessary.
Ablation strategies often include ablation on both sides Cardiac Venous Anatomy in cc-TGA
of the baffle suture line for CTI-dependent atrial flutter,
sometimes even for FAT (can be localized adjacent to baffle In cc-TGA, the CS develops with the morphologic atria
sutures), and biatrial ablation for IART. The original surgical and, in the majority (88%-96%) of cases, drains into the RA
note should be carefully reviewed regarding the disposition with a traditional anatomic course. The venous branches
of CTI. (including the great cardiac vein, lateral branches, etc)
Access to the surgically excluded CTI and biatrial ablation develop with the morphologic ventricles. There is often an
necessitate either a transbaffle or retrograde aortic approach. abundance of RV veins, although they rarely drain all the
A transbaffle approach to the pulmonary venous atrium (and way from the RV apex. There is extensive collateralization
CTI) avoids arterial and aortic valve complications. For trans- between the RV and LV at both anterior and posterior inter-
baffle access, radiofrequency perforation may be preferable to ventricular grooves via the anterior interventricular vein
needle puncture. A retrograde aortic approach can be used and middle cardiac vein, respectively. In cc-TGA patients
to access surgically excluded CTI (aorta to RV and then pos- without an identifiable CS, the majority (70%) have thebe-
terior toward the tricuspid annulus) and the posterior pul- sian veins with wide ostia (>1 mm), which may be a target
monary atrium (aorta to RV and then through the tricuspid for lead placement.
valve into the pulmonary atrium). Catheter ablation in such
patients has a high acute success rate but a moderate (10%) Common Arrhythmias and Arrhythmogenic
rate of recurrence. Substrate(s)
Unilateral or bilateral iliofemoral vein occlusion is com-
mon in adults who have had Mustard or Senning procedures Impaired AV conduction and AV block are common, and the
because of neonatal femoral venous catheterization with site of block is usually suprahisian or intrahisian because of
large sheaths for balloon atrial septostomy and subsequent histopathologic fibrosis of the His bundle. The rate of com-
multiple cardiac catheterization. Baffle obstruction or atresia plete AV block is 5% at birth and 2% yearly in previously
typically occurs at its superior limb (reported in 36%) and is unaffected patients, with a cumulative prevalence of 22% on
3.5 times more common after the Mustard procedure than long-term follow-up. In the presence of a VSD, complete AV
the Senning operation. Venography or MRI to assess the block can occur in more than 25% of patients. Therefore, pac-
lumen diameter prior to transvenous lead placement is criti- ing is necessary in many cc-TGA patients by adulthood.
cal, as stenosed areas may require angioplasty and stenting One or more accessory pathways (APs) occur in approxi-
before lead placement. Large preexisting baffle leaks must be mately 2% to 5% of cc-TGA patients. APs are more prevalent
closed surgically or using occlusion devices (such as a septal anywhere along the left AV (tricuspid) valve than along the
occluder like the Amplatzer device or covered stents) prior right AV valve. This is especially true when there is associ-
to endovascular lead placement, as transvenous leads incur ated Ebstein malformation of the left-sided tricuspid valve. In
a greater than 2-fold increased risk of systemic thromboem- L–TGA (cc-TGA) there is no tricuspid–aortic fibrous conti-
boli in patients with intracardiac shunts. This increased risk nuity, and therefore left anteroseptal and midseptal pathways
can exist. The conduction system is usually remote from the Ebstein Anomaly
tricuspid valve.
Anatomy of the Lesion
Implications of Clinical Anatomy for the
Ebstein anomaly is characterized by a failure of delamina-
Electrophysiologist
tion of tricuspid valve leaflets (more often involving the sep-
Lead Placement
tal leaflet than the posterior or anterior leaflets) from the RV
For CRT in cc-TGA patients with a patent RA CS, all leads myocardium with apical displacement of the septal leaflet and
may be introduced transvenously. The atrial lead is positioned the functional annulus, dilated “atrialized portion” of the RV,
in the RA, and the endocardial ventricular lead is placed in and tricuspid valve regurgitation.
the subpulmonary LV through the right AV (mitral) valve.
The systemic RV epicardial lead is introduced through the Surgical Correction of Ebstein Anomaly
CS. If a malformed or underdeveloped CS precludes RV epi-
cardial lead placement, then this may be done via a minitho- Tricuspid valve repair or replacement is performed.
racotomy as a hybrid approach. Depending on the position of the valve suture line, the CS is
In patients with a persistent left SVC draining into a either allowed to drain into the RA (when there is sufficient
patent CS and an absent right SVC, the former may be distance between the CS and the AV node) or into the RV (to
accessed through the left subclavian vein for lead placement. avoid injury to the conduction system).
Endocardial leads are placed through the CS into the RA and
subpulmonary LV, while the epicardial systemic RV lead is Common Arrhythmias and Arrhythmogenic
advanced through a venous branch of CS to pace the RV lat- Substrate(s)
eral wall.
Sometimes LV endocardial pacing or lead placement is Supraventricular tachycardia, including AV reentrant tachy-
not desirable (to avoid risking AV valve regurgitation), and cardia, FAT, and atrial flutter and fibrillation are noted in
CS access is also not possible because the CS is malformed 30% to 40% of patients with Ebstein anomaly and is the most
or unidentifiable. In such cases, epicardial LV pacing may common presentation in adults. APs are present in 20% to
be possible directly via thebesian veins or thebesian veins in 25% of patients with Ebstein anomaly and may be multiple
communication with major cardiac veins. Dilation of such in nearly half the cases. These APs are frequently right-sided,
veins may be attempted prior to lead placement. The thebe- and the majority are located in the inferior half of the tricus-
sian veins that drain into the subpulmonary LV may also pid annulus (right posteroseptal and posterolateral).
have extensive collateralization with the systemic RV free
wall along the posterior interventricular groove. Therefore, Sudden Death
thebesian veins can also be used for RV epicardial pacing or
lead placement for CRT. Venography performed to delineate Sudden death is reported in 3% to 4% of patients. Atrial flut-
the thebesian veins is useful prior to such procedures. ter and fibrillation with rapid ventricular conduction through
Alternatively, an entirely epicardial system may be APs may be the cause.
implanted, with leads positioned remote from one another, in
areas of late electromechanical activation. Implications of Clinical Anatomy for the
Electrophysiologist
Ablation
Left AV (tricuspid) annulus–related APs may be mapped Lead Placement
and ablated via a retrograde aortic or transseptal approach. RV apical pacing in patients with Ebstein anomaly may affect
The retrograde aortic approach requires entry via the aortic the tricuspid (native, repaired, or prosthetic) valve integrity
valve into the RV outflow tract (RVOT), negotiating through and function. Transvenous RV epicardial pacing through
the septal attachments of the tricuspid valve to reach its a patent CS may be preferable when the CS drains into the
annulus, which may be technically difficult. A transseptal RA or even when the CS is surgically excluded to the RV side,
approach is advocated by some groups to avoid risking dam- despite having to cross the tricuspid valve. CT angiography is
age to the tricuspid chordal tensor apparatus, which may useful in delineating the exact position of the CS. Intracardiac
be encountered with the retrograde aortic approach. In cc- echocardiography is helpful in guiding CS lead placement.
TGA patients, the fossa ovalis is more posteriorly located Deep AV septal pacing through the RA is a novel technique to
in the atrial septum, and an ultrasound-guided approach is activate the LV free wall with potential implications in these
helpful. Anatomic knowledge of the specialized conduction patients. Surgical epicardial lead placement is another option.
system is vital when ablating tachycardia (AV nodal reen-
trant tachycardia and AV reentrant tachycardia) substrates Ablation of AP
related to the right AV (mitral) valve and is discussed earlier This ablation may be challenging because of multiple APs,
in this book. fractionated electrograms, dilated right heart structures,
and risk of coronary artery injury while ablating along the VT After TOF Repair
thin AV groove. It is imperative to differentiate between the TOF-related VTs are typically macroreentrant and mono-
apically displaced valve leaflet edge and the true AV groove morphic. They are usually localized to the RVOT infundib-
in which the right coronary artery runs. A right coronary ulotomy scar or the septal surface of the VSD patch. When
angiogram is helpful in identifying the true AV groove. Thin- there is a transannular patch, VT circuits may encircle the
caliber electrode catheters have been used rarely to perform VSD patch and tricuspid annulus and go between the RVOT
intraluminal right coronary artery mapping along an excep- and superior tricuspid annulus in the region of the ventricu-
tionally thin AV groove, although the commercial availability loinfundibular fold. In patients with repaired TOF without a
of these leads may be limited. Catheter stability may be an transannular patch, the RVOT region from which the muscle
issue because of the dilated and dynamic nature of right heart bundles were excised may form a conduction barrier and
structures. Specialized long sheaths, intracardiac echocar- become a VT substrate. The prevalence of VT in these patients
diography, and transesophageal echocardiography are useful appears to be between 3% to 14%. Sudden cardiac death is the
in such situations. The published acute success rate is 85%, most common cause of late death in patients with repaired
with a recurrence rate of up to 25%. This recurrence rate is TOF, with an incidence of 0.15% per year and a cumulative
higher than that in patients with other types of CHD, poten- risk of 2% per decade, although there is likely an exponential
tially because of poor catheter contact in the dilated RA and increase with increasing age.
the presence of multiple pathways.
Implications of Clinical Anatomy for the
Electrophysiologist
Surgically Corrected TOF
Catheter ablation can be successful in a large percentage of
Anatomy of the Lesion
patients with atrial flutter and VT and is a useful adjunctive
TOF is the most common cyanotic heart disease in adults. or stand-alone therapy.
AT Ablation
Surgical Correction
An empiric ablation line between the lower margin of atri-
Surgical correction of TOF historically has entailed atriotomy otomy scar and IVC has a high success rate, but a moderate
and/or ventricular incisions and the use of patches. These recurrence rate.
incisions and patches predispose patients to the late devel-
opment of arrhythmias. In TOF repair, patch closure of the VT Ablation
VSD is universal, but the remainder of the surgical approach The areas of slow conduction amenable to radiofrequency
may vary. About 75% of repairs in the previous era involved catheter ablation (RFCA) are between the right inferior RVOT
a transannular patch from the distal parietal RVOT to the patch region and anterior tricuspid annulus, the RVOT inci-
proximal anterior main pulmonary artery, as dictated by a sion (superior septal pulmonary valve annulus) and VSD
small pulmonary valve annulus. When the pulmonary valve patch, and the rightward portion of the VSD patch and the
annulus is of adequate size, excision of the obstructive RVOT anteroseptal tricuspid annulus. In the last instance, injury to
muscle bundles alone may suffice. close-by specialized conduction tissue should be avoided. In
general, RFCA of VT in TOF patients has a high success rate
and a very low recurrence rate of VT.
Common Arrhythmias and Arrhythmogenic
Substrate(s)
Venous Anomalies
Patients with repaired TOF are predisposed to develop both
About 9% of patients with CHD may have anomalies of the
ventricular and atrial arrhythmias. In a multicenter cohort
superior veins. A detailed description of all the venous anom-
study, 10% of patients developed atrial flutter, 11.9% of
alies is beyond the scope of this chapter. The 2 relatively com-
patients experienced sustained VT, and 8.3% of patients died
mon variations in the venous anatomy discussed below have
suddenly.
implications for venous access to the heart.
Atrial Arrhythmias After TOF Repair Persistent Left Superior Vena Cava
Atrial arrhythmias were noted in more than one-third of
adult patients after repair of TOF. Risk factors included older A persistent left superior vena cava (LSVC) is the most com-
age at operation, increased atrial size, tricuspid or pulmonary mon systemic venous anomaly and is present in 2% to 5% of
regurgitation, and previous Waterston or Potts shunt (direct patients with CHD. It usually drains via the CS into the RA.
aorta-to–pulmonary artery anastomosis). Isthmus- or inci- In 8% of patients with an LSVC, it drains into the left atrium
sional circuit–dependent IART as well as atrial fibrillation through an unroofed CS. When present, an unroofed CS is
have been described. frequently associated with an LSVC. Rarely, the CS may be
absent, and the LSVC is attached to the superior aspect of the There is associated agenesis of the suprarenal segment of
left atrium. In both these situations, anticoagulation should the IVC.
be strongly considered when implanting transvenous leads
through this venous structure.
A persistent LSVC is more prevalent in heterotaxy syn- SUMMARY
dromes, complete AVSDs, conotruncal anomalies (eg, TOF,
D-TGA), pulmonary atresia or pulmonary stenosis, anoma- In summary, it is essential for the electrophysiologist to be
lous pulmonary venous drainage, cor triatriatum, and LV fully au fait with the patient’s surgical history and ready to
outflow tract obstructions. An LSVC may be associated with use advanced cardiac imaging to plan an ablation or device
a right SVC and an innominate vein that may be normal in approach. Preemptive discussion with surgical, imaging, and
size, diminutive, or completely absent. interventional CHD cardiology specialists may also be vital
In patients who undergo AVSD repairs who have a domi- in fully understanding the anatomy, surgical substrate, and
nant LSVC, the CS is incorporated on the right side of the potential variation in vascular access in anticipation of the
patch, instead of the usual preference of leaving it on the left procedure. This background serves to outline a safe, effective,
side of the patch. For single-ventricle patients with persistent and systematic approach to interventional electrophysiology
LSVC undergoing bidirectional Glenn or hemi-Fontan pro- procedures in CHD patients. The subsequent cases illustrate
cedures, the LSVC is either ligated distally when there are siz- the application of these principles.
able crossing veins draining into a right SVC or anastomosed
to the left pulmonary artery when there are no crossing veins
ABBREVIATIONS
or any right SVC.
When right SVC is absent, ICD placement may still be AP, accessory pathway
possible through an LSVC draining into RA. A left subclavian AV, atrioventricular
venous access is preferred. The RA lead is positioned through AVSD, atrioventricular septal defect
the CS into the atrium. Placement of an RV lead may be dif- cc-TGA, congenitally corrected transposition of the great
ficult as it is challenging to direct the lead from the CS ostium arteries
and advance it across the tricuspid annulus into the RV. A CHD, congenital heart disease
long sheath or a large atrial loop may be helpful in such cases. CRT, cardiac resynchronization therapy
The LV epicardial lead can be positioned directly in the pos- CS, coronary sinus
terior branch of the CS. The fact that the CS may also be quite CT, computed tomographic, computed tomography
dilated when an LSVC drains into it must be considered when CTI, cavotricuspid isthmus
pacing within it. In addition, other CS anomalies like ostial D, rightward
atresia and unroofed CS may be present. D-TGA, dextrotransposition of the great arteries
FAT, focal atrial tachycardia
Interrupted IVC IART, intra-atrial reentrant tachycardia
ICD, implantable cardioverter-defibrillator
Azygos Continuation of IVC IVC, inferior vena cava
The hepatic segment of the IVC is absent with azygos contin- L, left ward
uation of the infrahepatic segment into the right or left SVC. LSVC, left superior vena cava
Rarely, bilateral azygos veins may drain the infrahepatic seg- L-TGA, levotransposition of the great arteries
ment into right and left SVCs. Interrupted IVC is common LV, left ventricle, left ventricular
in heterotaxy with left isomerism (polysplenia syndrome). MRI, magnetic resonance imaging
Such patients usually undergo a Fontan palliation proce- RA, right atrial, right atrium
dure. Access of catheters to the heart is usually possible, yet RFCA, radiofrequency catheter ablation
manipulation can be difficult. RV, right ventricle, right ventricular
RVOT, right ventricular outflow tract
Left IVC With Hemiazygos Continuation SVC, superior vena cava
Persistence of the left supracardinal vein (instead of the TOF, tetralogy of Fallot
right supracardinal vein) results in a left-sided subrenal IVC VSD, ventricular septal defect
segment that continues through the left hemiazygos vein. VT, ventricular tachycardia
Section II
Case Studies: Testing the Principles
Glossary of Catheter Names
AA 1,2 to 19,20, ascending aorta distal-proximal

ABL dis/prox (ABL d/p), ablation distal/proximal
Aort Abl p, aortic ablation catheter, proximal
CS 1,2 to 19,20, coronary sinus distal-proximal
Epi 1,2 to 3,4, epicardial catheter
Epi Uni, epicardial unipolar
HBE 1–4, His bundle electrogram distal-proximal
HIS dist/prox, His bundle distal/proximal
HRA prox, high right atrium proximal
IS 1,2 to 19,20, isthmus distal-proximal
LAA prox, left atrial appendage proximal
LASSO 1,2 to 10,11, circumferential mapping catheter distal-proximal
LS 1,2 to 10,11, circumferential mapping catheter distal-proximal
LVOT UNI, left ventricular outflow tract unipolar
MAP d/p, mapping catheter distal/proximal
P1 ART, arterial pressure
PRES 1,2, arterial pressure distal-proximal
PV 1,2 to 10,11, pulmonary vein distal-proximal
RCA 1,2 to 7,8, right coronary artery distal-proximal
ROV 1,2 to 19,20, roving distal-proximal
RVa, right ventricular apex
RVOT (RVOT d/p), right ventricular outflow tract (distal/proximal)
RVOT UNI, right ventricular outflow tract unipolar
RV prox (RVp), right ventricle proximal
T 1,2 to 19,20, crista terminalis distal-proximal
217
Case 1
Where is the accessory pathway?
Figure C1.1
A 25-year-old patient with a history of attempted ablation for shows moderate preexcitation. One catheter (HRA prox) was
Wolff-Parkinson-White syndrome was brought to the elec- in the right atrial appendage and another catheter (HIS) was
trophysiology (EP) laboratory. The patient had intermittent in the anatomic region of the bundle of His. A catheter (CS)
preexcitation, and during catheter insertion, the electrogram was being inserted in the coronary sinus.
in Figure C1.1 was obtained. The surface electrocardiogram
Where is the likely site for successful ablation of this acces-
sory pathway?
Abbreviations are expanded at the end of this chapter. A. Near the His bundle region
Terms with “[f]” denote abbreviations that appear in the figures only. B. Left atrium lateral wall
219
220 Section II. Case Studies: Testing the Principles
C. Left atrium septum RVp catheter, placed near the apex, is also late, so an AP that
D. Connection between the atrial appendage and right connects directly into the right bundle (Mahaim) is unlikely.
ventricle Third, where is the early intracardiac ventricular poten-
E. None of the above tial? On initial perusal, the tracing has no apparent early site.
There is, however, a far-field ventricular signal on the HRA
The answer to this question will become apparent in the
prox catheter. Although APs rarely connect directly from
subsequent discussion.
the appendage to the right ventricle, in that situation, a fairly
What features in this tracing help determine the location near-field ventricular potential and more tightly coupled
of the accessory pathway (AP)? First, analyze the electrocar- atrial and ventricular signals are expected.
diogram for important clues. Although the electrocardio- Fourth, can the AP be near the His bundle catheter? The ven-
gram is noisy and truncated, it shows a strongly positive delta tricular potential at this site appears late. However, a complex
wave in lead II and lead aVF, a positive delta wave in lead I, signal is associated with the usual location of the atrial signal.
and a small delta wave but predominantly negative QRS com- If the findings are examined in a step-by-step manner as
plex in lead V1. This pattern is consistent with a right anterior described above, it becomes apparent that the key to under-
or right anteroseptal AP. standing this case relies on identifying the nature and cause
Second, what can be learned from the intracardiac trac- of the complex signal on the His bundle catheter. The electro-
ing? The coronary sinus has a far-field ventricular signal cardiogram tracing suggests an AP somewhere in the right
that is late relative to the onset of the QRS complex, and a anterior region where the His bundle is located, but the ven-
free-wall, left-sided pathway is unlikely. The signal from the tricular signal is late.
What is this?
Figure C1.2
During right atrial pacing, the heart shows maximal pre- Again, can an AP be present in this location when the local
excitation, with a clear left bundle branch block in lead V1 and ventricular potential is late? To answer this, the nature of the
a strongly positive delta wave in lead II (Figure C1.2). Note complex signal first must be better defined by asking several
that with rapid pacing, the complex signal from the His bun- basic questions: 1) Is it atrial? 2) Is it from the His bundle? 3)
dle catheter still appears around the same time as the atrial Is it an AP potential? and 4) Is it ventricular (ie, 2 different
potential. The local ventricular potential, however, is late. ventricular potentials, early and late)?
Case 1 221
It’s not a!
Figure C1.3
With a further increase in the atrial pacing rate, atrioven- D. A “halo” catheter placed along the tricuspid annulus
tricular (AV) block is followed by conducted beats showing E. All of the above
less than maximal preexcitation (Figure C1.3). The complex Answer: E—All of the above.
signal from the His bundle catheter is absent when the AV
block occurs (arrows), but the atrial signal remains. Thus, No standard catheter position exists for mapping the
the complex signal has been dissociated from the atrium and tricuspid annulus. (In contrast, coronary sinus catheteriza-
is therefore not atrial in origin. The complex signal returns tion is useful when mapping the mitral annulus, owing to
for the last 2 conducted beats in the tracing, when pathway the close proximity of the 2 structures.) Furthermore, it is
conduction recurs. In the last beat, where there is less pre- extremely difficult to obtain good catheter contact on the
excitation, the complex signal is located further from the free wall of the tricuspid annulus, and in certain patients
atrial signal. Thus, one can deduce that this complex signal (eg, those with Ebstein anomaly), the location of the annu-
is in some way associated with the manifestation of pathway lus can be difficult to defi ne fluoroscopically. For these rea-
conduction. sons, various techniques have been developed to help map
the tricuspid annulus. When catheter contact is extremely
Which of the following methods can aid mapping of the difficult (eg, with right anterolateral or right lateral APs),
tricuspid annulus? magnet-guided catheter mapping and ablation can be help-
A. Magnet-guided mapping ful. An endocardially placed multielectrode catheter, simi-
B. Mapping catheter placed in the right coronary artery lar to that used for typical atrial flutter ablation, also can
C. Mapping catheter with closely spaced electrodes placed be used. Another feasible technique involves placing a rela-
along the lateral tricuspid annulus, just ventricular to tively small, multielectrode catheter in the right coronary
the cavotricuspid isthmus artery.
RCA matches the FF
Figure C1.4
In Figure C1.4, the RCA catheter, inserted in the right coro- detected by the coronary sinus (CS 1,2 to 11,12) or right ventricu-
nary artery, was placed on the annulus. However, the single com- lar (RV prox) catheters. However, a distinct signal is apparent
plex signal suggests overlapping atrial and ventricular potentials. on the His bundle catheter. Note that the early onset of the delta
If in fact the right coronary artery electrode is detecting a ven- wave precedes the His bundle signal, resulting in a negative His
tricular signal, this may indicate where on the other catheters Purkinje to earliest ventricular activation (H-V) interval. Yet the
the earliest ventricular signals should be sought. Clearly, no local ventricular potentials on the HIS prox and HIS dist cath-
candidate potentials suggesting early ventricular activation are eters are much later than the onset of the QRS signal.
Block in the pathway, see atrial electrogram (HRA prox)
Figure C1.5
Case 1 223
What remains to be determined is whether the complex and a ventricular signal, yet the complex signal under scru-
signal originates in the His bundle or is a fractionated ven- tiny is absent from the ABL catheter. By using simple disso-
tricular signal (Figure C1.3 having now established that ciative maneuvers, it is reasonable to conclude that the signal
it was not an atrial signal). In Figure C1.5, note the atrial being analyzed is not originating in the His bundle or AVN.
pacing–induced block in the pathway but continued conduc- Note that the last beat on this tracing is ectopic—caused by
tion through the AV node (AVN), starting with beat num- the neighboring ventricular myocardium or possibly induced
ber 3. For this beat, there is atrial capture, a His bundle signal, by another catheter.
Block
Figure C1.6
During mapping with the ablation catheter in the region mechanical trauma is between the AP and its ventricular
close to the His bundle catheter, preexcitation is lost sud- insertion site.
denly (Figure C1.6). The ABL dis catheter detects the com- Can 2 ventricular signals be detected by a single mapping
plex signal fi rst seen on the His bundle catheter and shows catheter? Yes, a 2-for-1 phenomenon can occur when the
a distinct deflection. Th is probable atrial signal is followed atrial impulse simultaneously travels down the AP (activat-
by 2 potentials, neither of which appear with the His bundle ing the annular ventricular myocardium) and travels down
signal (HIS dist). Finally, a far-field–like potential coincides the AVN and His bundle (activating the relatively more api-
with the QRS complex. During mechanical trauma at this cal ventricular myocardium, close to the exit site of the right
site, AP conduction is lost and the second beat shows no pre- bundle). Afterward, the ventricular activation wave front may
excitation. With the loss of preexcitation, the second com- travel back toward the base. (Two-for-1 signals can also occur
ponent of the complex signal (yellow arrows) now occurs with dual AVN physiology or with anteriorly and basally
after the far-field ventricular potential. The fi rst component, located APs.) This phenomenon is very important to rec-
however, is unchanged (white arrows). Consider the possi- ognize because an inaccurate conclusion otherwise may be
bility that the fi rst component of the complex signal repre- reached, ie, that the ventricular potential is single and late—
sents AP conduction, the second component represents local but this would not map close to the site where all other deduc-
ventricular activation, and the location of the block due to tions in this case would point (near the His bundle).
Pathway potential and His
Figure C1.7
With the His bundle catheter clearly showing the com- of the ventricular potential. The pathway potential detected
plex signal (HIS dist, arrow) (Figure C1.7), the ablation by the ablation catheter (ABL prox, arrow) can now be
catheter is manipulated to maximize the fi rst component visualized.
Before ablation
Figure C1.8
Case 1 225
The ablation catheter is further manipulated to obtain others of known origin. In this case, it could be deduced
the largest near-field pathway potential signal (Figure C1.8) that the fi rst component of the complex signal was an AP
while maintaining reasonable AV balance (AB dist, atrial potential because it was dissociated from all other possible
and ventricular potentials). Th is site was targeted for signals in this location. Thus, the signal under consideration
ablation. sequentially was shown not to be atrial, ventricular (related
After ablation
Figure C1.9
Six seconds into energy delivery, AP conduction was lost to His bundle conduction), or from the His bundle. Finally,
(Figure C1.9). The complex signal was no longer seen with the in the mechanical trauma tracing (Figure C1.6), the fi rst
ablation catheter. Ablation continued, and further EP study component of the complex signal (associated with pathway
showed no subsequent evidence of AP conduction. conduction) was not ventricular, either. However strange
Although the case described above is unusual, it illus- or unusual that signal may be, the fact that it is not any of
trates a very commonly used maneuver in cardiac EP, these other possible signals means that it must be an AP
namely the concept of dissociating one electrical signal from potential.

Surface ECG
Stim Stim Stim Stim
A V A V A V A
Annular EGM
AP AP

Conduction

Recording Recording
catheter catheter
AP AP AP
AP AVN-only Block in
Figure C1.10 (Adapted from Macedo PG, Patel SM, Bisco SE, Asirvatham SJ. Septal accessory pathway: anatomy, causes for difficulty, and
an approach to ablation. Indian Pacing Electrophysiol J. 2010 Jul 20;10[7]:292–309. Used with permission of Mayo Foundation for Medical
Education and Research.)
The schematic representation in Figure C1.10 shows the signal is seen. In this situation, the potential being analyzed
simple technique of dissociating potentials as a method of is not likely to be atrial, although it could be an early ven-
determining the origin of an unexplained potential. The tricular signal.
recording catheter is placed on the annulus and records Th is simple maneuver of atrial pacing and observing
atrial and ventricular potentials when the adjacent tissue what happens with a pathway block and a block to the ven-
is depolarized. During preexcitation, the atrial and ventricle is usually sufficient to determine whether an unex-
tricular deflections on the electrogram are relatively close plained potential is from an AP. The case described above is
together, and between them is an unexplained potential a rare exception—a potential (eg, AP in Figure C1.10) that
(“AP”). In the third beat of the atrial drive train (“Stim”) can be attributable to 1 of 2 ventricular origins, specifically
pathway, conduction is lost and ventricular activation ventricular myocardial activation from an AP. Th is level of
occurs via the AVN. The unexplained potential is not seen. complexity should not overly concern the novice electro-
Th is strongly suggests that the potential under scrutiny is physiologist because as long as the potential is recognized
neither atrial nor ventricular in nature. The usual remain- as not atrial, it is an excellent site for further mapping and
ing possibility is that it is an AP potential, which would ablation. Th is is true regardless of whether it is a genuine AP
be an excellent target for ablation. A more common occur- potential or a local early ventricular potential from pathway
rence, however, is as shown in the fourth beat of the drive conduction (distinct from the ventricular potential from
train. Here, antegrade conduction is lost and only an atrial AVN conduction).
Case 1 227
Surface ECG
Stim Stim Stim Stim
A V AV V A
Annular EGM
AP AP AP
Anterograde Ventricular signal Very early PVC

AP conduction advanced by PVC dissociates ventricular
signal from A and AP
Figure C1.11
Note, however, that when doing the simple pacing maneu- coupling intervals. In the middle beat, the premature ventric-
ver, if AV block occurs whenever pathway block occurs (ie, the ular contraction (PVC) advances the ventricular potential,
effective refractory period is longer for the AVN than for the but there is no change in the AP signal. Thus, the ventricular
pathway), it is uncertain whether the candidate potential is signal is dissociated from the candidate potential (ie, it is not
ventricular in origin. In cases where such clarification is neces- ventricular). With an even earlier PVC, as shown in the third
sary, the maneuver shown in Figure C1.11 can be performed. beat, the AP potential still occurs after the atrial potential.
During atrial pacing and preexcitation, the questionable Of course, with this maneuver alone, the candidate potential
potential (“AP”) appears between the atrial and ventricular has not been dissociated from the atrial signal, but this usu-
deflections. Now, while atrial pacing continues, premature ally would have been resolved with the simple atrial pacing
ventricular extrastimuli are placed at progressively shorter maneuver described in Figure C1.10.
Surface ECG
Stim Stim Stim
A V A V V A
Annular EGM
AP AP APR
Antegrade AP A single PVC advances the ventricular signal;

fixed-rate atrial with atrial block; atrial stimulation is followed
pacing only by the atrial signal
Figure C1.12
If retrograde conduction (via the AP) and antegrade con- There are several situations in cardiac EP for which the sim-
duction both occur, preexcitation is present, as seen in the ple and fundamental dissociation and association of question-
third beat of Figure C1.12. Retrograde AP activation produces able potentials with pacing maneuvers can be immensely useful.
a new potential (“APR”) after the ventricular signal. A stepwise approach is summarized in Boxes C1.1 and C1.2.
Box C1.1 Box C1.2

How to Determine the Source of a Questionable Conditions for Which Associative and Dissociative
Potential Maneuvers Are Used to Ascertain the Source of a
Potential
1. List all possible sources for the potential (eg, atrial, ventricu-
lar, His bundle, pulmonary vein, appendage, etc). Accessory pathway potentials
2. Systematically perform pacing maneuvers from the cham- Antegrade versus retrograde His bundle activation
bers listed in the differential diagnosis enumerated in step 1. Pulmonary vein potentials
3. Systematically attempt to dissociate the candidate potential Left atrial appendage or vein of Marshall potential being
from each of the possibilities, either during pacing or during mistaken for pulmonary vein potentials
tachycardia. Pay particular attention to periods of atrioventric- Fascicular potentials during an intrafascicular or automatic
ular and ventriculoatrial block, pulmonary vein block, etc. fascicular tachycardia
4. When all the possible origins of the signal in question Remnant conduction tissue or supravalvar muscle tissue
(step 1) have been reviewed, whichever possibility remains potentials in outflow tract tachycardia
is the source of the potential, however unlikely it may seem. Picking the correct component of a fragmented potential during
entrainment maneuvers (eg, to measure postpacing intervals)
During atrial flutter ablation in patients undergoing congenital
heart surgery, to determine whether a given potential is
originating within the mapped chamber or elsewhere
(eg, adjacent neo-left atrial tissue)
Figure C1.13
During an EP study with planned ablation in a patient Which of the following diagnoses should be considered?
with a history of tachycardia and syncope, the electrogram in A. Intermittent AP conduction with an antegrade 2-for-1
Figure C1.13 was obtained. Note that the HBE 1 catheter is phenomenon
located in the distal His bundle and HBE 4 is proximal. The B. Intermittent fused PVCs
ABL catheter is located close to the His bundle region but just C. Intermittent nodoventricular conduction
off the septum. An unusual electrogram sequence is seen. Note D. Fragmented ventricular potential
that in the middle beat, the QRS morphology changes, and in E. Ventricular potential (Figure C1.13, arrow) from the
the first and third beats, a potential is seen after the ventricu- left ventricle, which is early during PVCs
lar deflection on the His bundle catheter (arrow). Note also F. All of the above
that the same potential is picked up on the ABL p catheter,
although it is small and more far field. Answer: F—All of the above.
Case 1 229
A wide range of diagnoses are possible. Sometimes, 2 sets occurs early and gets fused with the other set of ventricular
of ventricular signals may occur. If the second set is caused by signals.
pathway conduction, resulting in preexcitation, the signal also
Figure C1.14
The electrogram in Figure C1.14 was from a patient PVC morphology suggests an origin in the right ventricu-
with documented, frequent PVCs (20,000 per day). The lar outflow tract.
Figure C1.15
In Figure C1.15, the first beat is in sinus rhythm, with ante- His bundle potential (white arrow). Thus, with the principles
grade right bundle branch block. The questionable potential described above, the electrophysiologist should be alert to the
occurs late after the ventricular signal (yellow arrow). In the possibility that this electrogram is related to the mechanism
second beat, the morphology changes; the pattern is similar that produced the PVCs. Once this simple conclusion is drawn,
to the PVC, but a second potential now appears just before the efforts should focus on identifying the appropriate ablation site.
Case 1 231
Figure C1.16
The mapping catheter (ABL d) is now manipulated carefully bundle catheter. This excludes conduction via a nodoventricular
to find an area where this unusual potential is largest (Figure connection. Potentials caused by structures near the His bundle
C1.16). Note that in the second beat, when the PVC occurs, the region are important to recognize because they can produce vari-
large potential occurs even earlier than the atrial signal on the His ous clinical arrhythmias (Case 17 shows other examples).
Figure C1.17
The electrogram in Figure C1.17 was obtained from a patient As shown in Figure C1.18, the white arrow points to the
with atrial fibrillation and a known anomalous pulmonary circumferential mapping catheter and the yellow arrow points
vein connection to the superior vena cava. The circumferential to the ostium of the anomalous pulmonary vein. What is the
mapping catheter (LASSO) is placed in the superior vena cava nature of the complex signals captured by the mapping cathe-
about 1 cm from the superior vena cava–right atrial junction ter (Figure C1.17, arrows)? Could they be atrial in origin, or do
and proximal to the anomalous pulmonary vein connection. they represent superior vena cava potentials? In Figure C1.17,
the intervals vary between the initial set of signals (after the
pacing stimulus) and the questionable potentials. This occurs
because of fused ectopy from the superior vena cava, although
that conclusion cannot be immediately drawn from the elec-
trogram. Still, the electrophysiologist should realize that the
signal under consideration is not atrial because the interval
between the atrial potentials and this candidate potential var-
ies (indicating dissociation).
Figure C1.18
Case 1 233
Figure C1.19
As seen in Figure C1.19, this phenomenon occurs repeat- component of the complex signal (likely the superior vena
edly. Also note that the second and third components of the cava) is isolated, then conduction block will be observed (ie,
complex signal (seen on the circumferential mapping cath- all potentials will be eliminated, other than the normal atrial
eter) move together. Thus, even if this potential partially potential after the pacing stimulus). An isolation procedure at
originates in the superior vena cava and partially in the the superior vena cava–right atrial junction was performed,
anomalously draining pulmonary veins, if conduction from resulting in a successful entrance block in the superior vena
the right atrium to the structure responsible for the first cava, as well as within the anomalous pulmonary veins.
Figure C1.20
Figure C1.20 is a tracing from a patient with known with bundle branch block, the ablation catheter is placed
exercise-related ventricular tachycardia. This is another situ- in the region of the pulmonary valve. Note the fragmented
ation for which the principles of associating or disassociating signal, followed by a sharp near-field signal, on the ABL p
a questionable potential with other known potentials can be catheter and the ABL d catheter. The patient had not had any
used to select an ablation site successfully. In sinus rhythm, previous ablation.
Which of the following structures likely is responsible for D. Myocardial tissue superior to (extending beyond) the
the near-field potential? pulmonary valve
A. Right ventricular myocardium Answer: D—Myocardial tissue superior to (extending
B. Smooth muscle of the pulmonary artery beyond) the pulmonic valve.
C. Aberrant conduction tissue
Figure C1.21
Myocardial sleeves sometimes extend beyond the pul- the site of valve insertion. Currently, the exact incidence
monic valve. Figure C1.21 shows an example of myocardial of such potentials and the rate at which they are arrhyth-
tissue extending above the anterior pulmonary valve cusp. mogenic in a given patient are unknown. Thus, the electro-
(Note the heterogeneity of tissue at the valve level.) Similar physiologist must determine through an EP study and the
to what occurs in the pulmonary veins, an area of conduc- ablation procedure whether such potentials should be tar-
tion slowing can give rise to fragmented potentials around geted for ablation.
Case 1 235
Inlet-outlet ring of conduction tissue
Right AV junction Outflow tracts
Left AV junction
Dead-end tract
Compact node
Penetrating bundle
Trabecular
component of right Left Dead-end tract
ventricle ventricle
Ventricular bundle
branches on apical
AV AV
trabecular septum
groove Right groove
ventricle
Branching bundle
and bundle branches
Figure C1.22
As described later in Case 14, conduction tissue rem- such conduction tissue and be activated after the fragmented
nants may also be found in the outflow tract (Figure C1.22). far-field ventricular potential. Thus, conduction tissue is an
However, it would be unusual for a potential to arise from unlikely source for the potentials shown in Figure C1.20.
Figure C1.23
In Figure C1.23, the ablation catheter has been pulled catheter position in Figure C1.20, it was relatively closer
toward the commissure between the right and anterior to the right ventricle. Note that the near-field potential
leaflets of the pulmonic valve. With intracardiac ultra- occurred again after the fragmented potential and that the
sonographic guidance, the catheter tip was known to be conduction delay (measured by the ABL d catheter) was
almost exactly at the commissure; compared with the large.
Figure C1.24
With isoproterenol, tachycardia spontaneously occurred Answer: D—Further mapping is required.

(Figure C1.24), showing a QRS morphology identical to the
Comparison of the signals recorded by the ABL d cathe-
patient’s clinical arrhythmia (Figure C1.20). Now compare
ter during tachycardia and sinus rhythm shows an apparent
the electrogram characteristics (measured by the ABL d cath-
reversal of the near-field and far-field potentials. Th is sharp
eter) with those seen during sinus rhythm (Figure C1.23).
potential from the pulmonary valve musculature clearly
Which of the following likely is true? precedes the drawn-out, far-field, multicomponent ven-
A. The ablation catheter now is located at the site of origin tricular signal. However, careful analysis shows a far-field
of the tachycardia component before the near-field potential from the pulmo-
B. The tachycardia arises from musculature above the nary artery musculature. Th is suggests that the catheter is
pulmonic valve not located at the true earliest site of origin. The true early
C. The ablation catheter has moved to the His bundle site likely is above the pulmonary valve, although that is not
location defi nitively known from the tracing. Thus, further mapping
D. Further mapping is required is required.
Case 1 237
Figure C1.25
With the catheter now manipulated toward the left cusp of (arrow). It has no significant preceding far-field signal, and the
the pulmonic valve (Figure C1.25), an earlier, sharp, near-field greater delay between the near-field and far-field potentials sug-
potential from the pulmonary artery musculature is now found gests further exit delay at the site of origin of this tachycardia.
Figure C1.26
The ablation catheter is moved further anteriorly to potential. If this was the only electrogram available for
the mid portion of the anterior pulmonary valve leaflet review, it is possible that the musculature above the pul-
(Figure C1.26). Here, one clearly sees that the near-field monary valve is a bystander and that the true early site
potential occurs much later than the preceding far-field of activation (origin of the tachycardia) is the ventricular
myocardium below the pulmonic valve. Th is principle of a total understanding of the anatomy of the region being
assessing the relationship of a near-field signal with the mapped, can often clarify which regions are likely to be suc-
far-field signal in sinus rhythm and tachycardia, along with cessful ablation sites.
Figure C1.27
Another important principle regarding conduction another cusp). If the first possibility is true (infravalve cause
across a site of conduction delay is illustrated in the pacing of tachycardia), then ventricular pacing should produce a
maneuver shown in Figure C1.27. During ventricular pac- similar pattern, ie, a ventricular myocardial far-field poten-
ing from the region of the right ventricular apex, there is tial followed by an isoelectric period and then by near-field
fusion of the near-field and far-field potentials on the abla- suprapulmonary valve potentials. However, with ventricular
tion catheter. However, during tachycardia, the far-field pacing, little delay is seen and the potentials are fused. Thus,
potential is clearly separated from the near-field potential the far-field potentials (seen on the ABL p catheter) associated
(see the fi rst tachycardia beat after cessation of pacing). with the first beat of tachycardia represent a tachycardia ori-
Th is information suggests that the tachycardia origin likely gin site located in an adjacent supravalvar pulmonary cusp.
is above the valve but not at the site of the ablation catheter With ventricular pacing, conduction occurs in the culprit
(anterior cusp). cusp tissue and in the bystander cusp tissue (where the abla-
Considering the first tachycardia beat recorded by the tion catheter is located), producing the fused signal; however,
ABL p catheter (placed above the pulmonic valve in the during tachycardia, the true origin (which generates the first
region of the anterior cusp), the tachycardia site is either 1) in far-field potential on the first tachycardia beat) occurs con-
the ventricular myocardium, with passive activation of the siderably before activation of the supravalvar musculature in
supravalvar musculature; or 2) above the pulmonary valve the cusps being matched (later-occurring near-field potential
but not where the ablation catheter is located (perhaps it is at is late).
Case 1 239
Figure C1.28
The catheter is now moved back (Figure C1.28) to the cusp noted. A large, near-field potential with abrupt termination of
where the earliest activation (origin) for the tachycardia was the tachycardia is observed, likely from mechanical trauma.
Figure C1.29
Figure C1.29 powerfully demonstrates how the cause of than sinus rhythm. Note that in sinus rhythm with right bun-
arrhythmia can be determined through the principles of dle branch block, the near-field potential is late on the ABL d
association and dissociation. The first 2 beats are in sinus catheter. It gets progressively earlier as greater fusion occurs,
rhythm with right bundle branch block. The third is a fused and eventually just the PVC morphology is seen on the QRS.
PVC with sinus rhythm and bundle branch block. The last 2 This strongly suggests that this potential is associated with
beats are PVCs occurring earlier and then markedly earlier the origin of the tachycardia.
Figure C1.30
During ventricular tachycardia (Figure C1.30), the cycle potentials recorded during one QRS complex were respon-
length of the tachycardia varied spontaneously. The arrows sible for the generation of the next QRS complex. As the exit
clarify the relationship between the local potential and the delay increased, the appearance of the next QRS complex was
surface QRS complex. On the ABL p catheter, the near-field delayed (slower cycle length). One approach to ablation in
spike that at first clearly preceded the QRS complex subse- such cases is to ablate circumferentially around the pulmo-
quently was within the QRS deflection. This occurred after nary valve, which isolates the arrhythmogenic tissue respon-
radiofrequency lesions were applied in the region of the sible for the early near-field potential above the pulmonary
pulmonary valve. Now, the considerable delay between valve. This approach is similar to pulmonary vein isolation
the early near-field potentials and the QRS was such that the for atrial fibrillation.
Case 1 241
Figure C1.31
In Figure C1.31, whenever there is a loss of the near-field tachycardia or catheter trauma, the tachycardia stops.
potential, either from spontaneous termination of the
Figure C1.32
Further analysis of the cycle length variation in tachycar- the cycle length of tachycardia subsequently increases from
dia is revealing (Figure C1.32). When the interval from one 336 to 350 milliseconds. The driver of tachycardia therefore
near-field potential (ABL d, supravalvar myocardial electro- must be located at or near the site of the ablation catheter
gram) to the next increases from 334 to 345 milliseconds, (above the pulmonary valve).
Figure C1.33
Further evaluation shows that when the exit delay those less experienced, must always be alert to the possibility
increases from the near-field potential to the ventricular of applying knowledge gained from maneuvers used in one
potential (Figure C1.33, RVp), the cycle length also increases. arrhythmia to other less familiar arrhythmias or tachycar-
This is analogous to increased atrial cycle length when the His dias. Understanding the basic concepts (in this case, “wob-
bundle activation time increases, which can be used to dis- ble” and the concept of dissociating signals) underlying these
tinguish between AVN reentrant tachycardia and junctional maneuvers allows interpretation that may aid in the ablation
tachycardia (see Case 17). Electrophysiologists, particularly of tachycardias that are otherwise difficult to treat.
Case 1 243
Figure C1.34
Attempts to isolate the right ventricular outflow tract at of the proximate coronary arterial system. Which method
the level of the pulmonic valve were unsuccessful, although (supravalvar focal ablation or root isolation) is better if the
exit delay became very pronounced (the near-field poten- pulmonic root is unknown? As with the aortic root, supra-
tial associated with the first beat being related to the last pulmonary valve ablation (particularly in the left cusp
beat of the tachycardia). Because of this, the catheter was posteriorly) also can be associated with arterial damage
moved from the pulmonic valve up to the site of earliest (see Case 14).
activation of tachycardia. After ablation at that site, tachy- Electrophysiologists must have a thorough understand-
cardia was terminated; the near–field potential was lost, ing of how unexplained potentials can be analyzed using
and tachycardia was no longer inducible (Figure C1.34). As pacing maneuvers and observing changes of association and
with pulmonary vein tachycardias, suprasemilunar valve dissociation that occur between these unknown signals and
tachycardias can be approached either with direct elimina- other known potentials (ventricular, atrial, etc). These tech-
tion of the focus or with root isolation. In the case of the niques are useful in identifying the culprit sites and targets
aortic root, it may be better to isolate the root first because for ablation for several arrhythmias.
Abbreviations EGM, electrogram [f]

EP, electrophysiology
A, atrial [f] FF, far field [f]
AP, accessory pathway H-V, His Purkinje to earliest ventricular activation
APR, retrograde accessory pathway potential [f] PVC, premature ventricular contraction
AV, atrioventricular RVOT, right ventricular outflow tract [f]
AVN, atrioventricular node Stim, stimulation [f]
ECG, electrocardiogram [f] V, ventricular [f]
Case 2
A 47-year-old man was initially referred to the electrophysi- persistent, recurrent atrial arrhythmia that was refractory
ology (EP) laboratory because of highly symptomatic par- to medical therapy. He returned to the EP laboratory about
oxysmal atrial fibrillation. Pulmonary vein isolation, partial 6 months after his initial ablation procedure. In the baseline
isolation of the superior vena cava, and ablation of the cavotri- state (before catheter insertion), he had a persistent atrial
cuspid isthmus were performed. Despite this, the patient had arrhythmia that was associated with difficult palpitations.
Figure C2.1
Figure C2.1 shows the intracardiac electrograms obtained circumferential mapping catheter (LASSO 1,2 to 10,11) was
after initial catheter insertion. A catheter was placed in placed in the left upper pulmonary vein. A catheter was placed
the coronary sinus (CS 1,2 to CS 19,20), with the CS 19,20 on the mitral isthmus just posterior to the mitral annulus (IS
electrodes located at the ostium of the coronary sinus. The 1,2 to IS 19,20), with poles 1,2 located closer to the septum and
poles 19,20 at about the 3-o’clock position on the left anterior
Abbreviations are expanded at the end of this chapter. oblique (LAO) projection of the mitral annulus (lateral wall).
Terms with “[f]” denote abbreviations that appear in the figures only. The ABL catheter was located on the roof of the left atrium.
245
Which diagnosis can be excluded on the basis of the P wave during tachycardia was similar to the interval between
patient’s history and the intracardiac electrograms shown the local potential and P-wave onset, as measured with the
in Figure C2.1? ablation catheter placed on the roof of the left atrium.
A. Recurrent, cavotricuspid isthmus–dependent flutter
B. Automatic atrial tachycardia arising from the right atria Given this information, which statement regarding deliv-
C. Persistent but passive conduction into the left upper ery of radiofrequency energy is most accurate?
pulmonary vein A. Ablation at this site on the left atrial roof will eliminate
D. Reentrant tachycardia exiting near the right upper pul- tachycardia because it is the focus of the arrhythmia
monary vein B. Ablation at this site will eliminate tachycardia because
E. Automatic tachycardia arising from the right upper the slow zone for this circuit is located at this site
pulmonary vein C. Ablation at this site will have no effect because the
F. None of the above tachycardia is a cavotricuspid isthmus–dependent
flutter
Answer: F—None of the above.
D. Ablation at this site may terminate tachycardia, but the
The overwhelmingly likely mechanism of tachycardia arrhythmia is unlikely to be eliminated
after isolation of the pulmonary vein, especially in patients E. None of the above
with chronic atrial fibrillation, is a reentrant atrial tachy-
Answer: D—Ablation at this site may terminate tachycar-
cardia (atypical atrial flutter). Nevertheless, nothing in the
dia, but the arrhythmia is unlikely to be eliminated.
patient’s history or intracardiac electrograms excluded the
possibility of an automatic tachycardia. In fact, the only The results of entrainment mapping (the interval after
way to define the tachycardia mechanism was to perform pacing was the same as the tachycardia cycle length, and
entrainment maneuvers (see Chapter 5). The circumferential the interval between pacing stimulus to onset of the P wave
mapping catheter, placed in the left upper pulmonary vein, was similar to that between the local potential to onset of
showed evidence of remaining potentials that likely arose the P wave during tachycardia) strongly suggested that the
from the musculature of the vein. Because these were acti- catheter was located in the tachycardia circuit. There was
vated “late” in the patient’s arrhythmia, they likely represent no evidence of overdrive suppression, which would suggest
passive conduction into the vein. Neither an automatic focus an automatic focus. Single-point ablation occasionally can
nor a reentrant tachycardia in the right upper pulmonary eliminate an automatic tachycardia focus, but this is rarely,
vein vicinity or in the right atrium could be excluded as the if ever, completely effective for an atypical flutter circuit.
true source of the patient’s arrhythmia. Although a detailed Within the tachycardia circuit, entrainment characteristics
anatomic map may provide insight into the tachycardia, a were consistent with the catheter being located within the
necessary first step is to perform basic pacing maneuvers. slow zone of the circuit or at its exit site. Although ablation
This will define the tachycardia mechanism and suggest within certain regions of the arrhythmia circuit may tem-
(if a flutter is diagnosed) the likely locations of the critical porarily terminate the tachycardia, it will not be eliminated
elements of the flutter circuit. without complete ablation of the slow zone or linear ablation
The ablation catheter was moved to several locations in the transecting the tachycardia circuits and anchoring the lesion
right and left atria, and pacing was performed using the ABL d to anatomic obstacles (eg, scars, valves, etc).
electrode at a cycle length approximately 20 milliseconds faster Using the information described above, a linear ablation
than the tachycardia cycle length (entrainment). When pac- across the roof of the left atrium was performed. However, the
ing from the left atrial roof, the atrium showed a very similar tachycardia still was repeatedly reinducible, with little (if any)
P-wave morphology and intra-atrial activation sequence. Upon change in the activation sequence or entrainment characteris-
cessation of pacing, the return intervals, as measured on the tics. As shown in Figure C2.1, the ablation catheter placed on
ABL d electrode, approximated the tachycardia cycle length. the left atrial roof consistently revealed a far-field potential that
The interval from the pacing stimulus to the onset of the could not be completely eliminated with endocardial ablation.
Case 2 247
RAO LAO
Figure C2.2
After re-isolating the remaining pulmonary vein con- the margins of the cardiac silhouette, lateral to the coronary
duction (left upper vein and right lower vein, to prevent sinus catheter course. This strongly suggests that the catheter
recurrent atrial fibrillation), the circumferential mapping is actually in the pericardial space. However, the catheter in
catheter was removed and catheters were repositioned to the LAO view appears to come back toward the right side, and
address the recurrent tachyarrhythmia. During catheter it is very close to the shaft of the coronary sinus catheter that
repositioning, the above fluoroscopic images (Figure C2.2) was placed via the right internal jugular vein.
were obtained. How does a catheter placed in the pericardial space from
The right anterior oblique (RAO) and LAO projections are an inferior approach travel around the cardiac silhouette
shown. The black arrows point to a catheter—where is that and reach the superior vena cava (shaft of the coronary sinus
catheter located? catheter)? To comprehend this, fi rst understand the nor-
A. Right ventricular outflow tract (RVOT) mal pericardial reflection and know the distinctions among
B. Transverse pericardial sinus 3 important pericardial recesses, namely the transverse
C. Oblique pericardial sinus sinus, the oblique sinus, and the aortocaval recess. Why is
D. Aortocaval pericardial sinus the anatomy of the pericardial sinuses relevant to the car-
E. Right upper pulmonary vein diac electrophysiologist? Epicardial ablation in the oblique
sinus may be required for certain patients with atrial fibril-
Answer: B—Transverse pericardial sinus
lation, either for autonomic modifications or ablation of
In the LAO projection, the catheter’s course (black arrow) the vein or ligament of Marshall. The transverse sinus may
can be traced back to the subxiphoid region. Note that the need to be entered for an ablation procedure that involves
catheter was inserted into the pericardial space using a subxi- the left atrial roof. It is equally important for ablationists to
phoid approach. In the LAO view, the catheter appears to take know which cardiac structures are not accessible from the
a similar course as the coronary sinus, but then it is clearly at transpericardial root.
Figure C2.3
To fully comprehend the catheter position shown in are continuous with each other (reflected), the exact sites
Figure C2.2, the operator must visualize the pericardial at which this transition occurs posteriorly is what makes
space and understand the fluoroscopic correlation for the the pericardial space somewhat complex. The simplest sce-
recesses in this area. At fi rst glance, the pericardial space nario would be to examine the posterior aspect of the heart,
in Figure C2.3 appears to be a simple virtual space between where a similar pericardial reflection occurs on the aortic
the visceral layer of the pericardium and the parietal layer, and pulmonary trunk. What complicates the situation,
which has been opened. The anterior surface of the right however, is that the inferior vena cava, superior vena cava,
ventricle and RVOT are seen, as well as the proximal por- and pulmonary vein also need to come from an extraperi-
tion of the great arteries. A catheter that enters the pericardial course to an intrapericardial location as they drain
cardial space anteriorly can freely move in this space; it into the heart. These structures split the pericardial space
is limited superiorly only by the reflection of the pericar- into various recesses that must be fully considered when
dium, about 2 cm from the root of the aorta and pulmonary manipulating catheters in the pericardial space for ablation
artery. Because the visceral and parietal pericardium layers procedures.
Case 2 249
Figure C2.4 (Adapted from Gray H. Anatomy of the Human Body. Philadelphia: Lea & Febiger, 1918; Bartleby.com, 2000. www.bartleby.
com/107/. Used with permission.)
The posterior surface of the pericardium is depicted in The 3-dimensional anatomic relationships of the trans-
Figure C2.4. Note that the pulmonary veins and the vena verse sinus are important for operators to understand when
cava pierce the pericardium, causing separate visceral pari- performing ablations via a transpericardial route. Note that
etal reflections other than the single reflection seen anteri- the transverse sinus is posterior to the ascending aorta and
orly. The space between the right and left pulmonary veins main pulmonary artery. Medially (rightward), it is limited by
is separated from a pericardial recess (the transverse sinus, the pericardial reflection associated with the superior vena
which is superior to the superior pulmonary veins) by sepa- cava. Laterally, it is continuous with the main pericardial
rate visceral parietal reflections directly adjacent to the supe- space seen anteriorly in Figure C2.3. Inferiorly, it is separated
rior pulmonary veins. from the oblique sinus by the pericardial reflections directly
In all, there are essentially 4 pericardial recesses: 1) between adjacent to the upper pulmonary vein.
the pulmonary veins and below the reflection, directly adja-
If a catheter is placed on the floor of the transverse sinus
cent to the superior pulmonary veins (this is the oblique
in the pericardial space, what structure will be ablated if
sinus); 2) a recess above the line of the superior pulmonary
radiofrequency energy is delivered?
veins and continuing laterally on the left side with the peri-
A. Anterior wall of aorta
cardial space (this is the transverse sinus); 3) the pericardial
B. Bachmann bundle region
reflection and recesses to the right of the right-sided pulmo-
C. Vein of Marshall
nary veins and superior to the superior vena cava; and 4) a
D. Right atrial appendage
small pericardial recess between the transverse sinus and the
lateral recess between the aorta and superior vena cava (this
is the aortocaval recess or sinus). Answer: B—Bachmann bundle region.
Ao
Ao
PA
PA
LA
Anterior view Left lateral view

Figure C2.5
A normal heart, dissected to display the transverse sinus in artery. By going lateral to and above the left atrial appendage,
the anterior and left lateral views, will help clarify the answer the catheter will be on the roof of the left atrium. The roof of
to the question above. In Figure C2.5, note that in the lateral the left atrium has specifically directed fibers (the Bachmann
view, the arrow points to the transverse sinus. Again, the ante- bundle) that are continuous with the right atrium across the
rior wall of this region is formed by the posterior wall of the roof of the interatrial septum. Thus, ablation on the floor of
pulmonary artery and aorta (in the anterior view, a red rod the transverse sinus is one way to ablate the epicardial por-
is in the transverse sinus). Thus, ablation performed within tion of the Bachmann bundle. If the catheter is moved more
this space cannot injure the anterior wall of the aorta. In both rightward, the pericardial reflection behind the aorta can be
views, it is evident that the floor of this space constitutes the broken with gentle pressure, and the catheter can come back
roof of the atria, specifically the left atrium and interatrial out to the right side of the pericardial space. However, there
septum. Note that for a catheter to enter the transverse sinus is a thin, limiting pericardial reflection medially (rightward)
from the pericardial space, it must go lateral to (the outside that does not exist laterally (leftward). Notice that the vein of
of) the left atrial appendage and then behind the pulmonary Marshall has no relationship to the transverse sinus.
Case 2 251
Superior
Right Left
Inferior
Ao
LPA
LPA
SVC
SVC RPA
RPA
Transverse
sinus
Recess
Recess
Ao
Recess
Recess
LAO
Figure C2.6
Figure C2.6 shows the catheter position (LAO view) atrial roof (it is a likely target site for ablation if cannulat-
relative to the transverse sinus. Note that the diagram ing the transverse sinus). Otherwise, inadvertent damage
shows the aorta transected to expose the transverse sinus. can occur to the pulmonary artery superiorly or the pos-
The arching common pulmonary artery bifurcates into terior wall of the aorta anteriorly. Pericardial reflections
the right and left pulmonary arteries and forms the roof associated with the superior vena cava and the superior
of the transverse sinus. Ablation, when performed in the aspect of the pulmonary veins limit the transverse sinus
transverse sinus, must be directed downward to the left medially.
Figure C2.7 shows the superior view of the normal heart
and highlights the close relationship between the superior
vena cava and the lateral wall of the ascending aorta. Th is
also shows the pericardial recesses in relation to these struc-
tures. The medial wall of the superior vena cava is immedi-
ately adjacent to the lateral wall of the ascending aorta. Th is
anatomic fact gives rise to some important electrophysiologic
findings. First, medial perforation of the superior vena cava
can involve puncture of the aortic wall (eg, during transseptal
puncture and placement of the transseptal sheath more supe-
riorly). Second, a mapping catheter placed at the junction of
the superior vena cava and right atrium medially will pick up
far-field ventricular potentials from the left ventricular out-
flow tract (LVOT), close to the junction with the aortic valve.
Third, it is difficult to access the transverse sinus for ablation
LAA from a catheter route via the right atrial appendage or lateral
wall of the aorta. Important ganglionated cardiac plexuses
are in this small space between the trunks of the superior
RAA vena cava and ascending aorta.
In Figure C2.7, the yellow arrow points to the posterior
portion of the aortocaval sinus. We observe that this peri-
cardial sinus is cranial to the transverse sinus (white arrow),
and these 2 sinuses are separated by the right pulmonary
artery (aortocaval sinus cranial to the right pulmonary
Figure C2.7 artery).
If an ablation catheter is manipulated to the posterior D. Inappropriate sinus tachycardia

aortocaval sinus (Figure C2.7, yellow arrow), which of E. A and C
the following may be ablated when energy is delivered to F. B and D
this site? Answer: E—A and C (an automatic tachycardia in the pre-
A. An automatic tachycardia in the precaval bundles caval bundles and a ganglionated autonomic plexus).
B. The esophagus
C. A ganglionated autonomic plexus
SVC AZV
Aortocaval recess Precaval bundle
Pectinates
Transverse sinus
RPA
Ao
LA
Eustachian valve
Figure C2.8
Again, the aortocaval sinus is located between the poste-

rolateral wall of the aorta and the posteromedial wall of the
Phrenic nerve superior vena cava. A better understanding of the immediate
relationship of a catheter placed in this site can be obtained by
SVC Parasympathetic
reviewing Figures C2.8 and C2.9.
efferents
The left panel of Figure C2.8 shows an oblique section
Azygos through the aortocaval recess. The aortocaval recess is sep-
arated from the transverse sinus via the right pulmonary
artery. The right panel shows the internal structures in the
right atrium at the superior vena caval–right atrial junction.
Pericardial The pectinate muscles all insert into the longitudinal ridge,
reflection the crista terminalis. The crista terminalis is considerably
lateral to the location of the aortocaval recess. The superior
RA limit of the crista terminalis epicardially is the sinus node,
and thus, the sinus node is not expected to be ablated when
energy is delivered via a catheter in the aortocaval recess. The
precaval bundle, considered a medially oriented pectinate
muscle at the ostium of the superior vena cava, may some-
times be an origin of tachycardia, and if an epicardial focus
Figure C2.9
Case 2 253
at this site was diagnosed, treatment would be ablation in the Figure C2.10 shows the RAO projection in a patient under-
aortocaval recess. going ablation for atrial fibrillation. This patient had 2 prior
As for the nerves associated with the superior vena cava, ablation procedures but still was symptomatic, with docu-
both the anterior and posterior portions of the aortocaval mented arrhythmia. The coronary sinus catheter was placed
recess have parasympathetic efferents and plexinated ganglia via the internal jugular venous route. The yellow arrow points
(Figure C2.9). The phrenic nerve in its usual course, however, to a circumferential mapping catheter, placed at the ostium of
tends to be more lateral and typically is not injured when the right upper pulmonary vein.
ablating in the aortocaval recess.
A multielectrode catheter (Figure C2.10, black arrow) was
Because the pericardial reflection is at varying distances
used for mapping the atypical atrial flutter after ablation.
from the superior vena caval–right atrial junction, perfo-
Where is this catheter located?
ration of the superior vena cava (eg, from lead extraction
A. Posterior wall of right atrium
procedures, ablation for an extrapulmonary focus of atrial
B. Posterior wall of left atrium
fibrillation, etc) does not always result in a pericardial eff u-
C. Transverse pericardial sinus
sion. If sudden hypotension is noted when manipulating or
D. Oblique pericardial sinus
ablating in the region of the superior vena cava, the absence of
E. Right inferior pulmonary vein
a marked pericardial eff usion does not exclude a potentially
life-threatening exsanguination from a superior vena caval Answer: D—Oblique pericardial sinus.
perforation. The course of the multielectrode catheter (Figure C2.10,
The esophagus is located more immediately to the posterior black arrow) shows that it does not reach this sinus via either
wall of the left atrium, posterior surface of one or more pul- the jugular vein (superior) or the femoral vein (note the other
monary veins, and the coronary sinus. However, it typically is catheters approaching the heart from an inferior route).
not in close proximity to a catheter in the anterior or posterior Rather, it comes from an anterior location, namely the sub-
portions of the aortocaval recess. xiphoid pericardial approach. After entering the pericardial
space, the catheter is located very posteriorly, with the distal
electrodes overlapping the circumferential mapping catheter
in the right upper pulmonary veins. The posterior pericardial
recess behind the left atrium is the oblique sinus. Catheters
placed in the oblique sinus will be between the right and
left pulmonary veins and also between the posterior wall of
the left atrium (anteriorly) and the esophagus (posteriorly).
Occasionally, a typical atrial flutter will require ablation or
mapping from the oblique sinus. A more common (but also
rare) reason to enter the space is to ablate the structure on its
left ward or lateral limit, which is the pericardial fold associ-
ated with the left pulmonary vein; this area is rich in auto-
nomic innervation and often is the location of the ligament
of Marshall.
Figure C2.10
Details of the oblique sinus are shown diagrammati-

cally in Figure C2.12. Note the separation of the oblique
sinus from the transverse sinus by the pericardial reflection
directly adjacent to the superior pulmonary veins; note also
the small additional recesses of pericardium (left pulmonary
recess, right pulmonary recess, etc) between the pulmonary
veins. Unlike catheter placement in the transverse sinus
(Figure C2.2), minimal catheter manipulation is required to
reach the oblique sinus after the pericardial space is entered.
Ao Eso
LSPV
RSPV
LA
LIPV RIPV
Figure C2.11
Figure C2.11 shows the posterior surface of the pericar-

dium with the heart removed. Note the parietal pericardium
between the orifices of the pulmonary veins (3 in this case).
Immediately posterior to the oblique sinus in some locations Figure C2.13
would be the esophagus.
Figure C2.13 is a reconstructed, computed tomographic

(CT) image that shows the relationship of the esophagus to
Superior the posterior wall of the left atrium and the pulmonary vein.
In this example, the esophagus appears closer to the left
Ao Right Left
lower pulmonary vein. However, the exact site of the esopha-
Inferior gus varies, not only between patients, but in a given patient
Superior at different times (because of peristalsis, left atrial size, etc).
sinus
Separating the esophagus from the posterior wall of the
LPA left atrium is a variable amount of extracardiac fat and the
SVC RPA
Transverse oblique pericardial sinus.
PCR sinus
The atrioesophageal fistula is among the most feared com-
Oblique LPVR plications of ablation in the endocardial surface of the posterior
RPVR sinus
wall of the left atrium. Ablation in the oblique sinus itself should
proceed with extreme caution. In general, only bipolar ablation
(between an epicardial and endocardial electrode) should be
IVC
considered when ablation in the oblique sinus is required.
Figure C2.12
Case 2 255
Figure C2.14 (Adapted from Doll N, Borger MA, Fabricius A, Stephan S, Gummert J, Mohr FW, et al. Esophageal perforation during left
atrial radiofrequency ablation: Is the risk too high? J Thorac Cardiovasc Surg. 2003 Apr;125[4]:836–42. Used with permission.)
Figure C2.14 is obtained from a report describing a fatal E. Use of CT imaging to define the location of the esophagus
atrial esophageal fistula formation. In the left panel, the F. None of the above
white arrow shows free air in the mediastinum. Histologic Answer: F—None of the above.
details of the fistula’s tract are shown in the right panel
(hematoxylin and eosin; original magnification × 25). Single Various methods are used during atrial fibrillation abla-
arrow indicates intact tissue; double arrows indicate the tion to try and prevent atrioesophageal fistula formation.
injured area. However, no method to date has been shown to completely
prevent this dangerous complication.
Which method could prevent atrial esophageal fistula for- Clearly, early recognition of fistula formation is important
mation during ablation for atrial fibrillation? to prevent death. Any complaint of dysphagia or odynophagia
A. Placement of a temperature probe in the descending after atrial fibrillation should be taken seriously, and appro-
aorta priate imaging studies should be performed. The presenting
B. Placement of a temperature probe in the lumen of the syndrome may be one of infection or systemic embolism.
esophagus Any presentation after left atrial ablation consistent with
C. Watching for refractile microbubbles with ultrasonog- endocarditis should prompt a rapid investigation for atrio-
raphy when ablating on the posterior wall of the left esophageal fistula formation. Either air embolism (esophageal
atrium to atrial air) or embolism attributable to endocarditis may
D. Watching for pericardial eff usion in the oblique sinus also be the initial clinical indication of atrioesophageal fistula
with intracardiac ultrasonography formation.
Aortic
arch
LB
Asc RPA
aorta
Eso
LA Desc
aorta Figure C2.16
Figure C2.15
Most methods to prevent esophageal damage during abla- The sagittal CT image (Figure C2.16) shows compression
tion involve temperature monitoring, either on the endocar- of the posterior left atrium onto the esophageal lumen (arrow).
dial electrode or in the esophagus. Figure C2.15 shows the Importantly, the considerable thickness of the esophageal
intimate anatomic relationship of the posterior left atrial wall wall is also visible in this section. Thus, a temperature sensor
and the esophagus. Note that the descending aorta is separated in the esophageal lumen would detect a temperature increase
from the left atrium by the esophagus. An ablation catheter only after significant heating of the anterior esophageal
placed epicardially on the roof of the left atrium (transverse wall. In addition, the esophageal probe requires continuous
sinus) may also be relatively close to the esophagus if the repositioning to the appropriate site of endocardial ablation.
catheter inadvertently is directed posteriorly during abla- Damage to the esophageal arterial supply, by heating the
tion. The thin virtual space (oblique sinus) is hardly visible in exterior surface of the esophageal wall anteriorly, potentially
Figure C2.15, but it is between the left atrium and esophagus; contributes to infarction and the damage that leads to fistula
it should be clear that ablation via a catheter placed in this development. Altogether, intraluminal esophageal tempera-
pericardial recess would have a high risk of causing collat- ture monitoring has limited effectiveness in the prevention of
eral damage to the esophagus. A temperature probe placed in fistula formation.
the descending thoracic aorta obviously would be completely
ineffective in monitoring for esophageal damage during left
atrial ablation. Even placement of an intraesophageal luminal
probe has considerable limitation.
Case 2 257
Blood Tissue
Direct injury
Bubbles
Blood vessels
cooling
Tip Tissue
temperature temperature
Catheter
Thermal injury
Blood flow
cooling
Figure C2.17
Other methods intended to minimize esophageal ther- 120

mal damage include endocardial temperature sensing and Impedence (Ω)
100
intracardiac ultrasonography. Figure C2.17 illustrates
some of the important biophysical and ultrasonographic Tissue
80 temperature (°C) >20°C
phenomena relevant to distant structures (ie, the esopha-
Units
gus) with temperature-controlled ablation. To measure 60

temperature, either a thermistor or thermocouple is 40 Tip temperature (°C)
located at variable distances from the catheter tip of the
distal electrode. Refractile microbubbles may be observed 20
with intracardiac ultrasonography during radiofrequency
Power (W)
0
energy delivery. Certain bubble types (eg, coarse and per-
0 20 40 60 80 100 120
fused) precede impedance rise and formation of coagulum
or char, but they are not correlated with depth of tissue Seconds
heating. Thus, the presence of microbubbles during abla- Figure C2.18 (Courtesy of D. L. Packer, MD, Mayo Clinic,
tion has no bearing on whether the esophageal wall or Rochester, Minnesota. Used with permission.)
luminal heating is occurring. Similarly, significant dis-
crepancies have been observed between the temperature Figure C2.18 shows the relationship between tip tempera-
measured from the distal electrode sensor (provides feed- ture (measured from the distal electrode) and tissue tempera-
back for control of power delivery) and actual tissue heat- ture; in this example, the differences exceeded 20°C. Therefore,
ing at various distances within the myocardium or into even if the temperature limit is set for 55°, if the electrode is suf-
surrounding structures. ficiently cooled, the tissue temperature may be 75°C or higher.
160
120 Impedence (Ω)

Units
80
Esophagus, external wall (°C)
Catheter tip (°C)
40
Esophagus, intraluminal (°C)
Power (W)
0
0 20 40 60 80 100 120
Seconds
Figure C2.19 (Courtesy of D. L. Packer, MD, Mayo Clinic,
Rochester, Minnesota. Used with permission.)
A canine experiment used an irrigated tip catheter to per-

form ablation in the posterior left atrium. Figure C2.19 shows
the differences between catheter tip temperature, intralumi-
nal esophagus temperature, and esophageal external wall
Figure C2.20
temperature. Note the considerable heating of the external
wall (and associated vasculature) of the esophagus, without
clear evidence of increased temperature from the catheter tip
or the intraluminal probe. Various mapping systems, used to aid identification of the
course of the esophagus, may help prevent esophageal dam-
age during posterior left atrial ablation. (The more specific
uses of mapping systems in atrial ablation are discussed in
Chapter 3.) Figure C2.20 shows an electroanatomic image
fused with CT data of the pulmonary veins and posterior left
atrial wall (posteroanterior view). The black dots represent
the course of the esophagus, determined by a mapping cath-
eter placed in the esophagus. The red dots represent ablation
lesions, placed in a wide circumference around the pulmo-
nary vein. Although such imaging modalities potentially can
minimize collateral damage to the esophagus during abla-
tion, several limitations should be acknowledged. First, the
esophagus is a dynamic structure that may change position
during the procedure. Second, changes in the free load sta-
tus of the patient during ablation will alter the relationship
between the left atrium and esophagus, as well as the left
atrial geometry used to create these maps. Third, the lumen
of the esophagus may not be the best marker to use when
trying to avoid damaging the anterior wall and associated
vasculature.
Case 2 259
LA
PA
Figure C2.21
Although refractive microbubble visualization with the oblique pericardial sinus. When ablation is performed
intracardiac ultrasonography is not particularly useful on the left atrial posterior wall, hyperechoic tissue changes
as a preventive measure (ie, as a precursor of esophageal will be seen on the atrial myocardium itself. Transmural tis-
damage), the esophagus itself can be visualized posterior sue changes, signifying lesion creation, are an appropriate
to the left atrium. The linear, phased-array, intracardiac end point for ablation at a particular site on the posterior
ultrasound probe should be placed more anteriorly in the left atrium. If further tissue heating occurs from contin-
right atrium (closer to the tricuspid valve) and angled pos- ued power delivery, tissue changes in the oblique sinus and
teriorly to visualize the posterior wall of the left atrium and anterior wall of the esophagus may be observed, suggesting
the esophagus (Figure C2.21, black arrow). The small echo- unwanted heating or damage beyond the epicardial limit of
lucent space between the esophagus and the left atrium is the left atrium.
Figure C2.22
Sometimes, a pericardial eff usion specifically involving is noted or if a small oblique sinus pericardial eff usion
the oblique sinus may be seen (Figure C2.22). Th is poten- develops.
tially may progress to a more circumferential pericardial Thus, although many of the answer choices for the
eff usion. Thus, another method to survey for esophageal question after Figure C2.14 are used and are potentially
injury would be careful ultrasonographic monitoring of effective in preventing esophageal atrial fistula forma-
the posterior left atrial wall; energy delivery should be ter- tion, no technique can reliably avoid esophageal damage
minated if a change in echodensity in the oblique sinus altogether.
Figure C2.23
Figure C2.24
Figures C2.23 and C2.24 are electrocardiograms obtained C. Patient 2—the morphology suggests a LVOT origin
from 2 patients with symptomatic ventricular tachycardia. D. Patient 2—the morphology suggests an exit on the left
Patient 1, in Figure C2.23, was a 48-year-old woman with ventricular free wall
exercise- or emotion-related rapid tachypalpitation. The pal- E. None of the above
pitations were associated with severe presyncope on several
Answer: E—None of the above.
occasions. Patient 2, in Figure C2.24, was a 62-year-old man
with a history of coronary artery disease but no prior myo- With regard to epicardial ablation for arrhythmia, a deci-
cardial infarction. sion must be made about pericardial access before catheter
manipulation or ablation in the left ventricle. Currently,
Which patient’s arrhythmia is likely to be treated success- access to the pericardium via a subxiphoid approach is per-
fully with epicardial ablation? formed preferably without anticoagulants. Because of this,
A. Patient 1—the morphology suggests a LVOT origin the operator must reasonably judge whether epicardial access
B. Patient 1—the morphology suggests a left ventricular would be worthwhile (ie, whether the likely benefit outweighs
apical “slow zone” the risk) for a given patient.
Case 2 261
Several factors should be considered when making such epicardial access is unlikely to be worthwhile. Note also in
a decision. First, if the patient has multiple prior infarctions Figure C2.24 that the retrograde P wave (arrow) occurs with
or multiple prior attempts at endocardial ablation, the likeli- a very short R-P interval, and further, that the initial upstroke
hood of requiring epicardial mapping or ablation is relatively of the QRS complex is fairly sharp and relatively normal look-
high. Second, if the patient has undergone one or more surgi- ing. These characteristics suggest an origin close to or within
cal bypass procedures, mapping within the pericardial space the cardiac conduction system (fascicular tachycardia). With
may be difficult, and the catheter may not be manipulated most of the cardiac conduction systems being subendocar-
easily to the required site for ablation. Th ird, the electrocar- dial, epicardial ablation or mapping would be unnecessary
diogram during tachycardia should be analyzed carefully to and ineffective.
exclude certain morphologies that suggest either a septal or Thus, after analysis of these electrocardiograms, the abla-
LVOT origin or fascicular origin that would likely limit the tionist typically would not need to obtain epicardial access
usefulness of epicardial ablation. Finally, certain clues from before initial mapping and attempts at ablation endocardi-
the endocardial map before ablation should raise the clinical ally. Beyond the electrocardiogram, careful analysis of infor-
index of suspicion for an epicardial exit or slow zone (for a mation obtained from mapping (either point-to-point or with
reentrant arrhythmia). a mapping system) may give important clues about whether
Again, examine the electrocardiograms in Figures C2.23 epicardial mapping or ablation is likely to be required.
and C2.24. Neither electrocardiogram indicates whether The following features from mapping should alert the elec-
the mechanism is reentrant (with the successful ablation trophysiologist to a possible epicardial origin (slow zone) for
site being the slow zone of the circuit) or automatic. Rather, tachycardia:
the vector (morphology) of the QRS during tachycardia indi-
cates the exit site (if it were a reentrant tachycardia) or the site 1. The endocardial map shows several areas to be equally
of origin (if the mechanism was abnormal automaticity). early, relative to a fi xed reference. When mapping the
The electrocardiogram in Figure C2.23 has a clear right adjacent cardiac chamber (left ventricle, right ventricle,
bundle branch block–type morphology, with a tall R wave in etc) and no significantly earlier site is found, the epicar-
lead V1. This strongly suggests an origin (exit) in the left ven- dium should be mapped.
tricle. Leads II, III, and aVF are all positive, suggesting a supe- 2. Concealed entrainment cannot be found endocardially
rior origin (exit) for the tachycardia. A superior origin may be with a stimulus-to-QRS-onset interval between 20%
associated with sites on the anterior wall of the left ventricle or and 60% of the tachycardia cycle length (see Chapter 5
the LVOT. Note further that the QRS is negative in the basal for details).
lead aVR but positive in the apical lead V4. This excludes an 3. High-output pacing (from an endocardial site) is
apical or near-apical origin for the tachycardia and suggests required to reproduce an adequate “pace map” of the
the origin is in a more basal location or the outflow tract. Thus, tachycardia. When lower-output pacing is performed,
this tachycardia has either a LVOT or an anterior mitral annu- the paced morphology appears different.
lar origin (exit). Furthermore, a QS complex (negative QRS) is 4. High-output pacing (from an endocardial site) is
seen in leads aVR and aVL. This strongly suggests an origin for required to demonstrate concealed entrainment,
the tachycardia in the LVOT (infra- or supra-aortic valvular despite the fact that with low-output pacing, capture
or aortic mitral continuity). As discussed below, there is no does occur (not within a scar).
method of ablating the LVOT via a pericardial route because It is important to obtain separate maps of the endocardium
the LVOT is below (posterior to) the RVOT. Thus, given this and epicardium so that activation times, pace map results,
morphology for tachycardia, epicardial mapping or ablation is and entrainment results can be compared. If only epicardial
highly unlikely to be required. mapping is performed, the reverse error may occur (ie, fail-
Now examine the electrocardiogram during tachycar- ing to recognize the true early site or slow zone in the mid
dia in Figure C2.24. Here again, note a right bundle branch myocardium or endocardium). In an automatic tachycar-
block–like morphology (tall R wave in lead V1), virtually dia, simultaneous endocardial and epicardial mapping near
diagnostic of origin in the left ventricle. The strong posi- the early site of activation is important when endocardial
tive concordance (R waves in V1 through V6, as also seen in energy is being delivered, unless the epicardial site is clearly
Figure C2.23) would exclude an apical origin (exit) for the earlier. Epicardial ablation is more difficult to perform
tachycardia. The electrocardiogram does not show the char- because the coronary arteries may be injured and adequate
acteristic vector of LVOT origin (no strong positive R waves energy delivery in the closed pericardial space is challeng-
in leads II, III, and aVF, and aVL is not negative). Thus, at ing. Radiofrequency power delivery of greater than 10 watts
this point in the analysis, a mitral annular origin (exit) for often is difficult to achieve during temperature-controlled
the tachycardia is likely. However, lead I is all positive, thus ablation. Closed- or open-tip irrigation, cryoablation, or
excluding a free-wall origin (exit) for the tachycardia. A basal mechanical irrigation of the pericardial space to mimic
septal origin is likely. Because no epicardial access is avail- blood flow have been used to increase power delivery, result-
able to map or ablate the interventricular septum, obtaining ing in a better lesion.
With reentrant ventricular tachycardia, the operator may

have to consider epicardial ablation if repeated endocardial
ablation attempts have failed. Figure C2.26 shows a bipolar
voltage map (created using the electroanatomic mapping
system). The patient had a large, inferior-wall, myocardial
infarction and a mitral annular ventricular tachycardia
(isthmus tachycardia). The use of voltage maps in ablation
procedures for reentrant ventricular tachycardia is discussed
in detail in Chapter 3. In this example, a large area of poor
(small-amplitude) bipolar signals are displayed in red (red
dots are sites of ablation lesions). Multiple sites within this
zone showed concealed entrainment of the induced ven-
tricular tachycardia morphology. The ablationist decided
to perform a linear ablation that transected the scar and
attempted to anchor these lesions to the mitral annulus (to
eliminate the large slow zone). This approach is different
from the approach that connects scars or slow zones (dis-
Figure C2.25
cussed further in Chapter 3). Options to consider if this
approach fails include encirclement of the scar or epicardial
ablation to obtain transmural lesions through the slow zone
Figure C2.25 shows the epicardial activation sequence in for tachycardia.
a patient with an automatic ventricular tachycardia. In this Although epicardial ablation may be strongly consid-
electroanatomic map, the earliest site of activation is on the ered in several scenarios, the common practice is to first
posterolateral mitral annular region. An electrocardiogram attempt endocardial ablation whenever possible because
obtained during such a tachycardia would have a similar pre- of the difficulties associated with adequate energy deliv-
cordial lead access, as shown in Figure C2.24; however, both ery and the need for coronary angiography before and
leads I and aVL should be negative (QS complex). Epicardial sometimes during ablation to avoid damage to the arterial
ablation should be strongly considered (despite the limita- system.
tions described above) to eliminate the tachycardia focus
For the patient whose electroanatomic map is shown in
mapped in Figure C2.25.
Figures C2.25 and C2.26, which option is least likely to
be effective in ablating the presumed epicardial focus
(Figure C2.25) or slow zone (Figure C2.26) for the patient’s
tachyarrhythmia?
A. Using the coronary venous system for ablation
B. Using an 8-mm-tip catheter or an open-irrigation cath-
eter and ablating from an endocardial site
C. Increasing the duration of radiofrequency energy deliv-
ery from an endocardial site
D. Pericardial access via a subxiphoid approach
Answer: C—Increasing the duration of radiofrequency
energy delivery from an endocardial site.
When endocardial ablation is unsuccessful, either endo-
cardial ablation should continue or epicardial ablation should
be performed to increase the depth of the lesion.
Figure C2.26
Case 2 263
delivery. Furthermore, by increasing lesion depth, the area of

endothelial denudation necessarily increases, making a poten-
tial surface for thrombus formation. As seen in Figure C2.17,
the primary goal is tissue heating at varying distances from
where the “tip temperature” is being measured. To accomplish
this, significant power has to be delivered via the catheter.
After tissue electrode contact has occurred, power deliv-
ery can be limited by several factors. First, if the electrode is
located at a site of poor blood flow or wedged into the myo-
cardium (papillary muscle, pectinate, etc), the electrode may
heat very quickly, and power delivery will be limited with
temperature-controlled ablation. Second, any coagulum that
forms on the electrode surface will cause a quick rise in temper-
ature or impedance (or both), thereby limiting power delivery.
Methods to increase the amount of power delivered (and
thus the depth of the lesion) essentially are methods to cool the
Figure C2.27 (Courtesy of D. L. Packer, MD, Mayo Clinic,
catheter tip. An electrode with a larger surface area (8-mm tip
in the above question) or an electrode with open or closed irri-
gation can be used. Paradoxically, if the tissue electrode sur-
Although issues regarding lesion depth are germane to abla- face size increases without a corresponding increase in power,
tion at all cardiac sites, left ventricular ablation is of particular smaller lesions may be created because of a decrease in charge
concern. Figure C2.27 is a cross-section of a canine ventricle density. Lesions from open-irrigation tips can increase tissue
that illustrates some of the issues discussed. Note that the left depth and volume with less risk of coagulum formation, but
ventricle, particularly with normal myocardium, is thick; it endothelial denudation and failure to reach the epicardium
is often deeper than lesions created with high-power energy with lesion creation remain problematic (Figure C2.27).
Duration Dependence of
Left Ventricular Radiofrequency Lesion Dimensions at 25 Watts
10 7.14±2.63 15 800
7.25 388
± 9.50 ±
1.26 6.70 ± 286
6.50 ± 2.65 9.72
8 ± 0.97 ±
1.00
6.89
1.16 600 235
8.13 ±
4.75 ± ± 289
10
Diameter, mm
Volume, mm3
± 2.39 1.11 336

Depth, mm
6 0.96 ±
93.5
4.25 400 233
±
± 86.1
4 1.26
5
200 51.9
2 ±
41.9
0 0 0
5 10 20 30 60 5 10 20 30 60 5 10 20 30 60
Seconds Seconds Seconds
n= 4 11 4 4 5 n= 4 11 4 4 5 n= 4 11 4 4 5
Figure C2.28 (Data from Simmers TA, Wittkampf FHM, Hauer RNW, Robles de Medina EO. In vivo ventricular lesion growth in
radiofrequency catheter ablation. Pacing Clin Electrophysiol. 1994 Mar;17[3 Pt 2];523–31.)
Increased duration of energy delivery theoretically can Although epicardial ablation necessarily occurs via
result in a larger lesion. However, Figure C2.28 shows that subxiphoid pericardial access, other options remain. A
the lesion depth, diameter, and volume plateau rather quickly still-investigational technique is to purposely perforate the
when simply increasing the duration of energy delivery. Thus, right atrial appendage to gain access to the pericardial space.
if power is kept constant, increased duration of energy deliv- However, a method with a long clinical history is to use the
ery will not improve ablation of an epicardial focus or slow cardiac venous system to ablate epicardial foci.
zone from an endocardial catheter.
Several features of the cardiac venous anatomy can be

noted in Figure C2.29. First, the heart has fairly large veins
on all surfaces of the ventricle. Second, significant collateral
veins are located among the major veins, but they generally
are smaller in size. Third, the veins do not necessarily fol-
low the exact course of the arteries; thus, some ablations can
be performed from a vein without endangering the arterial
vasculature. Nevertheless, as observed in the biventricular
pacing practice, not all sites of ventricular myocardium have
sufficiently large veins that allow placement of an ablation
catheter (or pacing electrodes).
Figure C2.29
Posterolateral vein
3.8 ± 2.1
major branches
Coronary
sinus
Anterior
interventricular vein
Middle
cardiac vein
Figure C2.30 (Adapted from Asirvatham SJ. Biventricular device implantation. In: Hayes DL, Wang PJ, Sackner-Bernstein J, Asirvatham SJ,
editors. Resynchronization and defibrillation for heart failure: a practical approach. Oxford [UK]: Blackwell Publishing; c2004. p. 99–137.)
Figure C2.30 is an idealized image of ventricular venous Which branch of the coronary vein should be cannulated to
anatomy, based on our observations from approximately 600 reach the target site for ablation?
human hearts. Consistently present are large veins that drain A. Middle cardiac vein
the anterior ventricular walls to posterolateral ventricular B. Posterior cardiac vein
walls and the inferior wall. C. Posterolateral cardiac vein
If the epicardial focus for the annular automatic tachy- D. Anterior intraventricular vein
cardia is ablated epicardially (see electroanatomic map in E. Any of the above
Figure C2.25), options are to use a subxiphoid approach or a F. None of the above
cardiac venous approach. If the patient has previously under- Answer: E—Any of the above.
gone pericardiotomy (surgery) and adhesions are suspected,
the ablationist may decide to use the cardiac venous system.
Case 2 265
LA
CS
PLV
81%
Branch of middle
cardiac vein
Branch of anterior LV
interventricular vein
Left lateral view

Some patients may have a separate vein that drains the C. Via the internal jugular venous route, place the catheter
lateral left ventricular free wall. Often, however, collateral tip on the tricuspid annulus and apply clockwise torque
branches from the main cardiac venous system drain this until the catheter enters the coronary sinus; then apply
region of the heart. In most patients (81% in one series), venous counterclockwise torque while withdrawing the cath-
drainage of the lateral left ventricle is via a large branch of eter until the posterior vein is entered
the posterolateral vein (Figure C2.31); this vein must be can- D. Via the internal jugular venous route, place the catheter
nulated to ablate the focus shown in Figure C2.25. In many tip on the tricuspid annulus, apply counterclockwise
instances, the anterior interventricular venous system or the torque until the coronary sinus is entered; advance the
middle cardiac venous system must be cannulated first and catheter and then, bending the catheter and applying
then a large collateral vein will be subsequently cannulated, clockwise torque, withdraw the catheter until the pos-
and then a catheter will be manipulated through a large col- terior vein is entered
lateral vein to reach the appropriate site on the lateral left ven- E. A and C are correct
tricular free wall. F. B and D are correct
Answer: F—B and D are correct.
Which maneuver is appropriate for cannulating a postero-
lateral or posterior cardiac vein if the electrode is advanced The posterior veins (middle cardiac vein pathways, coro-
via a femoral or internal jugular vein to the heart? nary sinus diverticula, and epicardial ventricular tachy-
A. Via the femoral route, place the tip of the catheter on cardia on the posterolateral mitral annulus) are the most
the tricuspid annulus, apply clockwise torque to enter common cardiac veins that an ablationist should be familiar
the coronary sinus, then apply further clockwise torque with for selection and ablation. These veins can be cannu-
while advancing the catheter to enter the posterior vein lated via either a femoral or jugular (subclavian) approach,
B. Via the femoral route, place the catheter tip on the tri- but different maneuvers are required. The type of torque
cuspid annulus, apply clockwise torque, and advance used is independent of the side of the body that the catheter
the catheter in the coronary sinus; then apply counter- is inserted (eg, right femoral is the same as left femoral) but
clockwise torque while withdrawing the catheter until differs from the inferior (eg, femoral vs superior jugular)
the posterior vein is entered routes.
RAO
A B
Curl and rotate

clockwise
MCV
C D
Pull back to
engage the CS Advance sheath as
catheter is pulled back
Figure C2.32 illustrates techniques used to cannulate right atrium or ostium of the coronary sinus; from this rather
the middle cardiac vein with a deflectable catheter via the “straight” orientation, the catheter tip is advanced deeper
internal jugular venous route (RAO projection). Although into the middle cardiac vein. At this point, the sheath can
a sheath is pictured in conjunction with the catheter in this be advanced when gently pulling back the catheter to enter
example, the technique and maneuvers are the same with a the middle cardiac vein (panel D). This may be necessary to
catheter alone. Note the small, pericardial fat pad, which cre- perform selective angiography of the middle cardiac vein for
ates a radiographic translucency that defines the plane of the the purpose of defining a diverticulum or to identify lateral
atrioventricular (AV) annuli in the RAO view. In panel A, the annular branches that can be used to manipulate the catheter
catheter has been placed fairly deep in the coronary sinus. To to the target site.
enter the coronary sinus from the tricuspid annulus, sharp When the femoral route is used to advance the catheter to
counterclockwise torque is required while withdrawing the the heart, the opposite maneuvers are required. That is, after
catheter. Continued counterclockwise torque will cause can- placing the electrodes near the tricuspid annulus posterosep-
nulation of one of the atrial branches. In panel B, after the tally, clockwise torque is used to enter the coronary sinus, and
catheter tip is free in the coronary sinus, the catheter is made the catheter is advanced into this vein. Now, with anterior
to curl or bend until the distal electrode points to the ventri- curl (pointing to the ventricle in the RAO view) and counter-
cle (anterior in the RAO view). With application of clockwise clockwise rotation, the catheter is gently pulled back until the
torque and a steady curl, the catheter tip is slowly pulled back middle cardiac vein is cannulated. Fluoroscopic techniques
toward the ostium (panel C). Several ventricular veins can be used to identify and confirm cannulation of a coronary vein
cannulated using this technique. If subsequent cannulation are discussed in Chapter 1.
occurs in a vein deeper in the coronary sinus, for which abla- After the coronary sinus has been entered from a femoral
tion is not required, the same maneuver is repeated to fur- route, further application of clockwise torque will cause the
ther withdraw the catheter tip. Eventually, with the anterior catheter to enter an atrial vein. This is important to recognize
curl and clockwise rotation while pulling the catheter back for 2 reasons. First, if the catheter is pushed in further with-
close to the ostium, the catheter will engage the middle car- out realizing that an atrial vein has been selected, coronary
diac vein. After the middle cardiac vein is entered, if a sheath vein dissection may occur. Second, this maneuver is useful
is being used, the sheath initially must be pulled back to the when ablation in an atrial vein is the goal.
Case 2 267
Left atrial appendage
Left superior
pulmonary vein
Vein of Marshall
Left inferior
pulmonary vein
Coronary sinus
Figure C2.33
The most atrial vein that an ablationist may wish to enter Ablation may be performed either within the vein or at the
is the vein of Marshall. Th is remnant of the left superior vena ostium of the vein to isolate any arrhythmogenic tissue. Use
cava drains the left atrium into the coronary sinus, approxi- of atrial veins may be necessary when ablating the plexinated
mately 3 cm from the coronary sinus ostium. The postero- autonomic ganglia found behind the left atrium (necessary in
lateral ventricular vein is often located at the same place but some types of atrial fibrillation ablation). If a posterior atrial
drains the ventricle. After the coronary sinus is cannulated vein is cannulated closer to the ostium (1–2 cm), then this
with a catheter via a femoral route, further clockwise torque vein likely drains the left atrium just anterior to the oblique
is applied to select the vein of Marshall (counterclockwise sinus (Figure C2.33); just as caution is recommended when
torque would be used to select the posterolateral vein). This ablating in the oblique sinus (or posterior left atrium), abla-
vein courses between the left atrial appendage and the ante- tion through a posterior atrial vein should also be done with
rior surface of the left-sided pulmonary veins (Figure C2.33). care to avoid injury to the esophagus.
RAO LAO
Figure C2.34
Figure C2.34 shows the RAO and LAO projections during because of an endocardial ridge that can separate the vein of
ablation in a patient with a vein of Marshall origin for atrial Marshall from the endocardial site. This ridge is between the
fibrillation. The yellow arrow (RAO and LAO views) shows the left atrial appendage and the anterior surface of the left-sided
catheter tip engaging the vein of Marshall. Clockwise torque pulmonary vein.
has been applied to direct the catheter tip in the atrial direc- Sometimes, veins other than those of the coronary sinus
tion (posterior, in the RAO view). In the LAO view, it is not distribution need to be cannulated for mapping and ablation
clear if the catheter (yellow arrow) is engaging a ventricular purposes. This is usually when the coronary sinus is occluded
vein or an atrial vein or if it is still in the coronary sinus (see or cannot be entered for other reasons.
Chapter 1 for details on these fluoroscopic views). The black A 20-year-old man presented with recurrent rapid tachy-
arrow (RAO and LAO views) points to a catheter that is also palpitation. He had a history of multivalvular heart disease
mapping or attempting to ablate the vein of Marshall from and previously underwent aortic and mitral valve replace-
an endocardial route. Note that these catheters overlap in the ment with mechanical prostheses. An atrial septal defect
RAO view but are widely separated in the LAO view. This is (ASD) was repaired with a pericardial patch.
Case 2 269
Figure C2.35
The patient’s resting 12-lead electrocardiogram (Figure wave in lead V1 that is greater in amplitude than the S wave. If
C2.35) was clinically suspicious for preexcitation. What is neither feature is present, a right-sided bypass tract with ante-
the least likely diagnosis? grade conduction is unlikely. Whether conduction is robust in
A. Preexcitation from a left-sided accessory bypass tract an antegrade-conducting, left-sided bypass tract is difficult to
B. Preexcitation from a right-sided accessory bypass tract determine on the 12-lead electrocardiogram. This is because in
C. Prinzmetal phenomenon sinus rhythm, left lateral bypass tracts are sufficiently far away
D. A fasciculoventricular pathway from the originating impulse (in the sinus node) that even
E. A left-sided accessory bypass tract with robust ante- those with good antegrade conduction may present with subtle
grade conduction preexcitation, particularly if AV node conduction is strong.
Answer: B—Preexcitation from a right-sided accessory
Which of the following is not an appropriate method for
bypass tract.
ablation of an accessory pathway on the left free wall of the
Figure C2.35 shows sinus rhythm. The slurred upstroke of mitral annulus?
the QRS complex (delta wave) is best seen in leads II and III. A. Ablations via a catheter placed in the great cardiac vein
This may represent true preexcitation, or it may be a condi- B. Transseptal puncture and endocardial ablation on the
tion that mimics preexcitation (pseudo-preexcitation) such mitral annulus
as fasciculoventricular connections or Prinzmetal phenom- C. Ablation via a catheter placed in the small cardiac vein
enon. Fasciculoventricular tracts are not true accessory bypass D. Ablation via retrograde placement of a catheter across
tracts; they represent a relatively basal exit from the right the aortic valve and on the mitral annulus
or left bundle branch (see Chapter 4 for details). Prinzmetal E. Ablation with a catheter placed epicardially on the
phenomenon is another nonaccessory bypass tract condition mitral annulus via a subxiphoid approach
in which a slurred upstroke to the R wave may be present. In
Answer: C—Ablation via a catheter placed in the small
this situation, antegrade conduction is enhanced through the
cardiac vein.
bundle branch system, again with a relatively more basal exit.
Left ventricular hypertrophy and surgical procedures involv- Several methods commonly are used to ablate left-sided
ing the basal septum may give rise to this phenomenon. The pathways. With increased familiarity with the transseptal
preexcitation status (true vs mimic) cannot be determined on approach, the method described in answer C and a retrograde
the basis of the electrocardiogram alone. In the EP labora- transaortic approach are about equally common when placing
tory, pacing maneuvers as described in Chapter 4 can readily catheters on the mitral annulus for ablation. Occasionally, for
make the distinction. Right-sided bypass tracts with antegrade epicardial pathways, ablation can be performed with a cath-
conduction will have a positive delta wave in lead I or an R eter placed in the coronary sinus and advanced more distally
to the great cardiac vein, close to the mitral annulus. For epi- Although the 12-lead electrocardiogram shown in Figure
cardial pathways, particularly if coronary vein ablation was C2.35 strongly suggests a left-sided accessory pathway, the
unsuccessful (often because of inadequate energy delivery or left atrium must be mapped (using a method described above)
proximity of an artery), subxiphoid pericardial access can be before proceeding with ablation. The arrow in Figure C2.36
obtained and the catheter positioned on the mitral annulus points to a mechanical aortic valve, which precludes retro-
epicardially. The small cardiac vein is a rightward tributary of grade access to map the mitral annulus. The most common
the coronary sinus and arises very close to the coronary ostium method to map the mitral annular region is to place a multi-
(often between the ostia of the coronary sinus and the middle electrode catheter in the coronary sinus. However, when this
cardiac vein). This small vein drains the base of the right ven- procedure was attempted in the patient, only a stump of the
tricle, close to the tricuspid annulus. The small cardiac vein can coronary sinus was observed proximally, with no obvious
be cannulated (with some difficulty) and used to map or ablate reconstitution of the vein more distally. For unknown reasons,
right posterior epicardial accessory pathways. However, this some patients with valvular surgery (in this case mitral valve
vein does not provide access to left lateral accessory pathways. annuloplasty and procedures possibly related to ASD repair)
Accessing a left-sided, free-wall, bypass tract was consid- have abnormalities in the coronary sinus. Abnormalities
erably difficult for this particular patient. Retrograde access is can include coronary vein stenosis, dissection, or abrupt
contraindicated across a mechanical aortic valve. In addition, termination or absence of ventricular venous tributaries. In
a mechanical mitral valve is a relatively strong contraindica- Figure C2.36, the obviously abnormal coronary sinus can be
tion for catheter mapping and ablation in the left atrium (close seen with gentle angiography through an end-hole multielec-
to the valve) for fear of catheter entrapment. Most ablationists trode coronary sinus mapping catheter. In the corresponding
would avoid endocardial manipulation for a patient with a LAO projection (not shown), only about 1 cm of the coronary
Starr–Edwards valve; however, careful catheter manipulation sinus could be visualized or mapped.
(often with intracardiac ultrasonographic guidance) can be At this point, the remaining option for mapping the mitral
performed in a patient with a St. Jude bileaflet valve. annulus and possibly ablating a left-sided accessory pathway
A previous ASD repair can complicate transseptal punc- is to perform a transseptal puncture. As explained above, it is
ture. Initially, ablationists were reluctant to perform transseptal possible but less desirable in patients who have had repair (eg,
puncture on any patient with ASD closure. However, in cur- patch, pericardium, device, or suture) of an ASD.
rent practice, transseptal punctures are performed in patients Sometimes, it can be deduced from the electrograms
with pericardial patch closure of an ASD and across the supe- alone that the pathway (or site of earliest activation for a
rior limbus for patients with Dacron patch closure. Finally, focal arrhythmia) is left sided; this may be deduced from
multiple cardiac surgical procedures are likely to have resulted electrograms recorded on the right side. In other words, if all
in clinically significant pericardial adhesions that would make right-sided potentials occur later than the onset of the delta
epicardial ablation via a subxiphoid approach difficult, if not wave (or later than the surface P wave for an automatic atrial
impossible. Thus, given this patient’s history and the pat- tachycardia), transseptal puncture can be justified in a patient
tern of preexcitation (if present, and if pseudo-preexcitation with previous septal surgery.
is excluded after an EP study), coronary sinus or great artery
ablation may be a strong consideration.
Figure C2.36
Case 2 271
Figure C2.37
The intracardiac electrograms shown in Figure C2.37 are D. Pacing the atrium at cycle lengths shorter than those
highly complex but key to understanding the next step in used to maximize preexcitation does not lengthen the
the ablation procedure. The CS catheter was placed on the interval between the atrial signal and the candidate
cavotricuspid annulus, with the distal electrode (CS 1,2) just potential
engaging the stump of the coronary sinus. The HRA catheter E. All of the above
was on the lateral right atrial wall, close to the superior vena F. None of the above
cava. The HBE catheter was in the usual His bundle loca- Answer: E—All of the above.
tion. The MAP catheter was placed in the anterior fossa ova-
lis region. (Placement of the ABL catheter will be discussed A His bundle potential characteristically is not seen at
shortly.) pacing cycle lengths shorter than the effective refractory
Note that there are at least 5 discernable components period of the AV node (this helps distinguish between His
to the His bundle electrogram. To determine whether all bundle signals and complex atrial signals or pathway poten-
right-sided potentials are late (and thus to justify transsep- tials). The atrial-His interval should increase with shorter
tal puncture), one of these multicomponent signals must be pacing cycle lengths, but if the AV node is already blocked
used to compare timing of the onset of the delta wave on the (maximal preexcitation), the His bundle signal results from
surface electrocardiogram. As described in Chapter 4, the retrograde activation of the His. In this circumstance, fur-
electrophysiologist must symptomatically identify the cor- ther shortening the atrial pacing cycle length will not result
rect interpretation of each signal. The white arrow (HBE 1) in further prolongation of the atrial-His interval (no decre-
points to a potential that was shown to originate from the mentally conducting tissue is between the atrial pacing site
His bundle. and the retrograde His).
The yellow arrow (HBE 3) points to the key signal in this
Which of the following findings from pacing maneuvers case. As discussed in Case 1, sometimes a far-field ventricu-
suggest that the candidate potential indicated by the white lar signal or a pathway potential may occur very close to the
arrow is a His bundle signal? atrial signal; or, as in this patient with previous atrial surgery,
A. The potential is not seen when pacing the atrium at a the potential may represent a complex atrial signal.
cycle length in which AV block occurs A complete method to analyze highly complex electro-
B. The candidate potential is not seen when pacing the grams such as those on the His bundle catheter recording in
atrium at a cycle length with maximal preexcitation Figure C2.37 are reviewed elsewhere (Case 1 and Chapter 4).
C. When pacing the atrium at shorter cycle lengths, the The key component in this case, however, is understanding
interval between the atrial signal and the candidate the nature of the signal on the HBE 3 catheter (yellow arrow).
potential lengthens Given the patient’s history (atrial surgery, etc), this signal
could easily represent a fragmented atrial signal. Or, as illus- pacing maneuvers is that of relative dissociation (answer
trated in Case 1, septal pathways may have an early ventricu- choice C above is an example of such a finding). With atrial
lar signal followed by one or more delayed ventricular signals, extrastimulus testing, there is a delay from the atrial signal
with the first ventricular signal representing myocardial acti- to the candidate potential without a change in the degree of
vation via an accessory pathway. Thus, the key piece of infor- preexcitation. If the candidate signal was ventricular or oth-
mation required before considering higher-risk, left-sided, erwise associated with preexcitation (eg, pathway potential,
catheter placement in this patient is to know whether the etc), then causing a delay to signal activation would cause less
HBE 3 signal (yellow arrow) is atrial or an early component of preexcitation. During ventricular pacing with 1:1 retrograde
a preexcited ventricular signal. conduction, the absence of the candidate signal (Figure C2.37,
yellow arrow) does not exclude a fragmented atrial signal as
Which maneuver and outcome would most likely suggest its cause. This is because the wave front of activation (sinus
that the candidate signal (Figure C2.37, yellow arrow) is rhythm vs retrograde conduction) may be different, result-
a component of the atrial signal and not representative of ing in a different amount of delay between the 2 recorded
ventricular preexcitation? signals.
A. The signal is not seen during junctional ectopic beats Now consider the electrograms recorded by the ABL cathe-
B. Rapid atrial pacing results in loss of preexcitation and ter. The signal on the ABL d catheter (Figure C2.37, red arrow)
loss of the candidate signal had the following characteristics with pacing maneuvers.
C. With atrial extrastimulus testing, the interval between First, the potential was not seen when pacing the atrium at a
the initial atrial signal on the His bundle catheter and rate that produced loss of preexcitation. Second, the potential
the candidate signal increases without a change in the was not seen when pacing the atrium at the rate at which AV
degree of preexcitation block occurred. Third, the potential occurred later when pac-
D. The signal is not seen during ventricular pacing with ing the atrium at a rate that produced less preexcitation or no
retrograde conduction via the accessory pathway preexcitation. These characteristics strongly suggest that the
E. None of the above far-field potential (red arrow) represents ventricular activa-
tion caused by accessory pathway conduction. Further, this
Answer: C—With atrial extrastimulus testing, the interval
signal occurs earlier than any ventricular potential seen on
between the initial atrial signal on the His bundle catheter
the right-sided catheters.
and the candidate signal increases without a change in the
How was this early ventricular activation mapped? As
degree of preexcitation.
mentioned above, the coronary sinus was occluded and ret-
When a junctional beat occurs, conduction is entirely rograde access via the aorta was precluded by the mechani-
through the AV system, and thus preexcitation will be lost. cal aortic valve. We also were reluctant to perform the
If preexcitation persists with a junctional beat, a fasciculo- transseptal puncture through the previously repaired atrial
ventricular tract must be considered (see Chapters 4 and 6). septum unless clear evidence could be attained that showed
The absence of the candidate signal during the junctional ablation would likely be performed in the left side of the
beat does not help distinguish between a fragmented atrial heart.
signal and a ventricular signal associated with preexcita- In some situations, mapping through the extracardiac
tion. During rapid atrial pacing, if preexcitation and the venous system can be helpful to get an approximate idea of
candidate signal are lost simultaneously, the signal likely is the activation pattern of the left side of the heart. Almost
related to preexcitation. However, this phenomenon should universally, the vein used to map the left side is the coronary
be interpreted cautiously because an intra-atrial block to a sinus; however, several other less commonly considered veins
portion of the atrium can generate a fragmented signal dur- can be used. Such veins include remnants of the cardinal
ing rapid pacing, and the loss of preexcitation can occur by venous system, Thebesian vein, azygous vein, and the infra-
chance. As discussed in Chapter 4, a powerful finding during diaphragmatic vein.
Case 2 273
RAO LAO
Figure C2.38
In Figure C2.38, the RAO and the LAO fluoroscopic pro- map or pace the heart is rarely required, the ablationist should
jections illustrate infradiaphragmatic venous mapping with be aware of their existence. If emergent pacing is required,
the ablation catheter. Note the angiographic appearance of for example, in patients with the ventricles excluded from
the infradiaphragmatic venous system (arrows). These veins the systemic circulation (tricuspid atresia, Fontan, etc), these
sometimes are entered inadvertently during biventricular veins can be used for temporary pacing and capture when
pacemaker-related procedures. In the LAO projection, note the patient is intubated and likely will be unaware of inter-
the relative lateral and left ward course of this vein just below mittent phrenic diaphragmatic stimulation. Mapping either
the heart as it is seated on the diaphragm, with some branches the coronary sinus or extracardiac vein has similar value for
very close to the annulus and thus similar in course to the identifying activation patterns and mapping in the pericar-
coronary sinus. When mapping (with high gain settings) was dial space, although catheter manipulation is generally more
performed in this vein, a far-field signal with earlier ventricu- difficult and the mappable areas are more limited when using
lar activation was noted. Although the use of such veins to the venous system.
RAO LAO
Figure C2.39
Figure C2.39 shows the catheter position in a patient with The azygous vein is a large posterior vein that drains the
paroxysmal, symptomatic, narrow-complex tachycardia that posterior mediastinum and empties into the posteroseptal
was eventually diagnosed as a typical AV node reentry. In the aspect of the superior vena cava, typically about 2 cm from the
RAO and LAO projections, the arrows point to an octapolar superior vena cava–right atrial junction. Following the course
catheter. The catheter courses from right to left in the LAO of the catheter in question (RAO view), the catheter clearly
projection and from a ventricular to atrial course in the RAO entered into a more ventricular location at first. Then, as the
projection (distal electrodes close to the coronary sinus, prox- catheter was advanced, it approached and likely entered the
imal electrodes are more ventricular). When the sheath was coronary sinus. In the LAO view, the proximal electrodes of the
placed in the same location, a separate vein was confirmed, octapolar catheter clearly are more cranial, and the vein into
and the octapolar catheter was placed there. which it is being advanced courses more caudal (inferiorly)
as it approaches the coronary sinus. This would be a typical
Which is the least likely vein to place the octapolar course for a type of Thebesian vein that connects the coronary
catheter? sinus to the lumen of the right ventricle (venoluminal vessels).
A. Thebesian vein Thebesian veins more typically connect the intramyocardial
B. Venoluminal vessel capillary network to the lumen of the right ventricle. Rarely,
C. Azygous vein they connect an arterial wall to the right ventricle (atrial lumi-
D. Remnant of a cardinal vein nal vessel). Remnants of the cardinal venous system are more
E. Accessory coronary sinus commonly in the atria but may also occur in a relatively ven-
Answer: C—Azygous vein. tricular location. Thus, all possibilities mentioned in the ques-
tion may be correct, except for the azygous vein.
Case 2 275
RAO LAO
Figure C2.40
The RAO and LAO projections of a patient with supraven- but their importance mainly lies in their being recognized
tricular tachycardia are shown in Figure C2.40 (the case is when entered (ie, distinguishing it from cardiac perforation
discussed in detail in Case 20). The sheath used for contrast or transseptal entry into the left atrium).
angiography was placed in the right atrium. Because a far-field early signal during preexcitation
was identified on the left-sided venous mapping catheter
Which of the following structures is the least likely to be
(Figures C2.37 and C2.38), transseptal puncture was per-
opacified with contrast injection?
formed. As mentioned above, this patient had surgical closure
A. A ventricular Thebesian vein
of an ASD without the use of prosthetic material. Therefore,
B. An atrial Thebesian vein
the region of the fossa ovalis was punctured, similar to a stan-
C. Remnants of the cardinal venous system
dard transseptal puncture.
D. An epicardial atrial vein
Answer: A—A ventricular Thebesian vein. If the patient had a Gore-Tex patch closure or if a mechani-
cal patent foramen ovale closure device was in place, which
As discussed in detail in Chapter 1, the RAO and LAO would be an acceptable method of performing transseptal
views are very important for identification of unusual struc- puncture?
tures. In the RAO view, the coronary sinus catheter (arrow) A. Puncture through the inferior limbus
defines the plane of the annulus. Thus, any structure ante- B. Puncture anterior to the graft or closure device
rior to the annular coronary sinus catheter (closer to the ster- C. Puncture through the superior limbus
num) would be ventricular, whereas structures posterior to D. Puncture through the graft or closure device
the annular coronary sinus catheter (closer to the vertebral E. Transseptal puncture is contraindicated
column) would be atrial. The tip of the sheath clearly is in
Answer: C—Puncture through the superior limbus.
the atrium; thus, the opacified structure is emptying into
the right atrium. The arrows in the LAO view point to likely In patients with a prosthetic closure device or certain types
tributaries of this venous structure that drain the right and of prosthetic grafts, transseptal puncture through the fossa
left atria. This pattern is seen in the LAO projection, which ovalis (the preferred method) is either impossible or inadvis-
helps distinguish between right- and left-sided structures (see able. The fossa is bounded superiorly by relatively thick atrial
Chapter 1). Possibilities include an atrial Thebesian vein (usu- tissue, termed the superior limbus. Because of its thickness,
ally much smaller), remnants of the cardinal venous system it generally is unsuitable for routine transseptal puncture,
(levo-retro-atrial cardinal vein, dextro-retro-atrial cardinal but when puncture through the fossa is contraindicated, the
vein), or an epicardial vein on the roof of the left atrial wall, superior limbus can be targeted (with intracardiac echocar-
which, instead of draining into the coronary sinus, drains diography, if needed) to cross into the left atrium. Crossing
directly into the right atrium. These venous structures occa- at the level of the superior limbus should also be considered
sionally can be used for mapping or radiofrequency ablation, when it is difficult to push the transeptal needle through
the fossa ovalis and calcification of the interatrial septum is node are located more anteriorly on the inferior limbus and
evident fluoroscopically. In such cases, the superior limbus may be damaged when trying to enter the left atrium at this
approach may be preferred because transseptal puncture site. Anterior to the fossa ovalis is the fast pathway region and
through the fossa under increased pressure may give rise to beyond that are the aorta, the aortic cusps, and the ascending
calcific embolization. aorta. Therefore, if the fossa cannot be entered, a puncture
The inferior limbus is the septal portion of the eustachian into the left atrium, anterior to the anatomic location of the
ridge. The compact AV node and the fast pathway to the AV fossa ovalis, is contraindicated.
RAO LAO
Figure C2.41
Note in Figure C2.41 the location of the ablation catheter epicardial structure. Therefore, the ablation catheter should
(white arrow) relative to the prosthetic valves (black arrows). be at least 2 to 4 mm from the coronary sinus (best seen in
In the RAO projection, the ablation catheter just crosses the the LAO projection). If the ablation catheter appears superim-
plane of the prosthetic mitral annular ring. In the LAO proposed on the coronary sinus catheter, it likely is too atrial and
jection, the ablation catheter is just lateral (peripheral) to the is indenting the myocardium to approach the coronary sinus
mitral annular ring (black arrows). If a coronary sinus cath- relatively epicardially. In contrast, if the ablation catheter is
eter were placed, this would be seen lateral (peripheral) to too far (>1 cm) from the coronary sinus, it likely is not mak-
the ablation catheter. This is an ideal annular location for an ing contact with the annulus. The RAO projection shows the
ablation catheter at the site of pathway potential recognition. anterior orientation of the aortic (bileaflet) valve to the mitral
The ablationist should remember that the coronary sinus is an annular ring.
Case 2 277
Compare the relative position of the aortic valve and the

Box C2.1 mitral annulus in this patient to understand the maneuvers
Mapping the Mitral Annulus via a Retrograde required to map the mitral annulus in a retrograde aortic
Approach
approach (of course, that approach is contraindicated for this
1. Catheters must never be prolapsed across the aortic valve
with a leading tip. Rather, the tip should be deflected, form- patient with a prosthetic bileaflet valve). In the RAO projec-
ing a “U” shape to avoid injury to the valve and inadvertent tion, the mitral annulus is clearly more posterior (atrial) to
damage to the coronary arteries. the aortic valve, whereas in the LAO projection, the mitral
2. After the left ventricle is reached, the catheter deflection annulus is clearly seen to the left (lateral) of the aortic valve.
must be released, with the tip pointing toward the apex.
Th is is the rationale for the standard steps used to maneu-
3. Gently curve and move the catheter to and fro to free the tip
from the papillary muscles and chordae tendineae. ver a catheter via a retrograde aortic approach to map the
4. The catheter must be curved so that the tip points posteri- mitral annulus (Box C2.1). The RAO and LAO views also
orly in the RAO projection and laterally in the LAO projec- show that the aortic mitral continuity (region between the
tion. This is generally achieved by applying counterclockwise aortic and mitral valve) cannot be accessed via a pericardial
torque while deflecting the catheter posteriorly in the RAO
approach.
view.
5. The catheter tip may be placed on the annulus (above the Sometimes, an electrophysiologist will need to determine
valve) or between the valve and the ventricular myocardium whether an accessory pathway is present, even without having
(below the valve). catheters on the left side of the heart. As explained previously,
the coronary sinus in this patient could not be cannulated,
Abbreviations: LAO, left anterior oblique; RAO, right anterior and the electrodes labeled CS 1,2 to 9,10 were placed on the
oblique.
tricuspid annulus.
Figure C2.42
Figure C2.42 shows the electrogram recorded when pac- D. Differential site ventricular pacing; there is an acces-
ing the ventricle from the distal His bundle catheter. sory pathway
What is the maneuver being demonstrated and what is the E. Without the coronary sinus mapping catheter, the
interpretation? presence of a left-sided accessory pathway cannot be
A. Induction of retrograde right bundle branch block; determined
there is an accessory pathway
Answer: C—Parahisian pacing; there is no evidence of an
B. Parahisian pacing; there is an accessory pathway
accessory pathway.
C. Parahisian pacing; there is no evidence of an accessory
pathway
Although it is true that inclusion or exclusion of a left-sided atrium. Although it is true that a left-sided pathway cannot be
accessory pathway is best done with mapping electrodes in excluded with parahisian pacing, even with a coronary sinus
the coronary sinus or the left atrium (regardless of the pac- catheter in place (because of a possible delay in getting to the
ing maneuver performed), a careful analysis of the results of lateral ventricular site), if retrograde activation of the atrium
parahisian pacing can result in a reasonably certain conclu- was from a lateral pathway, in addition to the AV node, at
sion. The principles and pitfalls associated with parahisian least a subtle change in the atrial activation sequence would
pacing are described in Chapter 4. The first beat in Figure be expected. For example, the intervals between the His
C2.42 is pacing at relatively low output. The QRS interval is bundle catheter (HBE 1–4) and the catheter at the CS ostium
wide and the signal from the ventricular myocardium is cap- (CS 1,2) and the catheter placed higher on the right atrial
tured (RVp catheter). The His bundle signal is captured in septum (HRA) would have different relative timing, should
the second (narrower) beat but not in the first beat. Thus, the more distal coronary sinus activation occur. Thus, acces-
first beat is associated with ventricular myocardial capture, sory pathway conduction at this pacing cycle length likely
whereas the second and third beats are associated with myo- is absent, considering that the atrial activation sequence is
cardial and His bundle capture. The interval between the exactly identical and the interval between the stimulus and
stimulus and atrial signal is longer in the first beat, strongly atrial signal is longer when only a ventricular myocardial sig-
suggestive of AV nodal conduction from the ventricle to the nal is captured.
V5
V1
03:50:34-2 VT
V5
V1
04:31:09-2 Longest VT run
Heart rate versus time Total VT runs versus time

(Max, Min, and Avg)
Figure C2.43
The Holter tracing from a patient with frequent shocks Which cause of idiopathic ventricular fibrillation is best
from an implantable cardioverter-defibrillator is shown in ablated using an epicardial approach?
Figure C2.43. The patient had a structurally normal heart. A. The left posterior fascicle
Two prior ablation attempts (to decrease the frequency of B. The Purkinje network
device discharges) were unsuccessful. The Holter tracing C. The supravalvar aortic outflow tract
shows frequent premature ventricular contractions with D. None of the above
interspersed ventricular-paced beats, followed by a run of E. All of the above
polymorphic ventricular tachycardia or ventricular fibrilla- Answer: D—None of the above.
tion. The patient’s QT interval was normal, and the electro-
lyte levels were normal. When 2 prior endocardial ablation attempts have
been unsuccessful, the operator must determine whether
Case 2 279
epicardial ablation is worthwhile. Although little is known structures that generally can be easily ablated if appro-
about the initiating beats of ventricular fibrillation or priately mapped with an endocardial approach. In fact,
polymorphic ventricular tachycardia, reasonably estab- one problem that an electrophysiologist encounters with
lished causes include an origin in the fascicular system, fascicular tachycardias is mechanical “bumping” during
His-Purkinje network, and the outflow tract. The fascicu- catheter manipulation of the focus of the critical region of
lar system and His-Purkinje network are subendocardial a circuit.
Figure C2.44
Figure C2.44 shows a 12-lead electrocardiogram of the is an anterior structure that is in immediate proximity to the
initiating beats for the polymorphic ventricular tachycardia pericardial space.
sequence. Other cases presented in this textbook will describe Thus, a rare but potential reason for difficulty with abla-
a detailed method of analyzing the QRS vector to determine tion of a RVOT may be that the focus is epicardial. In that
the origin site of tachycardia. In this example, the right bun- case, pericardial access is a reasonable option to consider.
dle branch block morphology (tall R wave in lead V1) suggests However, for difficult LVOT tachycardia ablation, epicardial
an origin on the left ventricle. Further, a tall R wave is seen in access is of little value.
leads II, III, and aVF, along with a QS complex in leads aVR
and aVL. These suggest an origin in the superior portion of For a patient with previously failed or difficult LVOT abla-
the heart, the outflow tract. The LVOT is a relatively posterior tion, which access may be used to facilitate ablation?
and rightward structure (described below) compared with A. Subxiphoid pericardial access
the RVOT. Thus, the QS complex in lead I suggests an origin B. Distal coronary sinus access
in the left most part (closest to the left arm, lead I), namely C. Right atrial appendage access for mapping and ablation
the left coronary cusp region. Should the electrophysiolo- D. Left atrial appendage access for mapping and ablation
gist consider epicardial mapping for a potential outflow tract E. None of the above
focus? The answer depends on which outflow tract is being
Answer: B—Distal coronary sinus access.
considered. The LVOT is in the “center” of the heart, covered
anteriorly by the RVOT that wraps around from right to left; Anatomy of the LVOT, particularly the supravalvar por-
thus, access to the LVOT or the supra-aortic valvular region is tions, must be completely understood by ablationists before
limited from a pericardial approach. The RVOT, in contrast, attempting ablation.
Cardiac
vein
LVOT retrograde
approach Figure C2.46
Figure C2.45
Figure C2.46 is an anatomic dissection at the level of the
base of the heart showing important anatomic relationships
of the supravalvar aortic region. Observe how the aortic valve
In Figure C2.45, an LAO view of the heart shows the out-
is bounded on all sides by the other cardiac valve and a por-
flow tract region and its relationship to the coronary vascu-
tion of the RVOT. The white arrows point to the distal portion
lature. The lower white arrow shows a catheter placed in the
of the coronary sinus (great cardiac vein or anterior intraven-
LVOT (retrograde approach). This catheter was placed close
tricular vein). A catheter placed in the distal coronary sinus
to the aortic valve, just opposite of the mitral valve. About
and manipulated to the septal (rightward) branch of this vein
1-to-2 cm above this catheter was the left main coronary
would place it on the epicardial surface, close to the left coro-
artery as it bifurcated into the left anterior descending and
nary cusp or supravalvar LVOT. This dissection also shows
left circumflex arteries. The upper white arrow points to the
the very close relationship of the posterior pulmonary cusp
cardiac vein (junction of great cardiac veins and anterior
and the left main coronary artery. The right atrial appendage
intraventricular vein). A multielectrode catheter was placed
drapes over a portion of the right ventricle and RVOT, but it
in this vein to map the epicardial region, close to the outflow
is separated from the aortic valve and LVOT by the RVOT.
tract. The figure also shows the often unappreciated proxim-
The left atrial appendage typically drapes over a portion of
ity of the left main coronary artery to a catheter placed in the
the mitral annulus and the RVOT. Rarely, a second posterior
RVOT (yellow arrow).
lobe of the atrial appendage is “sandwiched” between the
RVOT and LVOT, very close to the left main coronary artery;
an anatomic proximity between the left atrial appendage and
the LVOT occurs only in this rare situation. Thus, of all the
“epicardial” approaches that can be taken with regard to the
LVOT, none are of significant value, except for the distal coro-
nary sinus vasculature.
Case 2 281
RAO LAO
Figure C2.47
Figure C2.47 shows the LAO and RAO projections of very close, which could give the mistaken impression that the
complex catheter placement in a patient with a supra-aortic outflow tract is being mapped via the epicardial approach.
valvar focus of ventricular fibrillation. The complete analy- However, by analyzing the simultaneously obtained RAO
sis of this fluoroscopic image and interpretation is presented image, the 2 catheters clearly are separated by the entire cir-
in Chapter 1 and Case 14. The figure is reproduced here to cumference of the RVOT. The relationship between the 2 out-
underscore the usefulness of an epicardial approach for abla- flow tracts should be compared with the relationship of the
tion of a focus in the region of the LVOT supravalvar aorta. distal electrodes of the coronary sinus catheter and the distal
The yellow arrows point to a catheter in the LVOT, with electrode of the LVOT catheter. In the LAO view, the distal
the shaft in the supravalvar region. The white arrows point electrodes of the coronary sinus catheter, epicardially placed
to a catheter in the RVOT. The red arrows define a catheter ablation catheter, and LVOT catheter appear to be fairly close
placed by a subxiphoid approach in the epicardium. In the together, but again, the RAO view shows the epicardial cath-
RAO image, note that the LVOT (yellow arrow) is sepa- eter (red arrow) is quite a distance away, whereas the distal
rated from the epicardially placed catheter (red arrow) by coronary sinus electrodes are reasonably close to the LVOT.
the entire RVOT (white arrow). In the LAO image, the tip This is consistent with the anatomic relationships shown in
of the LVOT catheter and the RVOT catheter appear to be Figure C2.46.
Figure C2.48
If the primary focus of the premature ventricular con- output for fear of complications. Which complication is
traction or ventricular tachycardia is located in the region of most likely to occur if inadvertent, high-power ablation
the left main coronary artery, careful examination of Figure results in an impedance “pop” when ablating this site of
C2.48 shows that nearly simultaneous (but not necessar- early activation?
ily early) activation occurs in the RVOT catheter, epicar- A. Damage to the right coronary artery
dial catheter, LVOT catheter, and the distal coronary sinus B. Damage to the left anterior descending artery
electrodes. C. Perforation into the left atrium
In Figure C2.48, the ventricular potentials in the distal cor- D. Perforation into the right atrium
onary sinus electrode (CS 1,2), the RVOT catheter (RVOT p), E. Damage to the AV conduction system
and the epicardial catheter (Epi 3,4) are all simultaneously early Answer: C—Perforation into the left atrium.
and time with the onset of the QRS complex. In a structurally
normal heart, the true earliest site of activation typically pre- Referring back to Figure C2.46, note that the noncoronary
cedes the onset of the QRS by almost 40 milliseconds. cusp, as the name suggests, is not immediately connected
to either main coronary artery. The left anterior descending
In a 47-year-old man with idiopathic ventricular fibril- artery is further anterior and has no immediate relation-
lation, the site of earliest activation is found when map- ship at any location in the noncoronary cusp. The posterior
ping the noncoronary cusp of the aortic valve, close to lesion of the noncoronary cusp may be the mitral annulus
its junction with the left coronary cusp. The operator (left ward) or the tricuspid annulus (rightward), as seen in
is reluctant to increase radiofrequency energy power Figure C2.46.
Case 2 283
LA
Figure C2.49
The arrow in Figure C2.49 shows the close relationship and the interatrial septum–left atrium region. Thus, as
of the noncoronary cusp and the left atrium. A thin wall observed in the RAO projection of Figure C2.47, epicar-
of valvular tissue and left atrial myocardium separates the dial access via a subxiphoid approach is of little value when
posterior aortic root from the left atrium. Thus, inadvertent attempting to reach the supravalvar aortic root. Also shown
high-energy delivery may promote perforation (perhaps via well in Figure C2.49 is the cranial caudal relationship of the
an impedance “pop,” which could cause fistula formation pulmonic valve, aortic valve, and ostium of the left main
between the aorta and the left atrium). coronary artery. Note that the most cranial structure is the
The His bundle penetrates the membranous septum pulmonic valve, followed closely by the ostium of the left
between the commissure of the noncoronary and right coro- main coronary artery; the most caudal structure is the aor-
nary cusp of the aortic valve and the commissure of the septal tic valve.
and anterior leaflet of the tricuspid valve. Thus, damage to the In approaching either RVOT or LVOT tachycardias,
conduction system is more likely when ablating at the junc- detailed knowledge of the anatomic relationship of these
tion of the noncoronary and right coronary cusp, rather than structures is essential. The most important relationship to
the noncoronary and left coronary cusp (as was done in the understand is that the RVOT is anterior (closer to the ster-
patient described in the question above). num) to the LVOT throughout its course. Portions of the
Again, well illustrated by the dissection in Figure C2.49 RVOT may be located to the left (suprapulmonary) or to the
is the “sandwiching” of the aortic root between the RVOT right (infundibulum) of the LVOT.
The discussion below pertains to Figures C2.50 and

C2.51. In Figure C2.51, an LAO view of catheter position-
ing in a patient with recalcitrant RVOT tachycardia is seen.
The white arrow points to a catheter in the pericardial space
(epicardial catheter) placed via a subxiphoid approach. The
nearby ablation catheter (black arrow) is in the RVOT at
the site of earliest endocardial activation. A far-field poten-
tial was observed to be early on the endocardial (ablation)
catheter. By manipulating the epicardial catheter close to the
endocardial catheter, a near-field signal that timed with the
far-field potential (earliest signal) on the endocardial cath-
eter was obtained.
When ablating from the epicardial catheter (Figure C2.51,
white arrow), which is the most likely ablation energy deliv-
ery profile (with settings of 60 watts, 65°C temperature-
controlled ablation)?
A. 10 watts, 65°C, 120 ohms
B. 60 watts, 65°C, 85 ohms
C. 60 watts, 47°C, 125 ohms
D. 10 watts, 65°C, 80 ohms
Answer: A—10 watts, 65°C, 120 ohms.
Although the electrophysiologist’s skill determines
whether subxiphoid pericardial access is obtained, the value
of mapping in the pericardial space is often limited by the
fact that delivery of adequate radiofrequency energy is dif-
Figure C2.50 ficult. Typically, because of the absence of circulating blood, a
quick rise in temperature (and often impedance) limits power
delivery. Thus, epicardial ablation is almost always ineffective
because of these limitations and power delivery. However,
for true epicardial foci (or epicardial slow zones for reentrant
tachycardia), subxiphoid epicardial mapping and ablation
may be effective if the focus or slow zones are mid myocar-
dial. Methods to overcome these problems include the use of
ablation catheters internally irrigated with saline, flushing
the pericardial space with fluids, or using cryoenergy.
Figure C2.51
Case 2 285
Figure C2.52
Figure C2.52 shows the relationship of the pericardial sac CT, computed tomography, computed tomographic
to the RVOT. A careful comparison of the dissection with the Desc, descending [f]
fluoroscopic image (taken from a similar orientation) shows EP, electrophysiology
that epicardial mapping can identify and potentially ablate an ESO (Eso), esophagus [f]
epicardial RVOT focus but, as mentioned above, cannot do so I, inferior [f]
for arrhythmogenic substrates in the LVOT. IVC, inferior vena cava [f]
A thorough understanding of the pericardial space adds L, left [f]
an important dimension to the diagnostic and therapeutic LA, left atrium [f]
armamentarium of an invasive cardiac electrophysiologist. LB, left bronchus [f]
Not only is it important to know how to access the peri- LAA, left atrial appendage [f]
cardium safely, but a detailed knowledge of the pericardial LAO, left anterior oblique
recesses (eg, oblique sinus, transverse sinus, aortocaval LIPV, left inferior pulmonary vein [f]
sinus, etc) is vital. Equally important is an understanding LPA, left pulmonary artery [f]
about the cardiac structures that are not readily accessible LPVR, left pulmonary vein recess [f]
via a pericardial approach (eg, the aortic root). Methods to LSPV, left superior pulmonary vein [f]
map and occasionally ablate an epicardial focus without LV, left ventricle [f]
accessing the pericardial space, instead using either the cor- LVOT, left ventricular outflow tract
onary veins or (more rarely) the Thebesian and other veins, MCV, middle cardiac vein [f]
should also be kept in mind. An accurate knowledge of the PA, pulmonary artery [f]
pericardial space and the anatomy of these associated veins PCR, pericardial recess [f]
can be helpful in various arrhythmias, including ventricu- PLV, posterolateral vein [f]
lar tachycardia, atrial fibrillation, and accessory pathway R, right [f]
ablation. RA, right atrium [f]
RAA, right atrial appendage [f]
RAO, right anterior oblique
Abbreviations RIPV, right inferior pulmonary vein [f]
RPA, right pulmonary artery [f]
Ao (AO), aorta [f] RPVR, right pulmonary vein recess [f]
Asc, ascending [f] RSPV, right superior pulmonary vein [f]
ASD, atrial septal defect RVOT, right ventricular outflow tract
AV, atrioventricular S, superior [f]
AZV, azygous vein [f] SVC, superior vena cava [f]
CS, coronary sinus [f] VT, ventricular tachycardia [f]
Case 3
Figure C3.1
The electrograms in Figure C3.1 were from a 27-year-old man Which diagnosis is consistent with the intracardiac elec-
with recurrent, medication-resistant paroxysmal supraven- trogram shown in Figure C3.1?
tricular tachycardia. The CS catheter (CS 1,2 to 17,18) was well A. Atrioventricular (AV) node reentry
seated and stable in the coronary sinus, with CS 17,18 located B. Orthodromic AV reciprocating tachycardia using a
at the coronary sinus ostium. The HRA catheter was located left-sided pathway
in the high right atrium laterally. The His bundle distal elec- C. Orthodromic reciprocating tachycardia (ORT) using a
trode (HBE 1) was located at the junction of the His bundle right-sided accessory pathway (AP)
and right bundle branch. D. Premature atrial contraction
E. All of the above
Abbreviations are expanded at the end of this chapter.
Terms with “[f]” denote abbreviations that appear in the figures only. Answer: E—All of the above.
287
Examine the tracings shown in Figure C3.1 and note the 3 orthodromic AV reciprocating tachycardia, with posterolat-
different atrial activation sequences for the 3 beats recorded. eral AP) and the entire coronary sinus activation is similar
If all tachycardia beats had the characteristics of the mid- to that seen in the middle beat, there is an important dif-
dle beat, AV node reentry would be a strong candidate for ference in the relative timing of activation of the high right
diagnosis. The ventriculoatrial (V-A) interval and His-atrial atrium. Examine the right atrial activation in the first beat
intervals are very short, and the earliest site of atrial activa- and compare it with a subsequent beat. In the first beat, the
tion is septal, close to the HBE 4 catheter (compare the second HRA signal is very early; it is later in the second beat and
and third beats to determine which signal is atrial). However, much later in the final beat, activating clearly after all other
when comparing the middle beat with the first and last beats, atrial activations.
2 important factors must be remembered when determin- What is the cause of early activation on the HRA cath-
ing the fundamental mechanism of this tachycardia. First, eter in the first beat? One possibility is a serendipitous
the rate of tachycardia does not change (His-His and inter- (catheter-induced or spontaneous) premature atrial contrac-
ventricular [V-V] intervals are constant). Second, the atrial tion (PAC) occurring at about the same time as the first tachy-
activation sequence in the mid and distal coronary sinus (CS cardia beat. Premature beats can fuse with tachycardia beats
11,12 to CS 1,2) is identical in all 3 beats. and bear no relationship to the mechanism of tachycardia;
These observations in turn give rise to 2 findings. One, such a diagnosis must be considered.
because the tachycardia cycle length is unchanged, all 3 beats A second possibility is a right-sided, retrograde-conducting
likely have the same tachycardia mechanism. Two, because the AP. Although several electrodes are used to map the mitral
distal coronary sinus activation sequence is the same for all 3 annulus, mapping of the right atrium free wall during rou-
beats, the mechanism activating this portion of the atrium tine computed tomographic ablation procedures is per-
and coronary sinus must be the same as the mechanism of formed only via the HRA catheter. If such an AP is present,
the tachycardia. Thus, while AV node reentry certainly is a the first beat shown in Figure C3.1 may represent ORT using
possible diagnosis, it is not the only mechanism of tachycar- that pathway. However, given that the mid to distal coronary
dia that should be considered, given the considerable changes sinus activation and cycle length of the tachycardia do not
in septal atrial activation sequence from beat to beat without change in the 3 beats shown, the more likely possibility is
changes in the tachycardia cycle length. that the right-sided pathway is a bystander during tachycar-
Now consider the third beat in Figure C3.1. The site of ear- dia. Subsequent tracings showed these changes in activation
liest activation in this beat is in the mid coronary sinus (CS sequence were frequent during the patient’s ablation proce-
11,12). This activation pattern is consistent with retrograde dure, which made it unlikely that any of the changes with
conduction via a left-sided (left posterior or left posterolat- the atrial activation sequence were from randomly occurring
eral) AP. If the mid to distal coronary sinus activation in the premature beats.
2 preceding beats are identical to that of the last beat, and In summary, given the single tracing, potential mecha-
the cycle length has not changed during tachycardia, assume nisms included ORT using the left-sided pathway, ORT using
the left posterior or posterolateral AP is active and likely is a right-sided pathway, AV node reentry, and possible PAC.
responsible for tachycardia in all 3 beats. Although all of these mechanisms were possible and thus
Now consider the first beat of tachycardia in Figure C3.1. needed to be verified (see Chapter 4), the most likely diag-
Note that although the mid to distal coronary sinus activa- nosis was ORT using the left-sided pathway (similar to distal
tion is similar to that seen in the third beat (consistent with coronary sinus activation and cycle length).
Case 3 289
Figure C3.2
In Figure C3.2, note that the retrograde atrial activation “sporadic” PAC occurred, it did so with a similar V-A inter-
sequence changes from a pattern typical of ORT using a val, strongly suggesting an AP as the mechanism of early
left-sided AP (the first 2 beats) to a sequence with unexpect- activation. Figure C3.2 shows an incidentally noted artifact
edly early activation in the HRA catheter (arrow). Given that after the second beat on the RVp and HBE 1 catheters. The
the cycle length of the tachycardia is unchanged, the most very sharp initial deflection and the simultaneous occur-
likely diagnosis is ORT using a left-sided pathway, with inter- rence in 2 closely situated electrodes strongly suggest that
mittent bystander conduction via a right-sided AP. Again, the artifact is from the catheters mechanically interacting
on the basis of a single tracing, the possibility of spontane- with each other. Subsequent analysis with pacing maneuvers
ous PACs cannot be excluded. However, at other times in and ablation indicated that this patient had a left-sided AP, a
the electrophysiology study, consistent tachycardia with the right free-wall AP, and inducible, nonsustained, typical AV
early HRA activation sequence was seen, and further, when a node reentry.
Figure C3.3
Figure C3.3 shows a change in activation sequence simi- with a left-sided pathway, when the bystander, right-sided,
lar to that shown in Figure C3.1. Th is occurred commonly free-wall pathway blocks (effective refractory period of the
during transition from the bystander, right-sided pathway bystander pathway), the retrograde AV nodal fast pathway
to the bystander, retrograde, fast pathway to the typical conducts and antegrade conduction during all subsequent
sequence of ORT using a left-sided pathway. Th is phe- beats of tachycardia is via the slow-pathway input to the
nomenon may be attributable to the fact that during ORT AV node.
Figure C3.4
Figure C3.4 shows a consistent activation sequence seen free wall, without resetting (changing the cycle length
during a prolonged observation period during the patient’s of) the tachycardia.
ablation procedure. Note the activation sequence similar to the 3. Radiofrequency ablation of the right-sided AP
first beat in Figure C3.1. If this activation sequence alone is seen, changes the activation sequence (late in the HRA
it is difficult to determine whether the basic mechanism is ORT catheter), without affecting the cycle length of the
with the left-sided pathway or with the right-sided pathway. If tachycardia.
a premature ventricular paced beat, placed during tachycardia,
preexcites the tachycardia (only by preexciting the early atrial If the ablationist has not already identified the culprit path-
signal in the mid coronary sinus) and then resets the tachycar- way and principal mechanism, an important practical con-
dia, the primary mechanism likely involves the left-sided path- sideration during ablation is that if the activation sequence
way. Other findings may also suggest that the culprit AP is on suddenly changes but the cycle length does not, ablation
the left side if they are observed only with an activation sequence should not be stopped. Although in this case, the ablated
like that in Figure C3.4. Such findings include the following: pathway is likely a bystander, it may still cause tachycardia
after the other (culprit) pathway is ablated. If ablative energy
1. A premature ventricular contraction (PVC) placed dur- is discontinued prematurely (incomplete ablation), edema at
ing tachycardia delays the next atrial activation with a the site may occur, making it very difficult to regain appropri-
similar atrial activation sequence (postexcitation), with ate catheter contact and find the pathway potential to target
the earliest atrial potential of the delayed beat occur- the site for ablation. Thus, the ablation sequence should be
ring in the mid coronary sinus. completed, with the understanding that a bystander pathway
2. A PAC or PVC placed during tachycardia variably has been ablated, and then attention should be turned to the
delays atrial activation on the septum or right atrial culprit AP.
Case 3 291
Figure C3.5
The tracing shown in Figure C3.5 is from the same patient of the heart (positive R wave in leads II and III). The atrial
discussed above (Figures C3.1-C3.4). This is a complex tracing, activation sequence for the first 3 beats (2 paced beats and a
with multiple findings that are instructive. Carefully analyze third beat) is both similar to and distinct from the sequence
this intracardiac tracing, starting with the maneuver being in the last 2 beats of tachycardia. Three different QRS mor-
performed, and explain each individual beat. It is worthwhile phologies are present; these are the ventricular-paced QRS,
to enumerate the findings observed and develop potential the QRS during the last 2 beats of tachycardia, and a different
explanations before reading through the ensuing discussion. wide QRS complex for the third beat. The electrograms have
Note that the first 2 beats are ventricular-paced beats, with subtle variations, as does the ventricular activation pattern
a right ventricular catheter placed relatively close to the base through the tracings.
Figure C3.6
In Figure C3.6, the yellow arrow points to a beat with a suggests an origin in the RVOT, fairly close to the pulmonic
wide QRS complex. What is the likely origin of this QRS valve (negative deflection in lead I). APs directly connecting
complex? to the outflow tract, although described in the literature, are
A. Right ventricular outflow tract (RVOT) PVC exceedingly rare.
B. Preexcitation via a right-sided AP The RVOT PVC (yellow arrow) does facilitate some impor-
C. Preexcitation via a left-sided AP tant observations in terms of the “slant” of the AP. Note the
D. Bundle branch reentrant echo beat ventricular activation sequence (white arrows) during ven-
E. Ventricular-paced beat tricular pacing and the RVOT PVC. With the RVOT PVC,
ventricular activation occurs from distal to proximal on the
Answer: A—RVOT PVC.
CS catheter (clockwise activation). In contrast, with the last
The QRS complex (yellow arrow) is markedly wide, with beat of ventricular pacing, the proximal coronary sinus elec-
slurring in both the initial and later parts, indicating slow trodes register the earliest ventricular activation (counter-
activation. Th is strongly suggests a ventricular origin for the clockwise activation). Note that the V-A interval at the site
beat, rather than bundle branch aberrancy or preexcitation. of earliest atrial activation (CS 9,10) is shorter with clockwise
Bundle branch reentrant echo beats are frequently seen at ventricular activation (RVOT PVC) than with counterclock-
the end of programmed ventricular stimulation. However, a wise activation (ventricular pacing). The atrial activation
tall R wave in leads II and III would be unusual for bundle sequence does not change, and no significant change in the
branch reentry because the exit is from the right bundle coupling interval is apparent between the last 2 paced beats
(close to the inferior wall of the right ventricle) rather than and that of the last paced beat and the RVOT PVC. The change
the outflow tract. Preexcitation via a left-sided AP typically in the local V-A conduction interval, close to the site of the
shows a right bundle branch block morphology; this pat- AP, occurs because of slant in the pathway (see Chapter 4).
tern clearly is not present, and this mechanism therefore can Because the local V-A interval is shorter when ventricular
be excluded. A right-sided AP is possible, but again, with activation proceeds from lateral to septal (clockwise activa-
the tall R wave in leads II and III and the S wave in lead tion), the ventricular insertion of the AP is likely to be lateral,
I, this mechanism is unlikely because the QRS morphology with the atrial insertion located more septally.
Case 3 293
A B C D
LA LA
p 4 3 2 d p 4 3 2 d p 4 3 2 d p 4 3 2 d
CS CS
LV LV
A1 A2 B1 B2 C1 C2 D1 D2
V1 V1
A A A A
V V V V
CSp CSp
AP AP
CS4 CS4
AP AP
CS3 CS3
CS2 CS2
AP AP AP AP
CSd CSd
A A A A
V V V V
Figure C3.7 (Adapted from Otomo K, Gonzalez MD, Beckman KJ, Nakagawa H, Becker AE, Shah N, et al. Reversing the direction of
paced ventricular and atrial wavefronts reveals an oblique course in accessory AV pathways and improves localization for catheter ablation.
Circulation. 2001 Jul 31;104[5]:550–6. Used with permission.)
The reason for this activation phenomenon is illustrated in can help with ablation in some difficult situations (dis-
Figure C3.7; this figure was published in the original report that cussed in more detail in Chapter 4). For example, if the ven-
described the usefulness and method to define the slant of an tricular insertion of an anteroseptal AP is off the septum
AP. In panel A, when the ventricular activation sequence pre- (rightward ventricular insertion of the AP) and the atrial
cedes counterclockwise from the septum to the lateral wall, the insertion is on the septum, given that the compact AV node
V-A interval on CS2 is short, whereas in panel B, when pacing at may be damaged during septal ablation, the slanted and
the same cycle length but from a different ventricular pacing site rightward-located ventricular insertion of that particular AP
to produce a clockwise activation pattern, the local V-A interval may be targeted deliberately.
is considerably wider. With a wider V-A interval, it is easier to Slant of an AP can also be defined by the superior-inferior
identify the AP potential. Panels C and D show the same phe- axis. For example, for septal pathways, pacing from an ante-
nomenon when pacing the atrium from a septal and lateral site rior and inferior location can help define whether the path-
to define the slant of an AP flux in the antegrade direction. way is slanted, with the atrial insertion being more anterior
In addition to using maneuvers, the slant of a pathway than the ventricular insertion (or vice versa).
to better identify the AP potential, understanding the slant
Figure C3.8
After the RVOT PVC, the atrial activation sequence and atrial potentials recorded by the His bundle and proximal
the QRS morphology change. coronary sinus catheters (Figure C3.8, red and yellow arrows,
respectively) occur nearly simultaneously. This finding can be
What is the likely mechanism by which the atrial activation seen in retrograde activation via the fast pathway because the
(Figure C3.8, white arrows) arose? true fast pathway exit site is slightly posterior and inferior to
A. Spontaneous PAC the His bundle (see Chapter 4).
B. Atrial tachycardia
C. Retrograde activation via the left-sided AP Having now considered the likely origin of atrial activation
D. Retrograde activation via the AV node (Figure C3.8, white arrows), how does this atrial activation
E. None of the above now conduct to the ventricle?
Answer: D—Retrograde activation via the AV node. A. Via the slow pathway
B. Via the fast pathway
As discussed above, a serendipitous premature contraction C. Via a left-sided AP
may be the underlying cause of a sudden change in activa- D. Via a right-sided AP
tion sequence. However, the next beat shows the same atrial E. Cannot be determined with the number of beats being
activation sequence (last beat on the tracing), making a PAC shown
unlikely. Induction of an atrial tachycardia is also a possibility.
Answer: C—Via a left-sided AP.
However, it also is unlikely because the earliest activation site
is close to where retrograde AV nodal conduction is expected Note that the last 2 beats shown in Figure C3.8 also have a
to occur (an unusual site for atrial tachycardias). The left-sided wide QRS complex, although it is relatively more narrow than
AP can be excluded as a cause because a clear change in activa- ventricular paced beats or the RVOT PVC. Importantly, the last
tion sequence is seen between the atrial activations (just after 2 beats show a fixed ventricular activation sequence and QRS
the RVOT PVC) and the next beat (white arrows). morphology that was consistent for the duration of the episode.
The most likely explanation for the origin of this beat is a Note that the earliest ventricular activation is a far-field ven-
relatively unique manifestation of a 2-for-1 phenomenon. The tricular signal recorded by the mid coronary sinus catheter (CS
RVOT PVC conducts to the atrium through the left-sided AP 9,10). This is occurring at a site near the site of earliest atrial
and then, after a long interval (likely from retrograde right activation during ORT. Note that the earliest site of ventricu-
bundle branch block), conducts again to the atrium via the lar activation clearly precedes the His bundle deflection (red
AV node. (However, we cannot completely exclude a septal arrow). Thus, the only 2 mechanisms for ventricular activation
AP that has a very long retrograde conduction time.) The occurring this early would be an antegrade AP or a PVC.
Case 3 295
Similar to the argument made to exclude PAC as a cause of in a retrograde fashion, but in addition, a 2-for-1 phenom-
early atrial activation in Figures C3.1 through C3.3, the ven- enon with now-retrograde conduction via the AV node ini-
tricular activation pattern and A-V interval help diagnose tiates antidromic tachycardia using the left-sided AP in an
antegrade AP conduction. In this tracing, start with ventricu- antegrade direction. A systematic analysis focusing on the
lar pacing and retrograde conduction via a left-sided AP. Next conduction intervals and activation sequences can help clarify
is a RVOT PVC that conducts via the same left-sided pathway mechanisms of tachycardia, even in fairly complex tracings.
Figure C3.9
In Figure C3.9, electrograms from the same patient show The preceding tracing (Figure C3.9) showed that the
spontaneous induction of atrial fibrillation, with a persis- patient had a left–sided AP capable of antegrade conduc-
tently wide QRS interval. A right bundle branch block pattern tion. Even without that information, however, electrophysi-
is evident, with the initial R wave taller than the R′ wave. The ologists may be asked to determine whether the mechanism
R wave is positive in all the chest leads (V1 through V6), and a of a wide QRS tachycardia is because of an AP (preexcited
QS pattern appears in lead I. tachycardia), AV node conduction with bundle branch
block, or ventricular tachycardia. Several features of the
What is the cause of the wide QRS complex seen during
QRS complex and axis should be analyzed to distinguish
atrial fibrillation in Figure C3.9?
preexcitation from bundle branch block and ventricular
A. Preexcited atrial fibrillation with conduction via the
tachycardia (see Chapter 6). Because the QRS is positive in
left-sided AP
all chest leads (V1 through V6), the origin of the ventricu-
B. Preexcited atrial fibrillation with antegrade conduction
lar activation likely is near the mitral annulus, close to the
via a right-sided AP
base of the heart. Th is type of axis immediately excludes
C. Ventricular tachycardia—QRS morphology should not
conduction via the left bundle (right bundle branch block).
vary significantly with preexcited atrial fibrillation
Analysis of the QRS complex itself in detail can also help
D. AV nodal conduction during atrial fibrillation with
identify the cause of QRS prolongation during tachycardia
right bundle branch block
(determine whether the primary abnormality causing the
E. AV nodal conduction during atrial fibrillation with left
delay in ventricular conduction occurs early or late in the
bundle branch block
QRS).
Answer: A—Preexcited atrial fibrillation with conduction
via the left-sided AP.
Bundle branch block Accessory pathway Ventricular tachycardia
Initial Later QRS Initial (δ wave) Later Initial and late QRS abnormal
upstroke wide (intra wide from downstroke (intraventricular conduction)
sharp from ventricular pathway normal from
normal conduction) conduction His-Purkinje
conduction to ventricle activation
(left bundle)
Figure C3.10
At times, a single-lead rhythm strip is all that is available AP should be suspected; in contrast, if the later portions of
for review when attempting to diagnose the cause of a patient’s the QRS are wide and abnormal but the initial deflection is
wide, complex tachycardia (Figure C3.10). Establishing a normal, bundle branch block may be present. Finally, if both
diagnosis requires careful analysis of the initial deflection early and late portions of the QRS complex appear abnormal
(upstroke) and later portions of the QRS and making a judg- (or bizarre), ventricular tachycardia is present.
ment about which portions of the QRS deflection are most Several exceptions to these rules should be kept in mind.
abnormal. In patients with wide QRS tachycardia from bun- With bundle branch block, the conducting bundle itself (left
dle branch block, initial ventricular activation occurs via the bundle branch in patients with right bundle branch block,
conducting bundle and is relatively normal. The second half etc) may be abnormal, or additional abnormalities may also
of the QRS complex reflects intraventricular conduction and be present in the distal His-Purkinje system. In such cases,
is clearly abnormal. When AP conduction causes wide QRS the entire QRS complex will be abnormal and thus will
tachycardia, initial activation of the ventricle (upstroke of mimic ventricular tachycardia. Certain APs may conduct
QRS) is via AP conduction to the ventricular myocardium. directly to the infrahisian conduction system (Mahaim path-
This produces the delta wave and is clearly more abnormal ways, etc). In such cases, the QRS complex is virtually indis-
than later activation (later portions of the QRS), which sug- tinguishable from bundle branch block (right-sided Mahaim
gests normal conduction via the His-Purkinje system. With pathway mimicking left bundle branch block). Finally, ven-
ventricular tachycardia, both the initial and late portions of tricular tachycardia may arise from the fascicular system or
the QRS typically are markedly abnormal. Thus, if the ini- from the septal myocardium close to the conduction system,
tial portion of the QRS is clearly more abnormal than the which produces a relatively normal initial deflection in the
later portion, antidromic activation of the ventricle via an QRS complex.
Case 3 297
Right bundle branch block Right accessory pathway LV tachycardia

Delayed RV Early RV and late LV early, RV late, and
activation LV activation slow ventricular conduction
LV RV RV LV LV RV
Figure C3.11
The QRS vector can also be used to distinguish bundle activation using an antegrade conducting accessory bypass
branch block from antidromic activation with an AP or ventric- tract), the earliest activation of the ventricle is typically at the
ular tachycardia (Figure C3.11). In wide QRS tachycardia caused base, resulting in concordant positive R waves in all pectoral
by bundle branch aberrancy, initial ventricular activation is via leads. Ventricular tachycardia may arise or exit at any portion
the conducting bundle (as mentioned above). Because the exit of of the ventricular myocardium, but when the focus is near
either bundle branch is midway between the base and the apex the apex of the heart, a QS complex will be identified in all
(right bundle exits about two-thirds of the distance to the apex), chest leads. Such a finding immediately excludes antidromic
the pectoral leads tend to “straddle” the apex and the QRS vec- activation via an AP or a bundle branch exit with contralat-
tor is never concordant among them. Thus, tachycardia or ven- eral bundle branch block (bundle branch or pathway-related
tricular exit on the mitral annulus near the base of the heart will aberrancy excluded). Of course, if the ventricular tachycardia
produce positive deflections (R wave) in all chest leads. happened to arise in the left posterior fascicle, the QRS vector
In contrast, tachycardia originating at the apex of the heart and morphology can be similar to supraventricular tachycar-
will produce a negative deflection (QS complex) in all chest dia with right bundle branch block and left anterior fascicular
leads. With bundle branch aberrancy, concordance of the pec- block. These findings are summarized in Table C3.1 and are
toral QRS axis is not present, with some chest leads positive also more extensively discussed in the context of wide QRS
and others negative. With bypass tract activation (antidromic tachycardias in Chapter 6.
Table C3.1
Wide QRS Tachycardia—Analyzing the QRS Complex
Specific Finding Significance Exceptions Comments
QRS width and normalcy

Initial portion of QRS Likely bundle branch block In severe infrahisian conduction ...
complex appears normal disease, both initial and later
deflections of the QRS are
abnormal
Initial portion of the QRS Likely preexcitation via an Ventricular tachycardia that ...
complex is slurred and antegrade-conducting AP enters into the conduction
abnormal, later portion of system, with later exit
the QRS complex is normal to multiple sites in the
ventricular myocardium via
the conduction system
Will also have an abnormal
early deflection, with the later
portion of the QRS complex
appearing normal
(continued)
Table C3.1
(Continued)
Specific Finding Significance Exceptions Comments
Both initial and later portions Likely ventricular Ventricular tachycardia that In patients with Ebstein
of the QRS complex are tachycardia arises from or near the anomaly and a right-sided AP,
abnormal (wide or slurred fascicular system will have a both initial and later portions
[or both]) relatively normal early portion of the QRS will appear
of the QRS complex abnormal (preexcitation
Septal ventricular tachycardia and bundle branch block,
may have a narrow QRS respectively) and may mimic
complex ventricular tachycardia
QRS axis
Discordance in pectoral Possibly bundle branch Ventricular tachycardia arising This finding is suggestive (but
leads, with some showing aberrancy from the mid portion (not not diagnostic) of bundle
positive R waves and others apical or basal) of the left branch aberrancy
showing negative QS ventricle However, if there is positive
complexes APs directly connected with the concordance in the
bundle branch system (no exit precordial leads (R waves
at the base) or QS complexes in V1
through V6), bundle branch
block aberrancy usually is
excluded
Positive concordance in Exit close to the base, often Septal and basal ventricular Positive concordance in the
precordial leads (all on the mitral annulus tachycardia, with conduction chest leads excludes bundle
positive R waves in V1 Strong consideration is into the heart’s normal branch block aberrancy,
through V6) given to antidromic infrahisian conducting system but findings can occur with
tachycardia via a standard ventricular tachycardia,
antegrade-conducting antidromic reciprocating
AP, but basal ventricular tachycardia, or other
tachycardia also is possible preexcited tachycardias
Negative concordance Suggests earliest ventricular Rare APs may exit closer to the ...
in the precordial leads activation, close to the apex than the base (variants of
(QS complexes in V1 apex of the heart Mahaim)
through V6) This is generally consistent
only with ventricular
tachycardia because APs
exit at the base and the
conducting bundle branch
block, typically about
two-thirds the distance
from base to apex
Abbreviation: AP, accessory pathway.
Case 3 299
Figure C3.12
Use the principles summarized in Table C3.1 to analyze the QRS tachycardia. However, as noted previously, this pattern of
12-lead electrocardiogram shown in Figure C3.12, obtained positive concordance can occur either with ventricular tachy-
from a patient with paroxysmal palpitation. Although the cardia arising from the base of the heart or from preexcitation.
reader may be familiar with multiple criteria to aid the dif- The relative normalcy of the second half of the QRS complex
ferential diagnosis of wide QRS tachycardia (based on the strongly suggests preexcitation. Ventricular tachycardia that
12-lead electrocardiogram), try to limit the current analysis arises close to the conduction system and enters the fasci-
to the principles regarding the QRS abnormality and axis. cles may have a relatively normal late part of the QRS. This
is unlikely in Figure C3.12, which shows negative signals in
Examine Figure C3.12. Based on the principles described leads aVL and I, suggesting an exit close to the ventricular free
above, what is the most likely diagnosis? The red arrow wall at the base of the heart. If this were a ventricular tachycar-
points to P waves seen throughout the tracing. dia arising or exiting from that site, it would not be possible for
A. Ventricular tachycardia as the retrograde P waves occur it to enter into (“hitch a ride” on) the specialized conduction
B. Bundle branch block during a supraventricular tachycar- system that is part of the intraventricular septum.
dia because the later part of the QRS is relatively normal The 1:1 atrioventricular relationship (Figure C3.12, red
C. Ventricular tachycardia because of “positive concor- arrow) does not help much in the differential diagnosis
dance” in the precordial leads (all positive R waves in because it can be associated with an atrial tachycardia with a
V1 through V6) long PR interval and bundle branch block, ventricular tachy-
D. Preexcited tachycardia because of an abnormal initial cardia with retrograde 1:1 activation, antidromic tachycardia,
deflection in the QRS complex and positive concor- or supraventricular tachycardia with bystander antegrade
dance in the precordial leads pathway conduction. However, the electrophysiologist should
E. Ventricular tachycardia because of the left ward frontal recognize some relatively subtle clues. The P wave duration is
axis seen in the tracing very short, suggesting retrograde activation from the septum,
likely the fast pathway (see Chapter 6). However, because
Answer: D—Preexcited tachycardia because of an abnor-
this is an unusual origin for preexcited atrial tachycardia, it
mal initial deflection in the QRS complex and positive con-
is unlikely. The V-A interval during tachycardia is relatively
cordance in the precordial leads.
long (start of the QRS to the start of the P wave [red arrow]).
In Figure C3.12, note that the early parts of the QRS com- This makes typical AV node reentry with antegrade preexci-
plexes showing tachycardia are markedly abnormal. This is well tation or bundle branch block also unlikely. Thus, the 2 most
seen in lead V1. The second half of the QRS complex (clearly likely diagnoses are a basal, lateral ventricular tachycardia or
shown in leads V1 and II) is sharp and appears normal. This is an antidromic tachycardia. Further analysis of the QRS (rela-
classical preexcitation. Note also the positive concordance—a tively normal throughout) strongly suggests an antidromic
tall R wave is present in leads V1 through V6. This essentially tachycardia with retrograde, fast-pathway activation as the
excludes bundle branch block as the mechanism for the wide most likely explanation.
I aVR V1 V4
II aVL V2 V5
III aVR V3 V6
Figure C3.13
Figure C3.13 is a 12-lead electrocardiogram obtained from abnormal, which is consistent with ventricular tachycar-
a 65-year-old man with recurrent, wide, complex tachycardia. dia. Given that the early QRS in leads I and II looks normal,
Again, the reader may be aware of several differential diag- bundle branch aberrancy should be considered. However,
nostic algorithms that could be used to establish the cause of concordance in the external leads excludes this possibility
this wide QRS tachycardia, but for the purpose of this ques- because exit from either conducting bundle branch is highly
tion, focus again on the QRS morphology and access. unlikely to occur on the base of the heart (mitral and aortic),
Observe positive concordance in the chest leads (tall and this pattern of ventricular excitation produces positive
R waves in lead V1 through V6). As explained above, this is concordance on the chest leads. This patient had ventricular
consistent with a basal ventricular tachycardia or an ante- tachycardia that was exiting from the lateral mitral annulus.
grade preexcited tachycardia. Th is time, the early part of the Careful comparison of this electrocardiogram with Figure
QRS complex is relatively normal in leads II, III, and V2, but C3.12 and the principles illustrated in Figure C3.11 will help
the QRS appears markedly abnormal in the late portion. In clarify principles useful in preparing an approach in the elec-
contrast, the early portion of the QRS in lead V1 also looks trophysiology laboratory.
Figure C3.14
Case 3 301
Consider again the patient with the left-sided AP and wide tachycardia in patients with dilated cardiomyopathy, reen-
QRS tachycardia. The intracardiac electrograms clearly show trant ventricular tachycardia in patients with prior myocar-
atrial fibrillation (Figure C3.14). The typical electrocardiogram dial infarctions, and RVOT tachycardia (tachycardia-induced
in patients with preexcited atrial fibrillation is a sporadically tachycardia). Dependent arrhythmia such as torsades de
irregular QRS interval and irregularity in the QRS morphol- pointes may also be triggered in susceptible patients (eg, those
ogy (specifically, width increase). This is because the rapid atrial receiving sotalol therapy for atrial fibrillation). Significant
arrhythmia conducting to the ventricle competes between the variability in the R-R intervals, consistent with some form of
AV node and the AP, and thus the QRS duration becomes vari- conducted atrial fibrillation, can be seen in Figure C3.14, con-
able. A wider QRS is associated with relatively more activation ducted via the AP.
via the AP (often with shorter cycle length), and a relatively Although the absence of significant variation in the QRS
normal QRS is seen when more conduction occurs via the AV duration or morphology during atrial fibrillation with a
node. The striking feature in this tracing is the uniformly wide known AP should alert the electrophysiologist to possible
and abnormal QRS complex (not an uncommon finding). AV node damage, this phenomenon is not uncommon even
when the AV node is relatively normal. This occurs because
Which is a possible explanation for the lack of significant the AV node or the infrahisian conduction system (or both)
variation in the QRS duration and morphology during blocks antegrade conduction, resulting in a fully preexcited
atrial fibrillation in this patient with a left-sided AP? beat. This will be evident near the initiation of atrial fibril-
A. Complete AV nodal block lation, usually when a short interval follows a relatively long
B. Ventricular tachycardia has been induced by the vary- interval. After the ventricle is activated entirely by the AP, the
ing cycle length of atrial fibrillation retrograde activation wave front may penetrate either into the
C. Retrograde penetration of the ventricular activation infrahisian conduction system or the compact AV node (con-
wave front into the infrahisian conduction system cealed conduction), resulting in perpetuation of complete
D. Retrograde penetration of the ventricular activation preexcitation. In such patients, when the pathway is ablated,
wave front into the compact AV node normal AV nodal and infrahisian conduction may be seen.
E. All of the above If the His bundle potential was consistently and clearly
F. None of the above seen in sinus rhythm (with or without preexcitation) but
Answer: E—All of the above. was absent during a rapid atrial tachycardia or atrial fibrilla-
tion, then a complete AV nodal block likely is present and is
Each of the options mentioned above should be considered responsible for the uniform, wide QRS complexes. However,
when a patient with atrial fibrillation and a known AP has a if the His bundle potential continues to be seen clearly but
uniformly wide QRS tachycardia. follows the wide QRS complex (constant V-H interval, with
Whenever an electrophysiologist is preparing to perform varying H-V intervals), then retrograde infrahisian penetra-
an ablation procedure in a patient with an AP, the following tion up to the compact AV node likely is occurring and is
features should raise concern about the possibility of an exist- responsible for the persistence of AV block after it is initiated
ing AV block: (see Chapter 6).
Generally, a multielectrode catheter (an 8-pole or 20-pole
1. Previous ablation attempt of a septal AP
catheter) preferably is used to record the His bundle or right
2. Very wide QRS from maximal preexcitation, particu-
bundle branch potentials (or both) in patients with wide QRS
larly if it occurred after an ablation attempt
tachycardia. Simply recognizing whether the His bundle or
3. Previous ablation attempt that resulted in continued
right bundle branch is being activated antegrade (proximal
preexcitation but with cessation of palpitations (ortho-
His electrode detects a potential before the mid or distal
dromic reentry)
electrodes) or retrograde can be helpful in narrowing down
4. Uniformly wide, irregular QRS during atrial fibrillation.
the differential diagnoses. Antegrade activation suggests
When such features are present, the patient should be that the mechanism of the wide QRS during tachycardia is
counseled on the possibility that the AV node may have bundle branch block, whereas retrograde activation is con-
already been damaged or ablated, and complete heart block sistent with either ventricular tachycardia or antidromic
may result after the remaining AP is ablated. tachycardia.
Ventricular tachycardia may be induced by atrial fibrilla- However, there are important exceptions to this simple
tion. The varying QRS intervals (eg, long-short-long sequence) use of multielectrode recording of the His bundle and right
are particularly likely to induce bundle branch reentrant bundle branch (see Chapters 4 and 6).
Antegrade His bundle activation
Proximal to distal His activation

A H V
Figure C3.15
Figure C3.15 diagrammatically shows the concept electrode and latest on the distal (first) electrode. AV node
of antegrade His bundle activation, as revealed by the reentry, ORT, and atrial flutter with bundle branch block
proximal-to-distal sequence of His potentials recorded by a would also show a similar proximal-to-distal activation pat-
multipolar catheter. In this particular example, atrial tachy- tern. It is dangerous to rely solely on this “rule” for excluding
cardia with left bundle branch block is seen. Note that the the causes of wide QRS tachycardia. Careful attention must
His bundle electrogram is earlier on the proximal (fourth) be given to placement of the multielectrode catheter.
Antegrade His bundle activation
Distal to proximal His activation

A H V
Atrial 4
tachycardia
3
Prox
RBBB 2
43 1
2
1
Figure C3.16
Case 3 303
Figure C3.16 shows a schematic for catheter placement in Ventricular tachycardia associated with distal retrograde
a patient with atrial tachycardia and proximal right bundle right bundle branch block can cause retrograde activation of
branch block. Here, the multielectrode catheter is placed in a the left bundle and His bundle but antegrade penetration of
relatively more ventricular location distal to the site of right the right bundle branch. Again, if the electrode is placed in a
bundle branch block. In this patient, antegrade activation is relatively ventricular location proximal to distal, activation
via the His bundle and then down the left bundle and ret- will be recorded on the multielectrode catheter, even though
rograde up the right bundle. Because the electrode is placed the His bundle and AV node are being activated retrograde
at the right bundle branch location, the multielectrode acti- during ventricular tachycardia. Thus, although placing mul-
vation sequence is from distal to proximal, even though His tielectrode catheters to record the His bundle and right bun-
bundle activation is antegrade. Other examples and excep- dle potentials can be very useful, careful attention must be
tions to these phenomena are discussed in Chapter 6. paid to such details.
Figure C3.17
Figure C3.17 (presented previously as Figure C3.5) shows a E. Atrial tachycardia

change in the “nature” of the atrial signals recorded by the CS Answer: C—An endocardial, left-sided AP.
catheter as the arrhythmia changes from retrograde activa-
Complex electrograms with near-field and far-field com-
tion via the AP to an antidromic tachycardia. Note that the
ponents occur in many arenas in cardiac electrophysiology. In
atrial signal is complex, particularly at sites of earliest ret-
general, double potentials suggest an area of slow conduction
rograde activation. A far-field potential (white arrow) is fol-
or conduction block. A catheter placed at the site of conduction
lowed by a near-field potential (yellow arrow).
delay or block will record 1 potential, and after the delay or con-
In Figure C3.17, what is suggested by the complex atrial duction circumnavigates the area of block, the second poten-
signal (ie, a far-field potential [white arrow] preceding a tial is recorded. In Figure C3.17, the catheter is not exactly on
near-field potential [yellow arrow]) on the CS catheter at the area of conduction delay or block; rather, it is to the side of
the site of earliest retrograde activation during tachycardia earlier activation from the propagating wave front. A near-field
and ventricular pacing? potential occurs first, and a far-field potential is observed after
A. AV node reentry conduction eventually occurs on the other side of delay or block.
B. Multiple retrograde APs Thus, in addition to diagnosing an area of conduction delay or
C. An endocardial, left-sided AP block, the catheter location (side) relative to the propagating
D. An epicardial, left-sided AP wave front of the conduction delay or block can be deduced.
additionally, because the coronary sinus is not directly con-

nected to the left atrium at the site of the AP, the near-field
potential from activation of the coronary sinus muscle
occurs somewhat later. APs that connect directly to the cor-
onary sinus muscle (ventricle to coronary sinus muscle to
left atrial musculature) are termed epicardial or venous APs.
In epicardial pathways, the near-field potential recorded by
the coronary sinus electrodes is expected to be earlier than
far-field endocardial activation. Note, in the last 2 beats
IVC
(antidromic tachycardia beats) shown in Figure C3.17, the
CS myocardial red arrows point to the near-field potentials within the
coat larger far-field potentials. Th is is because the activating
wave fronts for the left atrium and coronary sinus occur
almost simultaneously. Thus, during antidromic tachycar-
Figure C3.18 (Adapted from Asirvatham SJ. Cardiac anatomic dia, retrograde activation is via the AV node. From the exit
considerations in pediatric electrophysiology. Indian Pacing of the fast pathway, activation occurs via the Bachmann
Electrophysiol J. 2008;8 [Suppl 1]:S75–S91. Courtesy of Anton bundle or the fossa ovalis of the left atrial myocardium, as
Becker, MD, Academic Medical Center, Amsterdam, Netherlands.
well as activation from right to left via the coronary sinus
Used with permission.)
muscle itself. Because these wave fronts propagate about at
the same time, the potentials are fused; in contrast, dur-
Figure C3.18 is a dissection of the coronary sinus and ing retrograde activation via the AP, activation fi rst occurs
surrounding left atrial musculature. Note that a catheter in the left atrium (endocardial pathway) and then propa-
placed within the coronary sinus will record, in essence, gates via the left atrial–coronary sinus connection to the
2 different atrial potentials, one from the coronary sinus coronary sinus muscle. Remember that when mapping such
muscle activation itself and the second from the neighbor- endocardial pathways, a catheter placed in the left atrium
ing left atrial musculature. Looking back at Figure C3.17, (via a transseptal or retrograde aortic approach) should
note that the far-field signal (white arrow) is early on the record a near-field potential, equal to or earlier in timing
CS 9,10 trace. Th is suggests that the AP inserts directly into to the earliest far-field potential recorded on the coronary
the left atrial musculature (so-called endocardial pathway); sinus catheter.
Figure C3.19
Case 3 305
The concept is well illustrated in Figure C3.19. In this was placed on the mitral annulus via a transseptal route. Note
patient with 3 prior ablation attempts, the left-sided AP con- that the earliest atrial potential on the ablation catheter is a
duction pathway was targeted repeatedly. Note that the sig- near-field signal (white arrow) that times slightly earlier than
nals recorded by the coronary sinus electrode (CS 1,2 through the earliest far-field potential on the coronary sinus catheter.
CS 19,20) are highly complex, with multiple ventricular and This signal and a pathway potential (yellow arrow), identified
atrial components (see Chapter 4 for methods to distinguish after appropriate pacing maneuvers, strongly supported this
between these potentials). The earliest atrial potentials on the site as an excellent location to deliver radiofrequency energy.
coronary sinus catheter are far-field signals. The ABL d catheter Ablation at this site permanently eliminated AP conduction.
Figure C3.20
The electrograms in Figure C3.20 were obtained from potential was identified. Together, these features strongly
a patient with 2 prior ablation attempts for a left-sided AP. suggested the presence of an epicardial pathway that required
Note that the earliest signal seen on the CS 9,10 electrodes ablation.
is a near-field potential, with later far-field activation. The
ABL d catheter was placed within the coronary sinus for Which method likely is least effective for ablating an epi-
further mapping and possible ablation. As the catheter was cardial (venous musculature–related) AP?
placed in the coronary sinus, ectopy arising from the cor- A. Pericardial access, obtained via the subxiphoid
onary sinus musculature was seen in the third and fourth approach, with the catheter maneuvered to the mitral
beats (white arrows). This resulted in very early atrial acti- annulus
vation and shortened the V-A interval for those 2 beats, as B. Ablation from within the coronary sinus
recorded by the ablation catheter on the floor of the coro- C. Retrograde (transaortic) access, with the ablation cath-
nary sinus. Note that the pattern of early near-field and later eter placed “under” the mitral valve
far-field activation continued during coronary sinus ectopy. D. Retrograde (transaortic) access, with the ablation cath-
This figure illustrates the 2 main causes of early, near-field eter placed “on” the mitral annulus
activation within the coronary sinus during tachycardia— E. Transseptal access, with the catheter placed close
namely, an epicardial (venous musculature–related) path- to the mitral annulus and the ablation catheter and
way and an automatic tachycardia arising from the coronary the coronary sinus electrodes showing little or no
sinus musculature itself. When mapping the mitral annulus separation from each other in both the right ante-
with an endocardial catheter very close to the sites of earliest rior oblique (RAO) and left anterior oblique (LAO)
activation shown by the coronary sinus catheter, a far-field projections
Answer: D—Retrograde (transaortic) access, with the abla-

tion catheter placed “on” the mitral annulus.
Several methods can be used when attempting to ablate a
recognized or strongly suspected epicardial pathway. Each
approach has its own inherent advantages and disadvan-
tages. Pericardial access can be obtained via a subxiphoid
route, with the catheter manipulated to the mitral annulus.
However, this approach has 3 limitations. First, it is difficult
to attain sufficient power for epicardial ablation because of
rapid impedance rise (from the lack of cooling, attribut-
able to the lack of blood flow in the pericardial space). Th is
may be overcome to some extent by flushing the pericardial
space with saline, using an open- or closed-irrigation cath-
eter, or using cryoablation. Second, the pericardial fat in Figure C3.21
the atrioventricular groove makes it difficult to approach
this “epicardial” pathway from an epicardial route. It is This concept of multiple connections of epicardial path-
equally difficult to ablate from an endocardial route. Th ird, ways is illustrated in Figure C3.21. All patients have mus-
the circumflex coronary artery and proximal branches of culature associated with the coronary sinus, and nearly all
the obtuse marginal artery in the annular location may patients have multiple connections between the coronary
limit the ability to deliver radiofrequency energy with this sinus musculature and the left atrium. When this coronary
approach. sinus muscle also connects to the ventricular myocardium,
When ablating an endocardial pathway from a trans- an epicardial pathway results. Rare patients will have numer-
septal route, an ablation catheter well placed on the mitral ous connections between the coronary sinus muscle and
annulus will show little or no separation from the coronary ventricular myocardium, which creates multiple conduction
sinus electrode in the RAO view. However, in the LAO view, pathways. In contrast, even when a single ventricular connec-
they will be separated by 5 to 10 mm because the endocar- tion to an accessory pathway exists, the atrial end of the path-
dial ablation catheter and epicardial coronary sinus catheter way may have multiple connections to the atrial myocardium
are separated by the mitral valve and annular tissue. If both (as in patients without an AP). This results in multiple sites
views show no separation between the catheters, the abla- of early atrial activation with endocardial mapping, which
tion catheter probably is not on the annulus; rather, it likely hinders identification of the correct site for epicardial abla-
has been placed in the atrium, and with catheter manipu- tion (see Chapter 4). If the epicardial AP conducts only in the
lation or pressure (or both), the atrial myocardium (where retrograde direction, mapping can be very difficult, even in
the ablation catheter is located) is “overhanging” the mitral patients with a single ventricular connection, because of the
annulus and in fact is now fairly close to the epicardial coro- multiple sites of equally early endocardial activation. Finding
nary sinus electrode. Th is type of catheter positioning (ie, the pathway potential and distinguishing it from the normally
ablation and CS catheters in approximately the same posi- occurring coronary sinus muscle potentials is challenging,
tion in both RAO and LAO views) is not recommended for but the stepwise approach (discussed in detail in Chapter 4)
the standard endocardial pathway but may be tried for the will most likely identify an appropriate ablation site.
epicardial pathway.
Ablation from within the coronary sinus is often a last
resort. This method can be used safely for curative abla-
tion of an epicardial pathway, but it has several limitations.
First, coronary arteriography is required to ensure that there
is no major artery in proximity to the ablation site. Second,
as described earlier, power delivery from the coronary sinus
position is also difficult because of insufficient cooling and
the enhanced possibility of coagulum formation. Third, mul-
tiple potential connections among these pathways make it
difficult to ablate the entire coronary sinus musculature in
that particular region.
Figure C3.22
Case 3 307
A transaortic retrograde approach or transseptal catheters placed under the valve. Some electrophysiologists
approach may be used to place a catheter (Figure C3.22) might prefer to attempt ablation of an epicardial pathway
such that the distal ablation electrode is either between the using an under-the-valve approach, and in some cases, a
mitral valve and the ventricular myocardium (white arrow; catheter placed under the mitral valve may be a little closer
“under” the valve) or placed on the mitral annulus itself to the epicardial, coronary vein–related pathway. However,
(yellow arrow; “on” the valve). The nature of the electrogram the differences are not significant, except that catheter con-
recorded is quite different, depending on catheter posi- tact tends to be superior when the distal electrode is tucked
tion, with only a small atrial potential being captured with under the valve.
Table C3.2
Near- and Far-Field Potentials in Cardiac Electrophysiology
Electrophysiology Description Mechanism Electrophysiologic Significance
Phenomenon
Pulmonary vein In sinus rhythm, an earlier Slow conduction is seen across the With the catheter position
potential far-field potential (from left pulmonary vein musculature, unchanged, during pulmonary
atrial activation, proximal giving rise to 2 distinct potentials vein tachycardia, the near-field
to the site of ostial delay) In sinus rhythm, the near-field potential will seem to occur
is followed by a near-field potential is late when the catheter early (reversal of near-field and
potential (from actual is located in the pulmonary vein far-field signals)
activation of the pulmonary Analysis of the near- and far-field
vein musculature) potentials during tachycardia
activation of the pulmonary
vein versus tachycardia
(near-field potential early)
caused by the pulmonary vein
itself can be deduced
AP activation early Because the coronary sinus If there is no direct connection Tachycardias arising from the
in the coronary musculature is distinct from between the coronary sinus coronary sinus muscle or from
sinus the left atrium, catheters and left atrium at the site APs connected to the coronary
placed in this vein will record of catheter placement, the sinus will show a near-field
2 potentials wave front will activate the 2 potential early during
structures sequentially, resulting tachycardia
in 2 distinct potentials on the During left atrial tachycardias or
coronary sinus electrode at that endocardial APs, the far-field
site potential (indicating left
atrial activation) will occur
early in the coronary sinus
electrograms
Scar-related When mapping at the site of ... During mapping, if only the
tachycardia conduction delay or block, if earliest potential is mapped,
the near-field potential occurs when the catheter is moved to
first, the catheter is located the other side of the scar (away
to the side of the scar closer from the exit or origin of the
to the exit or origin of the tachycardia), 2 different sites of
tachycardia simultaneously early activation
will be mapped
In point-to-point mapping (with
or without a mapping system),
it is important to use only
the near-field potential for
recording the timing of the
potentials
(continued)
Table C3.2
(Continued)
Electrophysiology Description Mechanism Electrophysiologic Significance

Phenomenon
Automatic A fragmented or double There is no true conduction In this case (compare with
tachycardia potential may be seen on the between the sites showing previous row [scar-related
septum (atrial or ventricular) near-field and far-field potentials tachycardia]) the earliest
and with overlapping (overlapping or neighboring (near-field or far-field)
structures (right upper structures) potential should be recorded
pulmonary vein and posterior for mapping.
right atrium) Ablation should be performed
only after mapping a near-field
potential to the site that occurs
equal to or earlier than the
earliest far-field potential
recorded anywhere
Pulmonary vein Multiple far-field signals may be The “antenna” (field mapped by Pacing maneuvers described
potential that is recorded when a catheter is distal electrodes) of the mapping elsewhere (Cases 7 and 11) are
contaminated by placed in the pulmonary vein catheter picks up activation in the necessary to identify the true
potentials from Far-field signals can originate pulmonary vein and also that from pulmonary vein potential to be
neighboring in the neighboring left atrial neighboring structures targeted for ablation
structures appendage, vein of Marshall,
ipsilateral pulmonary vein, and
other sites
Abbreviation: AP, accessory pathway.
Table C3.2 enumerates several other situations in cardiac Marshall ridge will record not only the near-field atrial poten-
electrophysiology for which careful analysis of the near-field tial (often with relatively high amplitude in this location) but
and far-field electrograms is important. will also record potentials from the adjacent pulmonary veins,
possibly the left atrial appendage, and the vein of Marshall.
Abbreviations
A, atrial [f]
AP, accessory pathway
AV, atrioventricular
CS, coronary sinus [f]
d, distal [f]
LOM
H, His [f]
ridge IVC, inferior vena cava [f]
LA, left atrium [f]
LAO, left anterior oblique
LBBB, left bundle branch block [f]
CS LOM, ligament of Marshall [f]
LV, left ventricle [f]
ORT, orthodromic reciprocating tachycardia
Figure C3.23 PAC, premature atrial contraction
Prox (p), proximal [f]
Mapping within the coronary sinus, particularly when can- PVC, premature ventricular contraction
nulating the atrial veins (sometimes required in patients with RAO, right anterior oblique
atrial fibrillation), frequently results in highly fragmented RBBB, right bundle branch block [f]
signals. For example, a catheter placed directly in the vein of RV, right ventricle [f]
Marshall will record atrial potentials arising from the ligament RVOT, right ventricular outflow tract
of Marshall ridge and may also record signals from the coro- V, ventricle [f]
nary sinus musculature and the ostia of the pulmonary vein V-A, ventriculoatrial
(Figure C3.23). Similarly, catheters placed on the ligament of V-V, interventricular
Case 4
Figure C4.1
The tracing in Figure C4.1 is from a patient with atrial fibril- A. Peripulmonary vein pacing showed entrance block
lation diagnosed at age 17. The circumferential mapping B. Peripulmonary vein pacing showed persistent conduc-
(LASSO) catheter was placed in the left upper pulmonary tion into the pulmonary vein
vein, close to the ostium. The ablation catheter was placed C. Variable output pacing from the coronary sinus showed
more distally into the vein. The coronary sinus catheter was conduction into the pulmonary vein from the coronary
placed such that poles 1 and 2 were in the distal coronary sinus via an atrial vein
sinus and poles 19 and 20 were at the coronary sinus ostium. D. Parahisian pacing showed presence of an accessory
bypass tract
What maneuver was being performed and what did it
E. Left atrial appendage pacing showed a far-field append-
show?
age potential on the circumferential mapping catheter
Answer: C—Variable output pacing from the coronary
Abbreviations are expanded at the end of this chapter. sinus showed conduction into the pulmonary vein from the
Terms with “[f]” denote abbreviations that appear in the figures only. coronary sinus via an atrial vein.
309
Figure C4.2
When the coronary sinus was paced at a high output, circumferential mapping catheter (left atrial potential)
both the coronary sinus muscle and the nearby left atrium occurs later. However, the second potential on the mapping
were captured (Figure C4.2). When the coronary sinus was catheter (pulmonary vein potential) does not significantly
paced at a lower output, only the coronary sinus muscle change its timing relative to the pacing spike. From this, it is
was captured (arrow), which resulted in a second, more apparent that pulmonary venous conduction is independent
delayed left atrial potential. With low-output pacing when of the left atrium and is determined via the coronary sinus
the left atrium was not captured, the first potential on the musculature.
Case 4 311
Right superior LA PVP

pulmonary vein Left superior
pulmonary vein
SVC
Ostial delay
Ostium
RA LA
Left inferior
IVC Right inferior pulmonary vein
pulmonary vein
Figure C4.3 (Adapted from Asirvatham SJ. Pulmonary vein-related maneuvers: part I. Heart Rhythm. 2007 Apr;4[4]:538–44. Epub 2007
Jan 12. Used with permission.)
Several important concepts underlie the correct interpreta- Second, the vein of Marshall and other atrial veins are
tion of the maneuver shown. First, know that when a cath- remnants of the fetal venous circulation. Specifically, the vein
eter (eg, the circumferential mapping catheter) is placed in of Marshall is the remnant of the left superior vena cava. In
the pulmonary vein close to the ostium, 2 potentials are seen Figure C4.4, note that a probe placed in the vein of Marshall
(Figure C4.3). The first is an early, far–field potential from left extends from the coronary sinus ostium to the region of the
atrial activation; the second is a sharp, near-field potential left upper pulmonary vein.
from pulmonary vein activation. Typically, conduction to the Th ird, the coronary sinus has electrically active myo-
pulmonary vein occurs only via the left atrium across the pul- cardial sleeves of variable length that are distinct from the
monary venous ostium. adjacent muscle of the left atrium. In fact, it is instructive
to think of the coronary sinus as an additional atrium with
both venous and muscle components. As seen in Figure
C4.5, activation from the coronary sinus to the left atrium
Endocardial ridge location Left pulmonary veins (and vice versa) can occur through distinct muscular con-
nections. For example, pacing the left atrium from a site
adjacent to coronary sinus pole 1 will result in activation
of the coronary sinus muscle much more proximally (near
LAA pole 6), producing a disassociated pattern between the left
Ligament/vein of Marshall atrial electrograms and the electrograms from the coronary
sinus muscle.
Probe
Figure C4.4
CS
CS 9
CS 8
Pacing
CS 7 site
CS 6 * 1
LA CS
CS 5 catheter 2
CS 4 LA
CS 3 activation 3
CS
CS 2 10 4
CS 1 5
S 100 msec
9 8 7 6
CS activation
Figure C4.5 (Adapted from Antz M, Otomo K, Arruda M, Scherlag BJ, Pitha J, Tondo C, et al. Electrical conduction between the right
atrium and the left atrium via the musculature of the coronary sinus. Circulation. 1998 Oct 27;98[17]:1790–5. Used with permission.)
High Output Low Output
CS-LA connection CS-LA connection

11,12 11,12
9,10 9,10
7,8 7,8
5,6 5,6
3,4 3,4
1,2 1,2
CS LA CS LA
Figure C4.6
Fourth, with high-output pacing from the coronary sinus, sinus muscle alone is activated and, depending on the site of
parallel and simultaneous activation occurs in the coronary breakthrough activation to the left atrium, different patterns
sinus and left atrium. At low-output pacing, the coronary of left atrium activation are noted (Figures C4.5 and C4.6).
Case 4 313
Figure C4.7
Fift h, isolation of the pulmonary vein is important in the Figure C4.8 shows the right lateral view of the heart. What
ablation of atrial fibrillation. Although this concept is some- other reason might explain the inability to electrically iso-
what controversial, tracings like the one in Figure C4.7 clearly late a pulmonary vein, despite circumferential ablation
illustrate the arrhythmogenicity of the pulmonary veins. In around the vein (arrow)?
this tracing, the PV catheter shows rapid activation through- A. Atrial ventricular bypass tract
out the tracing, even after completion of circumferential iso- B. Right atrium to right upper pulmonary vein, muscular
lation of this vein and restoration of sinus rhythm (as seen on or electrical connection
the surface leads, HRA catheter, and CS catheter). If the pul- C. Left upper pulmonary vein to right upper pulmonary
monary vein is to be isolated from the rest of the atrium, then vein connection
in certain cases, connections other than those at the ostium D. Left upper pulmonary vein to left lower pulmonary
of the vein need to be diagnosed and ablated. One such con- vein connection
nection was shown in Figure C4.1. E. Azygous vein to right upper pulmonary vein connection
Answer: B—Right atrium to right upper pulmonary vein,
muscular or electrical connection.
Figure C4.8
Usually, the anterior surface of the right-sided pulmo-

nary vein is sharply demarcated and separate from the pos-
terior surface of the right atrium and superior vena cava
(Figure C4.9, arrow). In the autopsy specimen shown in Figure
SVC C4.8, a well-known (although somewhat rare) muscular con-
nection is seen; it can be an alternate route for arrhythmia
(arising from the pulmonary vein) to enter the atrium, despite
RAA adequate ablation at the ostium of the vein.
Diagnosis of this condition can be difficult but is usually
confirmed either because of continued initiation of atrial
fibrillation or persistent conduction into the vein (or both),
despite adequate ostial ablation. Another maneuver similar
SV to that described for vein of Marshall conduction can be used
to diagnose this condition.
Muscular
IVC
Figure C4.9
Connection
Activation sequence unchanged

= pulmonary vein potential
Activation sequence changed

at high and low output and
independent of pacing site
= connection

at high output only and
“moves” with pacing site
= far-field capture
Figure C4.10 (Adapted from Asirvatham SJ. Pacing maneuvers for nonpulmonary vein sources: part II. Heart Rhythm. 2007
May;4[5]:681–5. Epub 2007 Jan 12. Used with permission.)
With a multielectrode catheter placed in the right upper at a high or low output from various sites in the right atrium
vein (Figure C4.10) and pacing from the right atrium produces an identical pattern of distal early pulmonary vein
(“para-venous” pacing), early pulmonary vein potentials are potentials in the right upper vein, a connection with the right
seen more distal in the vein. These could be from far-field atrium can be diagnosed. In contrast, if this type of conduction
capture via the right atrial pacing catheter or conduction that is observed only with high-output pacing and varies with the
is occurring through a direct connection. However, if pacing site of pacing, then far-field capture can be diagnosed.
Case 4 315
Figure C4.11
Figure C4.11 shows electrograms captured by a linear, Abbreviations

multielectrode catheter that was placed in the left upper pul-
monary vein. Note that the pulmonary vein potentials are CS, coronary sinus [f]
earlier in the more distal electrode. The ablation catheter was IVC, inferior vena cava [f]
placed about 1 cm into the vein of Marshall. Note the early LA, left atrium [f]
ectopic beat with a spike-like potential in the ablation cath- LAA, left atrial appendage [f]
eter in the vein of Marshall. Following the vein of Marshall PVP, pulmonary vein potential [f]
activation, the pulmonary vein is activated even before any RA, right atrium [f]
left atrial activation is evident. Note also that the coronary RAA, right atrial appendage [f]
sinus muscle activation is late. This is because the muscula- S, stimulus artifact [f]
ture of the vein of Marshall is activated fairly distant from the SV, sinus venosus [f]
main body of the coronary sinus. SVC, superior vena cava [f]
Case 5
Figure C5.1

Terms with “[f]” denote abbreviations that appear in the figures only.
317
Retrograde His
Figure C5.2
A 37-year-old patient presented with a 10-year history of In addition, Figure C5.2 shows that when the ventricu-
sudden-onset, sudden-offset palpitations. The palpitations lar extrastimulus is placed, 2 findings supporting AV node
could be stopped reliably with carotid sinus massage or a reentry are observed. First, a retrograde His bundle potential
Valsalva maneuver. In sinus rhythm, no preexcitation was now is apparent (arrow) because the retrograde right bundle
noted. Figure C5.1 shows the intracardiac tracing during branch is refractory, owing to the prematurity of the extra-
tachycardia. Figure C5.2 shows the result of ventricular extrastimulus. Thus, instead of propagating up the right bundle
stimulus placement during ventricular pacing. branch, the wavefront must traverse the septum, enter the
left bundle, and then ascend to the His bundle. Th is delay
What is the likely diagnosis?
separates the timing of the ventricular and His bundle sig-
A. Left lateral accessory pathway nals such that the His potential is now visible (normally, it is
B. Two accessory pathways not seen because of simultaneous activation of the surround-
C. Atrioventricular (AV) node reentry with a bystander, ing ventricular muscle during ventricular pacing). Second,
left-sided pathway when the ventricle-to-His activation time is increased, the
D. Typical AV node reentry VA activation time is similarly increased, with no change in
E. Atypical AV node reentry the activation sequence. If a retrograde-conducting acces-
Answer: D—Typical AV node reentry. sory pathway was present, then VA conduction likely would
be independent of a delay in the His bundle activation. Thus,
Figure C5.1 shows an eccentric activation sequence in the even though the coronary sinus activation is eccentric, VA
coronary sinus, defined as activation of the distal coronary conduction is dependent on His bundle conduction (ie, AV
sinus electrodes (CS 1,2) with atrial potentials that are acti- node dependent). Note also that despite the eccentric acti-
vated ahead of more septal sites (CS 19,20, etc). This usually vation of the coronary sinus, the signal from the proximal
suggests a left lateral accessory pathway. In this case, how- His bundle catheter (surrogate for the fast pathway) is earlier
ever, a more likely diagnosis is AV node reentry. The inter- than any potential in the coronary sinus. Because the earliest
val between the first ventricular activation and the first atrial site of activation is the fast pathway, the patient has typical
activation (the ventriculoatrial [VA] interval) is extremely AV nodal reentrant tachycardia (earliest site of activation in
short; in fact, it is negative because atrial activity precedes atypical AV node reentrant tachycardia is the proximal coro-
ventricular activity. nary sinus).
Case 5 319
FP
FO
CS SP
Figure C5.3
HB
RAO
FO TT FP lesion
IVC CS SP lesion
TA
Figure C5.4
In the right anterior oblique view of the right atrium and

ventricle (Figures C5.3 and C5.4), the important anatomic
sites relevant to AV node reentry are noted. In Figure C5.3,
the arrows point from the respective pathway (fast or slow)
toward the compact AV node (circled area). Because of ana-
tomic obstacles such as the fossa ovalis and eustachian ridge,
the inputs to the AV node are discrete, not circumferentially
continuous. The anterior and superior input to the AV node is
termed the fast pathway, whereas the atrial myocardial fibers
that connect the ostium of the coronary sinus to the compact
AV node is termed the slow pathway. During ventricular pac-
ing or tachycardia, if the retrograde fast pathway is activated
first, the earliest site of activation is behind the eustachian LAO
ridge and tendon of Todaro. Thus, the earliest atrial potential Figure C5.5
will be captured either by a catheter specifically placed in this
(fast pathway) location or by the proximal His catheter, which Figure C5.5 shows the right and left anterior oblique fluo-
is in close proximity to the fast-pathway site. However, with roscopic projections. Note that the arrows point to an ablation
retrograde slow-pathway activation, a catheter at the ostium catheter placed at the fast-pathway site. The important obser-
of the coronary sinus will show the earliest activation. vation in the left anterior oblique projection is the leftward dis-
placement and angulation of the catheter at the fast-pathway
location. This occurs because the catheter has “fallen” behind
the tendon of Todaro and eustachian ridge, allowing it to point
more left ward. In difficult cases, for which AV node reentry is
not obvious but still is considered as a diagnosis, a catheter
should be placed specifically at this site and the activation
with that of the proximal coronary sinus.
Although the above discussion explains why a catheter at

the fast-pathway location records an early potential, it does
not explain why activation does not proceed directly from
this site to the coronary sinus ostium. Unlike the eccentric
activation (distal to proximal) observed in Figure C5.1, a
direct path would yield a concentric (proximal to distal) acti-
vation of the coronary sinus.
Figure C5.8
Consider how activation can proceed from the fast path-

way exit into the slow pathway, situated across the fibrous
Eustachian valve and ridge eustachian ridge, which is composed predominantly of non-
conducting tissue. In some patients, activation can indeed
Figure C5.6
progress through the eustachian ridge (Figure C5.8).
Fast pathway AV node
Slow pathway
Figure C5.7
Figure C5.9
In Figure C5.6, a human atrium dissection is shown as it
would be seen in a left anterior oblique projection. Note the
prominent eustachian valve and ridge. The fast pathway is
located behind the eustachian ridge, whereas the slow path- More commonly, however, the eustachian ridge forms an
way is more ventricular to the eustachian ridge, in the region electroanatomic boundary. Activation must proceed around
of the coronary sinus ostium. Figure C5.7 depicts a wavefront the eustachian ridge, gaining access to the slow pathway
propagating into the compact AV node from the slow path- inputs by traversing inferior to the crista terminalis (Figure
way, with a retrograde exit into the fast pathway (ie, typical C5.9). From there, it enters the cavotricuspid isthmus and
slow-fast AV nodal reentrant tachycardia). then the compact AV node and slow-pathway region.
Case 5 321
Figure C5.10 Figure C5.12
In some patients, the crista terminalis and the eustachian Less commonly, because of these anatomic boundaries,
ridge together form a boundary, and the fast-pathway exit site the right atrium does not allow any conduction from the
activation must proceed around the crista terminalis, on the fast-pathway exit site to the slow-pathway region and compact
ventricular side of the eustachian ridge (Figure C5.10). AV node. Activation must then proceed by crossing either the
fossa ovalis or the Bachmann bundle region to first enter the
left atrium (Figure C5.11). After the left atrium is entered,
connections between the left atrium and coronary sinus are
used to activate the musculature of the coronary sinus, which
in turn determines the atrial activation sequence on the coro-
nary sinus catheter (Figure C5.12).
Figure C5.11
CS catheter Noncontact map of adjacent LA
LAA LAA
LA LA
Proximal to distal Proximal to distal

19/19 (100%) 4/19 (21%)
LAA
LA
Distal to proximal
4/19 (21%)
LAA
LA
Fused
11/19 (58%)
Figure C5.13
Why then does distal-to-proximal coronary sinus acti- activation of the left atrial tissue (adjacent to the coronary
vation occur? Why can’t the left atrial wavefront enter a sinus) occurs in a distal-to-proximal manner. If the patient’s
more proximal coronary sinus location and proceed to the AV node reentry circuit uses left atrial activation and the
left atrium? Figure C5.13 shows the results of a study that patient has distal-to-proximal activation of the left atrium,
compared global left atrial activation sequences during then the coronary sinus connection will be entered more lat-
sinus rhythm using noncontact mapping. In some patients, erally, resulting in eccentric coronary sinus activation.
Case 5 323
II II
CL = 395 msec CL = 395 msec
RV prox RV prox
HRA HRA
VA = 120 msec VA = 120 msec
His His

CS prox CS prox
CS mid CS mid
CS dist CS dist
Before RFA After RFA

Figure C5.14 (Adapted from Luria DM, Nemec J, Etheridge SP, Compton SJ, Klein RC, Chugh SS, et al. Intra-atrial conduction block
along the mitral valve annulus during accessory pathway ablation: evidence for a left atrial “isthmus”. J Cardiovasc Electrophysiol. 2001
Jul;12[7]:744–9. Used with permission.)
Another surprising manifestation of a conduction path- distal coronary sinus (concentric activation), with no change
way through the coronary sinus muscle and left atrium is the in the tachycardia cycle length. This outcome can occur
observation shown in Figure C5.14. Before radiofrequency with typical AV node reentry after ablation of a left, lateral
ablation, a distal-to-proximal (eccentric) activation of the bystander pathway. However, this patient clearly did not have
coronary sinus was noted, consistent with the presence of a AV node reentry, a finding confirmed later in the study by
left, lateral accessory pathway. After a single ablative lesion, ablation of the lateral accessory pathway. Diagnostic maneu-
an abrupt change in the activation sequence occurred such vers confirmed that the pathway was a critical constituent of
that the proximal coronary sinus was activated before the the circuit.
His bundle
catheter Two possible explanations can account for this change
AP in activation pattern. Figure C5.15 shows the left anterior
connection
oblique view of the mitral annulus. Ablation may have been
performed proximal to the actual site of the accessory path-
way, leading to conduction block in the isthmus between the
left inferior pulmonary vein and the mitral annulus. After
ablation, left atrial activation could not proceed from lat-
eral to medial because of the block, so it instead proceeded
LIPV
in a clockwise pattern, resulting in concentric activation of
the coronary sinus catheter. This explanation presupposes
a small isthmus between the left inferior pulmonary vein
RFA lesion in and mitral annulus, as well as the absence of musculature in
left “isthmus” the left inferior pulmonary vein that can participate in the
circuit.
Coronary sinus
catheter
Figure C5.15 (Adapted from Luria DM, Nemec J, Etheridge SP,
Compton SJ, Klein RC, Chugh SS, et al. Intra-atrial conduction
block along the mitral valve annulus during accessory pathway
ablation: evidence for a left atrial “isthmus”. J Cardiovasc
Electrophysiol. 2001 Jul;12[7]:744–9. Used with permission.)
CS
CS 9
CS 8
Pacing
CS 7 site
CS 6 * 1
LA CS
CS 5 catheter 2
CS 4 LA
CS 3 activation 3
CS
CS 2 10 4
CS 1 5
S 100 msec
9 8 7 6
CS activation
Figure C5.16 (Adapted from Antz M, Otomo K, Arruda M, Scherlag BJ, Pitha J, Tondo C, et al. Electrical conduction between the right
atrium and the left atrium via the musculature of the coronary sinus. Circulation. 1998 Oct 27;98[17]:1790–5. Used with permission.)
Another explanation for the change in activation after abla- through the pathway that inserts into the left atrial muscle
tion is that a connection from the lateral coronary sinus to the can activate the coronary sinus only through a more proxi-
left atrium has been eliminated. Now, retrograde conduction mal left atrium coronary sinus connection (Figure C5.16).
Figure C5.17
In Figure C5.17, the IS catheter was placed in the left atrium, recordings. Within the left atrium, atrial activation proceeds
just opposite the CS catheter; note the similar amplitude of from IS 7,8 to IS 1,2. The absence of lateral propagation from
ventricular and atrial signals in both catheters, consistent IS 7,8 to IS 9,10 is because of conduction block. Instead, the
with an annular position. Whereas atrial activity on the CS tracing shows activation from the Bachmann bundle or the
catheter proceeds smoothly from the proximal to distal elec- left atrial roof, resulting in propagation from IS 19,20 to IS 7,8.
trodes, intra-atrial conduction block is seen in the left atrial IS Double potentials are seen at IS 7,8 at the site of block (arrow).
Case 5 325
This tracing clearly demonstrates the potential for dissocia- FP, fast pathway [f]
tion of coronary sinus activation and left atrial activation. This HB, His bundle [f]
important observation can be the key to understanding dif- IVC, inferior vena cava [f]
ficult accessory pathway or atypical left atrial flutter ablation LA, left atrium [f]
in this region. LAA, left atrial appendage [f]
LAO, left anterior oblique [f]
LIPV, left inferior pulmonary vein [f]
Abbreviations RAO, right anterior oblique [f]
RFA, radiofrequency ablation [f]
AP, accessory pathway [f] S, stimulus artifact [f]
AV, atrioventricular SP, slow pathway [f]
CL, cycle length [f] TA, tricuspid annulus [f]
CS, coronary sinus [f] TT, tendon of Todaro [f]
FO, fossa ovalis [f] VA, ventriculoatrial
Case 6
A 31-year-old man who was a lifelong long–distance run- Valsalva-like maneuvers terminated most episodes, but
ner presented with palpitation episodes that had troubled early recurrences were frequent. In the past few months,
him for the past 5 years. Symptoms were exacerbated with he had become fatigued even when not experiencing
exercise, and the palpitations often had a sudden offset. palpitations.
Figure C6.1
327
http://medical.dentalebooks.com
Figure C6.2
Figure C6.1 is the 12-lead electrocardiogram obtained Typical AV node reentry usually presents as a short R-P
while the patient was having typical symptoms. Figure C6.2 tachycardia; however, in certain situations, retrograde con-
shows event monitor strips recorded during termination and duction through the fast pathway is much quicker than the
initiation of the tachycardia. antegrade conduction through a portion of the compact AV
Which of the following diagnoses can be excluded? node and His bundle. Thus, from the turnaround point in
A. Ectopic atrial tachycardia from the coronary sinus the AV nodal reentrant tachycardia (AVNRT) circuit, atrial
musculature activation occurs markedly before ventricular activation, giv-
B. Atypical atrioventricular (AV) node reentry ing rise to a long R-P tachycardia. The electrocardiograms
C. Typical AV node reentry presented do not exclude this unusual possibility, which
D. Sinus tachycardia sometimes is seen in young children with very fast, retro-
E. None of the above grade, fast-pathway conduction or in older individuals with
bundle branch block and infrahisian conduction disease. It
Answer: D—Sinus tachycardia.
exemplifies the concept that the R-P interval (ventriculoatrial
The salient features of the electrograms in Figures C6.1 [VA] interval) is a pseudo-interval and does not represent VA
and C6.2 are the long R-P interval and the prominent nega- conduction.
tive P waves in the inferior leads. Several additional details on Note the beat in Figure C6.2 shown with the arrow, the
the tracings are worth noting. P wave is negative, as is the P wave during tachycardia.
The 12-lead electrocardiogram shows a narrow complex However, the P wave is narrow. Retrograde, fast-pathway
tachycardia with a long R-P interval. The P-wave morphology conduction (such as from this likely junctional beat) exits
during tachycardia suggests an origin in the inferior, poste- in the true interatrial septum and gives rise to a narrow
rior region of the atrium. The P wave is negative in leads II, P wave, whereas retrograde, slow-pathway activation
III, and aVF. This P wave axis can be seen in coronary sinus occurs via the coronary sinus (not part of the true inter-
tachycardia, posterior right or left atrial tachycardia, and atrial septum) and is associated with a wider P wave but
junctional tachycardia with an atrial exit through the slow– with a similar axis.
pathway region. It can also be seen in accessory pathway– Examine the initiating beat of tachycardia in the lower panel
mediated AV reentrant tachycardia, with a pathway located of Figure C6.2. No P wave is discernible, which suggests that a
in the posteroseptal region of the atrium; a variant of this junctional beat was responsible for tachycardia initiation. This
specific tachycardia is permanent junctional reciprocating argues against the diagnosis of ectopic atrial tachycardia. In
tachycardia (PJRT), in which the accessory pathway exhib- most instances (except with triggered activity), the initiating
its retrograde decremental conduction. Tachycardias arising beat in automatic atrial tachycardia has a P-wave morphol-
from the peri–sinus node region, Bachmann bundle region, ogy that is identical to the subsequent beat. Possible explana-
or left atrial roof consistently show a positive P wave in leads tions in this case would be a junctional beat with retrograde,
II, III, and aVF because of the supero-inferior axis of atrial slow-pathway conduction or a junctional beat with decremen-
activation in arrhythmias. Thus, the P-wave morphology tal, accessory-pathway conduction. These mechanisms would
alone virtually excludes sinus tachycardia. then initiate atypical AVNRT or PJRT, respectively.
Case 6 329
Figure C6.3
After catheter insertion (in the same patient), the trac- unchanged both in timing and activation sequence, despite a
ing in Figure C6.3 was obtained. The arrow points to a significant delay in the ventricle-to-His time, this is diagnostic
retrograde His bundle potential. When retrograde right of VA activation via an accessory pathway (see Chapter 4).
bundle branch block occurred (as with this premature ven-
tricular contraction [PVC] after a pacing train), ventricular
activation crossed the intraventricular septum and a wave
Box C6.1
front traveled up the left bundle to activate the His. Th is is
Points to Remember
observed frequently during electrophysiology studies and
ablation procedures. • Activation sequence is as important as ventricle-to-atrium
activation time when analyzing the effect of retrograde right
Given the observation described above, which conclusion bundle branch block or parahisian pacing.
• Retrograde right bundle branch block may reveal useful
can be drawn?
clues about the mechanism of ventricle-to-atrial activation.
A. Retrograde activation is occurring via an accessory
pathway
B. Retrograde activation during ventricular pacing is via
the AV node This phenomenon can be useful for identifying the mech-
C. Retrograde activation during ventricular pacing occurs anism of VA activation when the activation sequence does
via more than 1 mechanism not change. In the tracing in Figure C6.3, there is an obvious
D. None of the above change in the atrial activation sequence after the beat with
retrograde right bundle branch block. (The arrow points to
Answer: D—None of the above.
the retrograde His bundle deflection.) Thus, several possible
Several concepts must be understood to correctly inter- mechanisms remain, including 1) conduction via an acces-
pret this tracing. When retrograde right bundle branch block sory pathway during ventricular pacing, with a block in the
occurs and His bundle activation is markedly delayed com- accessory pathway when retrograde right bundle branch block
pared with ventricular activation, analysis of the subsequent occurs and subsequent conduction is via an AV nodal path-
effect on atrial activation can be revealing. If the retrograde way; 2) complete VA block with initiation of an ectopic atrial
His activation is delayed and the atrial activation is also tachycardia; 3) accessory pathway and AV nodal conduction
delayed by a similar amount (with no change in the activa- during ventricular pacing; and 4) either accessory pathway
tion sequence), then this is strongly suggestive of retrograde or AV nodal conduction only in the beat after the retrograde
activation via the AV node. In contrast, if VA activation is bundle branch block (Box C6.1).
Figure C6.4
Figure C6.4 shows electrograms recorded while para- analyzing tracings with retrograde right bundle branch block.
hisian pacing was being performed. The first beat was with With parahisian pacing at low output, the local ventricular
high-output pacing, which resulted in a narrow QRS complex. myocardium is captured, but the His bundle is not directly
The second beat was with low-output pacing, which resulted captured. The ventriculo-His interval is increased when the
in a wider QRS complex and the appearance of a retrograde His is not captured. In this case, the ventriculo-His interval
His bundle potential (arrow). increased the VA interval, with no change in the atrial activa-
What can be concluded from this maneuver? tion sequence. This finding is diagnostic of VA activation via
A. Retrograde conduction is via an accessory pathway the AV node. Note that the eccentric sequence does not exclude
B. Retrograde conduction is via the AV node AV nodal conduction. This is because the mid coronary sinus,
C. Retrograde conduction is from both the accessory and in some instances the distal coronary sinus, may be acti-
pathway and the AV node vated before the proximal coronary sinus, despite retrograde,
D. Retrograde conduction cannot be determined with fast-pathway activation. This is true for patients with retro-
this maneuver because the atrial activation sequence is grade, fast-pathway conduction who have a block between the
eccentric fast pathway and the ostium of the coronary sinus (see Case 5).
Note, however, that if an atrial potential was seen on the His
Answer: B—Retrograde conduction is via the AV node.
bundle catheter or if an ablation catheter was placed in the
The logic behind the interpretation of parahisian pac- fast-pathway region, activation at these sites would have been
ing is very similar to that described above, with reference to earlier than the earliest site in the coronary sinus.
Case 6 331
Figure C6.5
Tachycardia was initiated during atrial pacing (Figure sequence is more similar to tachycardia than atrial pacing.
C6.5). Given this mechanism of initiation, which mecha- Because this occurs at the pacing rate, the tachycardia may
nism of tachycardia can be excluded? have already initiated by the time of the paced event. The fact
A. Automatic atrial tachycardia that the second atrial paced beat occurs at the pacing cycle
B. Reentrant atrial tachycardia length suggests a reentrant mechanism or a triggered-activity
C. PJRT mechanism, which (in the case of reentry) reflects entrain-
D. AV node reentry ment by the second paced beat.
E. None of the above When a supraventricular tachycardia is initiated during
atrial pacing without a significant change in the atrial-His
Answer: E—None of the above. (AH) interval, an automatic mechanism is likely; however,
Several key points in the tracing in Figure C6.5 deserve several other mechanisms of tachycardia still are possible.
attention. The coronary sinus activation sequence during For example, if the first atrial paced beat resulted in a 2-for-1
tachycardia is similar but not identical to the first paced beat. phenomenon (antegrade conduction down the fast and slow
This suggests that the tachycardia has its earliest site of acti- pathways) and if the retrograde activation of the fast pathway
vation either in the right atrium, where pacing is being per- was much faster than antegrade conduction from the tachy-
formed, or on the intero-atrial septum. Sometimes, analyzing cardia turnaround point to the His bundle, then this type of
the differences between these sequences can shed light on the initiation is possible. This is sometimes seen in left-sided AV
site of origin or earliest site of activation of tachycardia. Note node reentry and also when typical AV node reentry occurs
that in the second paced beat, the coronary sinus activation in the extremes of age.
Figure C6.6
PJRT is also possible with this type of initiation. Here, conducting pathway. Of the mechanisms of tachycardia
very slight (sometimes imperceptible) changes in atrial described above, however, the subtle fi nding of the change
pacing cycle lengths can initiate tachycardia by retro- in atrial activation in the second beat supports a reentrant
grade activation through a very decremental and slowly mechanism (Figure C6.6).
Figure C6.7
Case 6 333
In Figure C6.7, observation of the atrial cycle length and sequence), which suggests either AV nodal reentry or AV
the atrial activation sequence shows that tachycardia already reentry. However, as the atrial activation sequence and
had been initiated during the ventricular pacing train. Even the atrial cycle length do not change, ventricular pacing is
very subtle changes in the coronary sinus activation sequence not entraining the tachycardia. One-to-one entrainment
(eg, reversal of far-field and near-field signals) suggest that VA is required for further analysis of the Morady maneuver.
activation is occurring through a connection distinct from Finally, ventricular pacing in long R-P tachycardias can be
that used for tachycardia propagation. particularly difficult to interpret because VA times can be
Similar reasoning is also used when analyzing the long with PJRT or atypical AVNRT. The phenomenon of
Morady maneuver (see Chapter 4). For example, in this postexcitation, with ventricular pacing delaying the next
instance, ventricular pacing may be occurring during atrial beat, can be powerful evidence of a decremental VA
tachycardia. Upon cessation of ventricular pacing, the fi rst connection (access pathway or AV node) as the mechanism
return potential is atrial (ventricle-atrial-ventricle [V-A-V] of tachycardia.
Figure C6.8
Just as it is important to analyze the initiation of tachy- dependent on the AV node (eg, AV node reentry or AV reen-
cardia, a study of termination can provide important clues trant tachycardia).
about the tachycardia mechanism and the potential sites for Note that the termination occurred after a PVC
ablation. In the tracing in Figure C6.8, tachycardia terminated (Figure C6.8). The PVC was coupled very late and did not sig-
with an atrial electrogram sequence identical to previous beats nificantly affect the AV interval during the tachycardia. The
of tachycardia with no QRS or ventricular potentials (termi- PVC likely penetrated into the AV node or infrahisian tissue,
nation with an atrial potential). This phenomenon of termina- which caused an antegrade block of the subsequent beat. A
tion with an atrial potential was repeatedly seen during the clear His bundle deflection is not seen in this tracing, so the
procedure. penetration and site of block was unknown.
Th is type of termination is highly unlikely to occur in Another observation from this tracing was that the PVC
atrial tachycardia because it would require simultaneous morphology suggested a right ventricular outflow tract or sep-
termination of antegrade conduction to both the ventricle tal origin, and yet there was no postexcitation of the retrograde
and the focus of the atrial tachycardia. Occasionally, vagally atrial activation, which had an earliest site near the septum.
responsive atrial tachycardias may terminate in this way This argued against a septal, decrementally conducting pathway
with a Valsalva maneuver or with adenosine. However, the and could be considered minor evidence for AV node reentry
repeated occurrence of such a termination argues against over AV reentry using a decremental, retrograde-conducting
atrial tachycardia and strongly favors an arrhythmia pathway (not diagnostic, but a subtle consideration).
105 msec
Figure C6.9
A consistent prepotential is noted on the ABL d catheter surrounding atrial tissue from the site of origin. If this were
(Figure C6.9) when mapping posteriorly near the roof of the an automatic tachycardia, the electrogram with a far-field
coronary sinus (about 105 milliseconds before the onset of the early potential and near-field late potential in the roof of the
surface P wave). coronary sinus would have suggested an origin in the atrial
musculature.
Which statement is most consistent with the above Reentrant arrhythmias of any kind have continuous
finding? electrical activity, and thus electrical signals can be found
A. Automatic atrial tachycardia arising from the left far ahead of the surface P wave. In PJRT, such early signals
atrium in a patient with a normal heart may represent a pathway potential. In AV node reentry or
B. Automatic atrial tachycardia arising from the coronary reentrant atrial tachycardia, these early potentials represent
sinus musculature in a patient with a normal heart portions of the atrium being activated at or proximal to the
C. A reentrant tachycardia mechanism slow zone (AVNRT lower common pathway or AV node). In
D. Junctional tachycardia patients with diseased atria, reentrant arrhythmias are more
common, but automatic tachycardias may also occur. If they
Answer: C—A reentrant tachycardia mechanism.
do occur, there may be an inordinate delay between the earli-
Automatic tachycardias in a normal heart, regardless of est site of activation (origin of the tachycardia) and recruit-
coronary sinus or atrial origin, will rarely precede the onset ment of the surrounding atrial tissue. Even so, activation
of the surface P wave by more than 40 milliseconds. This is 105 milliseconds ahead of the surface P wave (Figure C6.9)
because of the relatively rapid recruitment and conduction of would be unusual in an automatic tachycardia.
Case 6 335
Figure C6.10
In this patient, several maneuvers confirmed the diagnosis (linear, slow-pathway ablation). During ablation, the tracing
of AV node reentry. These included parahisian pacing, induc- in Figure C6.10 was obtained.
tion of retrograde right bundle branch block, and differential Note the occurrence of junctional beats. At times, it may
ventricular pacing. All showed that retrograde conduction be difficult to distinguish between junctional beats vs a slower
was entirely through the AV node. Furthermore, the tachy- form of AV node reentry. Note that sinus rhythm gradually
cardia could be reset from the ventricle with closely coupled gets faster, and in doing so, easily advances the antegrade His
premature ventricular extrastimuli, without changing the and ventricular potentials, while the AH interval remains
retrograde atrial activation sequence, and only by advancing normal. This finding is consistent with junctional rhythm. In
the retrograde His potential by approximately 40 millisec- AV node reentry, only tightly coupled atrial beats can advance
onds. Because of these findings, the slow pathway was ablated, the circuit, and this may occur only with prolongation of the
and ablation continued into the ostium of the coronary sinus AH interval (see Chapter 4).
Figure C6.11
During catheter manipulation (before radiofrequency

Box C6.2 ablation), the tracing in Figure C6.11 was obtained. Note that
Points to Remember the tachycardia continued with an atrial activation sequence
• Careful analysis of both initiation and termination of identical to that previously observed but with complete AV
supraventricular tachycardia can be revealing. block (Figure C6.11). Such a finding usually suggests atrial
• Attention must be paid to the atrial cycle length and detailed
tachycardia as the mechanism of the arrhythmia, but this
activation sequence to know when exactly the tachycardias
started. patient had AV node reentry. Catheter manipulation likely
• Repeated termination of tachycardia with an atrial potential resulted in mechanical trauma to either the lower common
argues against atrial tachycardia. pathway or the compact AV node, distal to the turnaround
• In a normal heart, prepotentials more than 40 milliseconds point of the tachycardia circuit. In fact, in some patients with
before onset of the surface P wave suggest reentry.
atypical AV node reentry, ablation of the lower common path-
• AV dissociation may occur in AV node reentry, with a level
of block at the lower common pathway, AV node, or infra- way can leave the patient with a propensity for atrial tachycar-
hisian tissue. dia. This frequently is misdiagnosed as a second arrhythmia
• Junctional tachycardia, rather than AV nodal reentrant but likely represents atypical AVNRT with lower common
tachycardia, is suggested by the ability of an atrial rhythm pathway block (Box C6.2).
to reset an AV nodal reentrant tachycardia–like rhythm
with late, coupled, atrial activation and a short atrial-His
interval.
Abbreviations
AH, atrial-His
AVNRT, atrioventricular nodal reentrant tachycardia
PJRT, permanent junctional reciprocating tachycardia
PVC, premature ventricular contraction
VA, ventriculoatrial
V-A-V, ventricle-atrial-ventricle
Case 7
Figure C7.1
The electrocardiogram in Figure C7.1 was obtained during C. There is marked capture latency
ventricular extrastimulation during an electrophysiology D. There is ventricular failure to sense
(EP) study. E. This is bundle branch reentrant tachycardia
What can be concluded from this tracing? Answer: D—There is ventricular failure to sense.
A. Ventricular pacing is being performed from the right During ventricular extrastimulation testing, ventricu-
ventricular outflow tract lar fibrillation or polymorphic ventricular tachycardia may
B. It shows an abnormal finding occur. The significance of these events is unknown. Generally,
a patient with a normal heart and good long-term progno-
Abbreviations are expanded at the end of this chapter. sis can have ventricular fibrillation induced by 3 or 4 tightly
337
coupled ventricular extrastimuli. Even more difficult to inter- duration from stimulus to capture, termed capture latency, is
pret is the finding of so-called ventricular flutter (ie, rapid, minimal, which suggests that the heart is structurally normal
sine wave–like, but monomorphic ventricular tachycardia) (Table C7.1). Conditions such as ischemia, sodium channel
that is induced by aggressive extrastimuli. blocker or amiodarone use, and prior cardiac surgery prolong
In this tracing, the pacing site is the right ventricular apex, capture latency. In ischemic cardiomyopathy, when pacing
as shown by a left bundle branch block pattern in lead V1 and in an area within a scar with slow conduction, an extreme
a prominent S wave in leads II and aVF (superior axis). Note delay can occur between the pacing spike and the exit site,
also that aVR and aVL are both positive, which suggests an at which point the QRS is inscribed. During left ventricular
inferior or apical pacing location. In contrast, remember that lead implantation for cardiac resynchronization therapy, cap-
aVR and aVL are both negative when the site of origin (pacing ture latency and capture thresholds should be assessed. Even
or ventricular tachycardia) is from the outflow tract region. with good capture thresholds, if capture latency is inordi-
nately long, effective biventricular synchronization will not
be accomplished. Table C7.1 summarizes the clinical electro-
Table C7.1 physiologic significance of capture latency.
Significance of Capture Latency Note that pacing spikes are seen during the ventricular
Duration of Latency Significance arrhythmia, which is evidence of failure to sense. This finding
occurs fairly frequently during EP studies and may re-induce
Normal or short Structurally normal heart
fibrillation or flutter; if inappropriate ventricular pacing con-
Marked increase Confusion with entrainment mapping,
in which capture latency may give tinues as a result of failure to sense, it may give the impression
the impression of failure to entrain a of a sustained arrhythmia. This is because spontaneous ter-
reentrant arrhythmia mination is not recognized, and the continued pacing reiniti-
In cardiac resynchronization, marked ates the tachycardia.
capture latency on the left ventricular In certain situations, induction of ventricular fibrillation
pacing lead will render therapy may be an abnormal finding, such as when the arrhythmia
ineffective is induced with a single or double extrastimuli but without
a short coupling interval. It is also abnormal for the initial
induction of a monomorphic ventricular arrhythmia to
Note that for even the third extrastimulus, the time from degenerate into a polymorphic ventricular tachycardia or into
the pacing stimulus to the QRS complex is short. Thus, the ventricular fibrillation.
Figure C7.2
Case 7 339
Figure C7.3
The 12-lead electrocardiograms were obtained before Sometimes, significant J-point elevation can be seen in
(Figure C7.2) and after (Figure C7.3) an intervention. young, athletic males; however, the extent of J-point elevation
Which statement is most consistent with the data shown? typically is no more than 25% of the height of the T wave.
A. Right bundle branch block occurring in the setting of Thus, the overall finding in these young individuals is a tall,
cardiomyopathy peaked T wave, with relatively minimal J-point elevation.
B. Right ventricular dysplasia In this tracing, taken after the infusion of procainamide
C. Acute right ventricular ischemia (Figure C7.3), J-point elevation is about 75% of the height of
D. Brugada syndrome showing the results of procain- the T wave. If atypical right bundle branch block is observed
amide infusion in a patient with a family history of syncope or sudden death,
E. Nonspecific finding often seen in male athletes the diagnosis of Brugada syndrome should be considered.
Brugada syndrome is a primary arrhythmic syndrome
Answer: D—Brugada syndrome showing the results of pro-
characterized by an electrocardiogram with apparent right
cainamide infusion.
bundle branch block and ST elevation plus T-wave inver-
On the baseline electrocardiogram (Figure C7.2), a right sion in the right precordial leads (V1 through V3). Because
bundle branch block pattern is seen. With right bundle of the T-wave inversion in the right precordial leads, dis-
branch block, usually an rSR′ pattern and a tall R wave are tinction from right ventricular cardiomyopathy is required.
seen in lead V1, in addition to a broad and sometimes deep These electrocardiographic changes are exacerbated by the
S wave in leads V5 and V6. When the changes in leads V5 and administration of class I antiarrhythmic medications, with
V6 are absent, conditions that mimic right bundle branch concomitant conduction abnormalities and the induction of
block should be considered. ventricular fibrillation.
properties. Diminished sodium currents cause loss of the

Box C7.1 “dome” in epicardial cell action potentials and create a
Salient Features of Brugada Syndrome voltage gradient between the epicardium and endocar-
Reduced peak sodium currents and loss-of-function mutations dium. Th is in turn causes the characteristic ST elevation,
of SCN5A (encoding voltage-gated, cardiac sodium channel) which promotes phase II reentry and development of ven-
Abnormal ST segment in right precordial leads V1 through V3 tricular fibrillation. The male preponderance in this syn-
Use of class I antiarrhythmic medication to unmask ST-segment
abnormalities
drome (75%) is thought to be due to the greater transient
Ventricular fibrillation occurs in 40% of patients with 5 years outward potassium currents seen in men, which render
of follow-up them more susceptible to loss of the dome in the epicar-
Syndrome overlaps with short QT syndrome or long QT dial action potential. The electrocardiographic changes are
syndrome type 3 dynamic (may come and go), and repeated tracings may be
Identical to sudden unexpected death syndrome in Southeast
Asia
required. Frequently, class I antiarrhythmic medications
are used to unmask the ST- and T-wave abnormalities. It is
important to note that the same SCN5A mutation can pro-
Brugada syndrome is inherited in an autosomal domi- duce overlapping syndromes. Members of the same family
nant pattern, and 20% of patients have a loss-of-function can have long QT syndrome type 3, Brugada syndrome, or
mutation in SCN5A, encoding a voltage-gated, cardiac other nonspecific, progressive diseases of the cardiac con-
sodium channel. The mechanism of arrhythmia is thought duction system. Box C7.1 summarizes the salient features
to be due to spatial heterogeneity of action potential of Brugada syndrome.
5 AM
Midnight
Figure C7.4 (Adapted from Nademanee K, Veerakul G, Nimmannit S, Chaowakul V, Bhuripanyo K, Likittanasombat K, et al.
Arrhythmogenic marker for the sudden unexplained death syndrome in Thai men. Circulation. 1997 Oct 21;96[8]:2595–600. Used with
permission.)
Sudden unexplained death syndrome is well documented the syndrome may have agonal respirations, brief and non-
in Southeast Asian males and now is known to be a manifes- sustained polymorphic ventricular arrhythmia, and labile ST
tation of the Brugada syndrome. During sleep, patients with segment changes, culminating in sudden death (Figure C7.4).
Case 7 341
Figure C7.5
The electrocardiogram in Figure C7.5 was obtained from a The relatively normal PR interval and the right bundle branch
patient with syncope that resulted in significant injury. It is block on the conducted beats strongly suggest infrahisian
most consistent with which diagnosis? disease as the cause of AV block. Note that the PR interval is
A. Brugada syndrome a strong predictor of the level of AV block; an increased PR
B. Infrahisian conduction disease interval in the conducted beats suggests compact AV nodal
C. Cardiac trauma block, whereas a short (normal) PR interval in the conducted
D. Overdose of digoxin beats suggests infrahisian block. There are exceptions to this
E. Arrhythmogenic right ventricular cardiomyopathy rule, particularly when the conducting bundle is abnormal
and slowly conducting. For example, in right bundle branch
Answer: B—Infrahisian conduction disease.
block, the left bundle conducts. If the left bundle also has sig-
When a patient presents with right bundle branch block and nificant disease, then the PR interval will be prolonged. Thus,
syncope, more extensive conduction abnormalities should be compact AV node disease and infrahisian disease may coex-
considered. Generally, right bundle branch block is an asymp- ist, giving rise to a long PR interval with an infrahisian level
tomatic, benign finding that occurs in patients with normal of block. However, the plasticity in the infrahisian system
hearts. Note the deep and long–duration S wave in leads V5 and (amount of delay that can occur before the block) is limited
V6; this is a typical finding in right bundle branch block (compare compared with the AV node. Thus, if the PR interval appears
this with Figures C7.2 and C7.3, showing Brugada syndrome). extremely prolonged, then the level at which maximal con-
Analysis of the relationship between the P wave and QRS duction slowing is present is almost always in the compact
complexes shows that there is atrioventricular (AV) block. AV node.
Figure C7.6
The electrocardiogram shown in Figure C7.6 is a complex during right bundle branch block. Furthermore, the extrasys-
tracing from the same patient described above. Note that the tolic beat has a right bundle morphology suggesting an origin
first beat shows sinus rhythm and a normal QRS complex. either in the AV node or left bundle branch. This extrasys-
Next are beats with a typical right bundle branch block pat- tolic beat may have caused left bundle branch block, and if
tern (tall R wave in V1 and slurred S wave in V6). The fift h conduction occurred via the AV node to the fast pathway,
beat is premature, with an incomplete right bundle branch then a block in the fast pathway may have given rise to a long
block pattern and a sharp initial upstroke; this suggests that PR interval (antegrade slow pathway conduction, left bundle
the beat originates above the Purkinje level and represents branch block, relatively slow conduction down the conduct-
either a conducted beat or a premature junctional beat. After ing right bundle, or a combination of these elements).
this beat is a long PR interval and then a QRS complex with Alternation between right and left bundle branch block
a left bundle branch block pattern that is considerably wider or right and left bundle branch blocks being seen at different
than both the extrasystolic beat and the previously conducted times is strongly suggestive of severe and labile infrahisian
beats. Again, a long PR interval usually signifies a conduction conduction disease. Although severe infrahisian disease typi-
abnormality in the compact AV node. However, in this patient, cally occurs in later stages of cardiomyopathy or advanced
after the left bundle was blocked, the right bundle conduc- age, it may precede the onset of overt cardiomyopathy in
tion was much slower than the left bundle conduction seen some situations (eg, Kearns-Sayre syndrome).
Case 7 343
Figure C7.7
The electrocardiogram in Figure C7.7 was obtained from the marked sinus arrhythmia, with greater than 25% varia-
another patient with syncope that resulted in injury. Brugada tion in the P-P intervals. These findings can occur in right
syndrome should again be considered. With a persistent ventricular trauma after chest or cardiac injury. An echocar-
T-wave inversion in leads V1 and V2 and a QRS complex that is diogram can be very helpful in this situation because severe
wider in the right precordial leads compared with the left pre- right ventricular wall motion abnormalities would be antici-
cordial leads, arrhythmogenic right ventricular cardiomyo- pated. The echocardiogram and the temporal profi le will help
pathy also should be considered. Note the deep S wave in lead distinguish echocardiographic changes attributable to syn-
V6 that suggests a true right bundle branch block. Also, note cope and trauma from primary electrical abnormalities.
60 ms
250 ms
V1
190 ms
V2
70 ms
Figure C7.8
In arrhythmogenic right ventricular cardiomyopathy, an arrhythmogenic right ventricular cardiomyopathy closely

epsilon wave may be present (Figure C7.8, arrow) because resemble those of cardiac trauma, additional imaging studies
of delayed activation of portions of the right ventricular can assess for the presence of myocardial fat or diverticulae,
myocardium. This deflection may give the appearance of an and an EP study can assess the inducibility of arrhythmias
incomplete right bundle branch block. Because of increased and late potentials. Such studies can help identify patients
right ventricular conduction delay, the QRS duration is typi- with arrhythmogenic right ventricular cardiomyopathy who
cally wider in the right precordial leads compared with the may benefit from an implanted cardioverter-defibrillator or
left precordial leads. Because echocardiographic findings of other antiarrhythmic therapy.
Case 7 345
I V1 I V1
II V2 II V2
III V3
III V3
aVR V4
aVR V4
aVL V5
aVL V5
aVF V6 aVF V6
Figure C7.9
The electrocardiogram in Figure C7.9 is from a patient Abbreviations

with arrhythmogenic right ventricular cardiomyopathy
(arrows point to the changes immediately following the QRS AV, atrioventricular
complex). Note the classic features of an epsilon wave and EP, electrophysiology
deep T-wave inversions (persistent, juvenile, T-wave pattern)
in leads V1, V2, and V3. Also note that, similar to Brugada syn-
drome, a right bundle branch block appears to be seen, but no
S wave is apparent in leads V5 or V6.
Case 8
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Figure C8.1
The electrocardiogram in Figure C8.1 is consistent with The main findings are a short PR interval and a clearly
which diagnosis? abnormal upstroke to the QRS complex (delta wave). This is
A. Dual atrioventricular (AV) nodal physiology best seen in lead I, where the delta wave is positive. In lead
B. A left-sided accessory bypass tract V1, the delta wave is isoelectric or slightly negative. These fea-
C. A right-sided accessory bypass tract tures are consistent with a right-sided bypass tract. Because
D. Dilated cardiomyopathy the degree of preexcitation is somewhat subtle, it is difficult
E. Left bundle branch block to ascertain from leads II, III, and aVF whether the accessory
Answer: C—A right-sided accessory bypass tract. pathway is anterior or inferior.
347
Portion of QRS
Showing Abnormality Electrocardiogram Cause of Abnormality
Initial Preexcitation
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Late Bundle branch block

I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Both parts Ventricular tachycardia,

I aVR V1 V4
(initial and late) preexcitation, and
bundle branch block
(Ebstein anomaly)
II aVL V2 V5
III aVF V3 V6
Figure C8.2
In patients with left bundle branch block, the initial por- this is an important finding that will help differentiate
tion of the QRS complex will appear normal, but the second between preexcitation and bundle branch block conduction
half of the QRS complex will be slurred (abnormal). When abnormalities (Figure C8.2).
analyzing tracings from Holter monitors and rhythm strips,
Case 8 349
Figure C8.3
Intracardiac catheters were placed in the patient. The CS was earlier than the ventricular deflection on the RVp cath-
15,16 electrodes were around the coronary sinus ostium, eter (positioned close to the apex). In sinus rhythm, the
and the CS 1,2 electrodes were in the distal coronary sinus. breakthrough site in the right ventricle usually is closer to
The electrocardiogram in Figure C8.3 was obtained. (The the apex, at the right bundle exit site; thus, the earliest ven-
artifact between the fi rst and second beats can be ignored.) tricular depolarization on the right side typically would be
Note that the His-ventricular (HV) interval is very short (12 seen on a right ventricular apical catheter, rather than the
milliseconds). Th is fi nding was consistent with an accessory His bundle catheter. When the right ventricular base depo-
bypass tract. Note also that the site of earliest ventricular larizes earlier than the apex, an AV bypass tract should be
activation was on the His bundle catheter (HBE 1–4) and considered.
Figure C8.4
Figure C8.4 shows an electrocardiogram from the same not decremental, the degree of preexcitation increases as con-
patient, taken while decremental atrial pacing was being per- duction via the AV node decreases, with more of the ventricle
formed at a cycle length of 400 milliseconds. Note that the being depolarized via the accessory pathway. The atrial-His
PR interval has lengthened. When atrial decremental pacing (AH) interval is expected to lengthen, as was noted in this
is performed in a patient with an AV accessory bypass tract patient, and the HV interval also is expected to become
(Table C8.1), decrement in conduction through the compact shorter and eventually negative (the ventricular potential pre-
AV node is expected. However, because AV conduction also is ceding the His potential) because of increased preexcitation.
determined by the bypass tract, the interval between stimulus Thus, the findings of this tracing were not consistent with the
and QRS onset does not change. Because most pathways are AV accessory pathway that was suspected initially.
Table C8.1
Effect of Decremental Atrial Pacing on Bypass Tracts and Related Phenomenon
Clinical Entity Stimulus-to- PR Interval AH Interval HV Interval Degree of Differential Effect of Parahisian Pacing Induction of Differential
QRS Interval Preexcitation Atrial Pacing Adenosine Retrograde RBB Ventricular Pacing
Block
Typical AV bypass No change Increased Increased Decreased Increased, with Increased Increased No change in VA No change in VA Decreased VA
tract and/or eventual preexcitation preexcitation interval (with interval with interval when
Becomes complete with atrial that may or without His development pacing at a
negative preexcitation pacing at become capture) if AP of RBB similar rate
a similar complete retrograde block if AP closer to the
rate closer conduction is retrograde base compared
to the atrial present conduction is with the apex
insertion of present
the AP
Decremental AV May increase Increased Increased Decreased Decreased Increased Both AP and ... ... ...
bypass tract or or preexcitation AV node
No change Increased with atrial may block,
or or pacing at resulting in
Slightly No change a similar complete AV
increased Depends on rate closer block
whether the to the atrial
decrement is insertion of
more in the the AP
AP or AV
node
Fasciculo- Increased Increased Increased No change No change No change No change in Parahisian Increased VH Decreased VA
ventricular preexcitation pacing cannot interval, interval when
bypass tract with AV block be performed increased VA pacing closer
Both low and interval, and to the base
high output no change compared with
produce in atrial the apex
a narrow, activation
complex QRS sequence if
if retrograde the fasciculo-
conduction via ventricular
the fasciculo- connection
ventricular is distal to
fiber is present the blocked
proximal right
bundle
(continued)
Table C8.1
Continued
Clinical Entity Stimulus-to- PR Interval AH Interval HV Interval Degree of Differential Effect of Parahisian Pacing Induction of Differential
QRS Interval Preexcitation Atrial Pacing Adenosine Retrograde RBB Ventricular Pacing
Block
Nodo- Mostly no Increased Increased Decreased Increased No change Transient No change in VA . . . Decreased VA
ventricular or change or or increase in interval (with interval when
nodoventricular- No change No change preexcitation or without His pacing closer
nodofascicular or AV block, capture) if AP to the base,
bypass tract depending on retrograde with nodo-
preferential conduction is ventricular
effects on the present and proximal
AV node Decreased VA nodofascicular
interval with tracts having
His or RBB retrograde
capture (or conduction
both) in a
nodofascicular
tract with
a distal
insertion into
the bundle
branch system
of the tract
Prinzmetal Increased Increased Increased No change No change No change AV block AV node Increased VH Decreased VA
phenomenon or response interval and interval when
May increased VA pacing closer
increase interval to the apex
compared with
the base
Abbreviations: AH, atrial-His; AP, accessory pathway; AV, atrioventricular; HV, His-ventricular; RBB, right bundle branch; VA, ventriculoatrial; VH, ventricular-His.
Case 8 353
Figure C8.5
Figure C8.5 illustrates the concept of differential atrial cycle length closer to the bypass tract will result in increased
pacing. In the first 2 beats, pacing is from the distal coronary preexcitation and a shorter HV interval. In this patient, the
sinus. In the last 2 beats, pacing is from the high right atrium. HV interval and preexcitation pattern did not change when
If a usual type of AV bypass tract is present, pacing at the same the pacing site was varied.
Figure C8.6
Figure C8.7
In Figure C8.6, an atrial extrastimulus was placed. Note clearly increased. Again, the HV interval did not change.
that the AH interval is slightly longer. In Figure C8.7, when These fi ndings were not consistent with a typical AV
a tighter atrial extrastimulus was placed, the AH interval bypass tract.
Case 8 355
Figure C8.8
In Figure C8.8, more rapid pacing resulted in a clear pro- changing the HV interval or the intraventricular activation
longation of the AH interval (121 to 162 milliseconds) without sequence.
Figure C8.9
Adenosine was then administered, and the electrocardio- strongly argues against the patient having a typical AV bypass
gram in Figure C8.9 was obtained. Note that the pattern of tract. Certain AV connections (eg, Mahaim fiber) may have dec-
preexcitation remains subtle and that the HV interval remains remental properties. However, adenosine and rapid atrial pac-
the same until AV block occurs. The occurrence of complete AV ing preferentially affect either the Mahaim fiber or the AV node;
block without an intervening period of incr hange preexcitation and the HV interval.
Figure C8.10
Another tracing from the same patient shows retrograde placed at a cycle length of 360 milliseconds during a drive
conduction (Figure C8.10). A ventricular extrastimulus was train of 600 milliseconds.
Figure C8.11
Figure C8.11 shows a more tightly coupled ventricular activation sequence. This suggests that retrograde conduction
extrastimulus at 340 milliseconds. Note that the ventricu- occurs via the AV node.
loatrial (VA) interval increases with no change in the atrial
Case 8 357
Figure C8.12
Figure C8.13
A maneuver resembling the differential atrial pacing respectively. Pacing from the base is associated with a shorter
described above can be performed from the ventricle to deter- VA interval (105 and 146 milliseconds, respectively, for base
mine whether retrograde conduction occurs via a bypass tract and apex) and no change in the VA activation sequence. This
or the AV node. Figures C8.12 and C8.13 show pacing from finding is consistent with conduction via an accessory bypass
the right ventricular base and from the right ventricular apex, tract that inserts near the base of the heart.
To summarize the findings from this patient thus far, preex- activation remains constant. Thus, the degree of preexci-
citation was present, but findings from atrial pacing maneuvers tation also remains constant. Any maneuver to cause AV
were not typical of an accessory bypass tract (decremental pac- block will result in loss of AV conduction without changing
ing prolonged the PR interval, stimulus-to-QRS interval, and the extent of preexcitation.
AH interval but did not change the pattern of preexcitation or For this patient, findings from the antegrade pacing
the HV interval). Similar paradoxic information was obtained maneuvers were consistent with the diagnosis of a fascicu-
after assessing retrograde conduction—decremental conduc- loventricular tract. Preexcitation and a short HV interval
tion consistent with AV nodal conduction was seen, but pac- resulted from premature activation of the ventricle from
ing near the base of the heart resulted in a shorter VA interval, either the His bundle or proximal right or left bundles.
which is more typical of bypass tract retrograde conduction. What explains the paradoxic findings with ventricular pac-
Under normal circumstances, a sheath of annular tis- ing and assessment of VA conduction? Retrograde conduction
sue exists around the His bundle and proximal right and does not always occur in a fasciculoventricular pathway that
left bundles. Th is insulating tissue prevents activation of conducts in the antegrade direction, but if retrograde conduc-
the neighboring ventricle. Conduction to the ventricle tion is present, then a parahisian maneuver cannot be performed
occurs from the mid to distal bundle branches, which is effectively. This is because any capture of the local myocardium
why the HV interval is normally 35 to 55 milliseconds. In will also capture the His bundle, and the usual distinction of
some patients, this insulating tissue may be breached, and narrow and wide QRS complexes will not occur. In fact, the
then activation of the ventricle occurs soon after activa- normal insulation of the His and proximal right bundles is
tion of the His bundle. Th is is termed a fasciculoventricular what makes parahisian pacing possible. Nevertheless, some
tract. Because conduction must fi rst go through the com- patients with a fasciculoventricular tract can have parahisian
pact AV node, decremental properties (ie, increases in the pacing performed, either because there is no retrograde con-
stimulus-to-QRS interval, PR interval, and AH interval) are duction through this tract or because the ventricular pacing
seen. Regardless of the rate of pacing in the atrium, however, site is more proximal to the site of the fasciculoventricular tract
the time from the His bundle activation to the ventricular (basal pacing with a distal fasciculoventricular tract).
Figure C8.14
In this patient, parahisian pacing could be performed conduction is dependent on the AV node (as also evidenced
(Figure C8.14). Note that the VA interval is longer in beat 2 by the decremental properties described above). Why, then,
(wide QRS) without His bundle capture than in beat 3 (narrow is the VA interval shorter when pacing at the base than with
QRS) with direct His bundle capture (82 vs 45 milliseconds, apical pacing? This is because the fasciculoventricular tract
respectively); in addition, the atrial conduction sequence is is relatively closer to the base than the apex, such as with a
the same for both beats. This finding suggests that retrograde proximal location of the right bundle branch.
Case 8 359
Figure C8.15
It is important to understand certain limitations before pacing at 400 milliseconds with isoproterenol could show
drawing conclusions on the basis of parahisian pacing. In the a different atrial activation sequence. In this case, para-
tracing in Figure C8.15, parahisian pacing is repeated with hisian pacing was repeated to ascertain whether this dif-
administration of isoproterenol. ferent sequence was also AV node dependent or whether
If varying activation sequences are seen with isopro- an accessory pathway was manifesting its retrograde
terenol or at different pacing cycle lengths, parahisian conduction. In this tracing, even with isoproterenol, the
pacing needs to be repeated for each observed change in wider QRS complex is associated with a longer VA conduc-
the activation sequence. In other words, parahisian pac- tion time and no change in the atrial activation sequence.
ing performed with ventricular pacing at 600 milliseconds This is consistent with retrograde AV node–dependent
may show a complete AV nodal response, but ventricular conduction.
Figure C8.16
Another important consideration is shown in Figure C8.16. there was capture of the junction of the His bundle and right
Here, a paradoxic response is noted. The narrow, complex, bundle (the usual site of His bundle capture); and second, the
third beat is associated with a longer VA interval—this is the atrium was no longer captured directly. As with any maneuver
exact opposite of what is expected with retrograde AV nodal performed in electrophysiology, a thorough knowledge of the
conduction. This is also inconsistent with retrograde accessory limitations and exceptions are necessary before coming to a
pathway conduction because a change in the VA interval going conclusion based on findings after a specific maneuver.
from the wide beat to a narrow, complex beat would not be
expected. In this case, with pacing from the His bundle cath-
eter, the catheter had drifted proximally and resulted in direct Abbreviations
capture of the atrium in the first 2 beats of the tracing (best
seen in beat 2). Because the insulation is more noted in the AH, atrial-His
proximal His bundle, the beat with direct atrial capture failed AV, atrioventricular
to directly capture the His bundle. As the catheter drifted more HV, His-ventricular
into the ventricle, 2 simultaneous phenomena occurred. First, VA, ventriculoatrial
Case 9
Figure C9.1
Figure C9.1 was obtained with linear, phased-array, intra- C. Intrapulmonary shunting of blood
cardiac echocardiography. The probe was placed in the right D. Likely Eisenmenger physiology
atrium, and an oblique view of the left atrium was obtained E. Atrial esophageal fistula formation
during an ablation procedure. Answer: B—Refractile microbubbles seen during radiofre-
quency ablation.
What can cause the bubble-like structures (arrow) in
Figure C9.1? The ablation catheter is placed in the left atrium, and the
A. Inadvertent air injection into the left atrium microbubbles are seen where ablation energy is delivered.
B. Refractile microbubbles seen during radiofrequency Although the actual origin of these microbubbles is subject
ablation to some controversy, they clearly can occur during ablation,
particularly at sites with good tissue-electrode contact. The
settings on the ultrasound imaging system are important
when visualizing these bubbles to distinguish among their
Abbreviations are expanded at the end of this chapter. various types. A high acoustic power or mechanical index
Terms with “[f]” denote abbreviations that appear in the figures only. setting may obliterate finer bubbles.
361
Blood Tissue
Direct injury
Bubbles
Blood vessels
cooling
Tip Tissue
temperature temperature
Catheter
Thermal injury
Blood flow
cooling
Figure C9.2
The schematic in Figure C9.2 illustrates the principles of

radiofrequency energy delivery and underscores the possibil-
ity of temperature differences at the catheter tip (where tem-
perature is monitored) vs deeper in the tissues. When energy
is delivered, heating at the catheter tip may directly injure
the tissue, with microbubbles forming at the tissue-electrode
interface. The catheter tip itself is cooled by blood flow, but
further increases in power delivery will cause thermal injury
deeper in the tissue; this may occur even if other blood ves-
sels at these deeper sites exert some cooling effect. Sometimes,
deep tissue temperatures may increase to 100°C or higher
without significantly changing the catheter tip temperature.
When this occurs, tissue vaporization (and steam formation)
may cause the steam bubble to rupture, either epicardially
or at times endocardially, resulting in a large outpouring of
coarse bubbles that are strikingly different from those seen Figure C9.3
during ablation. The impedance during ablation, which typi-
cally decreases by about 5 to 10 ohms during energy delivery, The intracardiac ultrasound image in Figure C9.3 was
will abruptly increase when tissue vaporization occurs. When obtained with the probe in the right atrium and shows an
coarse bubbles are seen, ablation energy should be decreased. image of the left atrium during catheter ablation. What is
Intracardiac ultrasonography was used during catheter abla- the likely origin of the structure indicated by the arrow?
tion in the ventricular myocardium, with the ultrasound cathe- A. Coagulum
ter close to the electrode-myocardial interface. A clear evolution B. Perforation
in bubble size from fine to coarse and the steam “pop” was seen. C. Thrombus
D. Atrial endocardial dissection
Answer: C—Thrombus.
One of the most feared complications during left atrial
or left ventricular ablation procedures is the formation of
Case 9 363
clinically significant thrombi. Thrombi may form through through the superior limbus. Intravenous hepariniza-
various mechanisms (eg, from coagulum, dissection, previ- tion, preferably before any left atrial access, decreases the
ously existing thrombus, etc). However, in the absence of ade- risk of thrombogenic complications, except for coagu-
quate heparinization or when catheter sheaths are placed for lum formation during energy delivery. During ablation,
extended periods in the left atrium, a thrombus can enlarge coagulum forms on the catheter itself, even with intrave-
and, in some instances, become massive enough to increase nous heparin; coagulum formation is associated with an
the patient’s risk of embolization. impedance rise.
Pulmonary
artery
Aorta
Figure C9.6
In Figure C9.6, note that no catheters have been placed in

Figure C9.4 the aorta. What is the likely cause of the bubbles here?
A. Ablation within the aortic wall for supravalvular out-
flow tract tachycardia
In this patient, a suction apparatus and a distal protec-
B. Perforation of the aorta during transseptal puncture,
tion system was used to successfully extract the thrombus
with the puncture being performed too anteriorly
(Figure C9.4), with no untoward sequela.
C. Perforation of the aorta during transseptal puncture,
with the puncture being performed too superiorly
D. Perforation of the aorta from the esophagus
E. Perforation of the aorta during transseptal puncture,
with the puncture being performed too posteriorly
Answer: C—Perforation of the aorta during transsep-
tal puncture, with the puncture being performed too
superiorly.
To understand the significance of air bubbles in the aor-
tic circulation (an alarming fi nding), review the anatomy of
transseptal puncture and have a clear understanding of the
3-dimensional anatomic relations of the ascending aorta,
aortic arch, and descending aorta. Specifically, the impor-
tant relationships are those of the aorta to the atria, the His
bundle, the superior vena cava, and pulmonary artery. Note
Figure C9.5
how the pulmonary artery or right ventricular outflow tract
represent the anterior aspect of the aorta. Because the bub-
bles were mainly seen more posteriorly and superiorly, the
Figure C9.5 is an ultrasonogram from a patient with aortic perforation did not occur via an anterior structure.
endocardial dissection; this highly thrombogenic event The ascending aorta has no anatomic relationship with the
can occur during left-sided ablation procedures. More esophagus. However, as explained below, the aorta is located
common dissection sites include venous structures, near near (superior to) the superior vena cava.
sites of perforation, and sites of transseptal puncture
A right anterior oblique view of the interatrial septum,

with the free wall of the right ventricle and right atrium
removed, is presented in Figures C9.8 and C9.9. Several ana-
tomic points should be carefully noted. First, the fossa ovalis
is located in the same plane as a line connecting the supe-
Aorta
rior vena cava and the inferior vena cava (in a fairly posterior
plane). Second, note that the structures separating the fossa
ovalis from the tricuspid annulus include the eustachian
ridge, the atrioventricular (AV) conduction system, and the
coronary sinus (more inferiorly). Third, note that anterior
and superior to the fossa ovalis is atrial musculature and part
of the conduction system, including the His bundle overlying
the aorta.
Thus, one way in which inadvertent aortic puncture may
occur is with anterior angulation of the catheter. Instead of
Figure C9.7 entering the left atrium at the level of the fossa ovalis, rela-
tively posteriorly, the catheter can disrupt the AV conduction
In Figure C9.7, a long-axis view of the aorta is shown. Note system or the aorta itself.
the relationship between the aorta, right atrium, and superior
vena cava. Note also that after perforation, a partial dissection
occurred, with thrombus formation.
RSPV
Tricuspid valve
LA
Aorta RA
RV LV
Figure C9.10
Figure C9.8
Figure C9.10 shows a 4-chamber view (coronal section)
of the heart. Note the fossa ovalis, which is the target for
transseptal puncture. The superior limit of the fossa ovalis
is the superior limbus, a relatively thick structure with com-
plex musculature. Transseptal puncture may be performed
through the superior limbus, but that causes considerable
disruption of the myocardium and endothelium. Note that
Aorta inferior to the fossa ovalis (arrow) is musculature that is
between the levels of the tricuspid valve and the mitral valve.
This portion of the heart, termed the AV septum, is techni-
Fossa cally still within the right atrium, but the tissue in that region
AVS includes left ventricular musculature. Inadvertent puncture
through the AV septum may damage the compact AV node
and give rise to fistulas between the left ventricle and right
atrium (Gerbode shunt). This dissection also illustrates how a
posteriorly and superiorly angled puncture may enter the
Figure C9.9 (Adapted from Asirvatham SJ. Cardiac anatomic right superior pulmonary vein.
considerations in pediatric electrophysiology. Indian Pacing
Electrophysiol J. 2008 May 1;8[Suppl. 1]:S75–91. Used with permission
Case 9 365
LAO RAO
Figure C9.11
The fluoroscopic image in Figure C9.11 shows an

attempted transseptal puncture. Note the location of the
coronary sinus catheter, which defi nes the inferior border
of the mitral annulus. Note the position of the His cath-
eter (arrow). In this projection, it is not possible to know
whether the aorta would be entered when advancing the
needle during attempted transseptal puncture. Although it
is commonly stated and true that the His bundle catheter is
a surrogate for the aorta and aortic root, this concept applies
primarily only to the right anterior oblique view, where an
anterior puncture at the level of the aorta can be confi rmed.
However, in the left anterior oblique projection, it is impos-
sible to know whether a puncture occurred very anterior,
with the catheter entering into the aortic root itself. Use of
contrast injection is helpful in this regard. Contrast stain-
ing will show a marked left ward extension when trying to
advance the transseptal catheter and needle. Th is would not LAO
occur anteriorly because of the fibrous annulus, and left- Figure C9.12 (Adapted from Asirvatham SJ. Cardiac anatomic
ward extension of contrast strongly suggests that the needle considerations in pediatric electrophysiology. Indian Pacing
tip is at least posterior to the eustachian ridge (eg, at the Electrophysiol J. 2008 May 1;8[Suppl. 1]:S75–91. Used with
level of the fossa ovalis). permission of Mayo Foundation for Medical Education and
Research.)
This concept is also useful when identifying the position

of the fast pathway to the AV node (Figure C9.12). Because
the fast pathway is located posterior to the eustachian ridge, a
catheter placed at the fast pathway region will appear left ward
in the left anterior oblique projection.
Intracardiac ultrasonography can be extremely helpful in
improving the understanding of the anatomy needed for suc-
cessful transseptal puncture. It likely improves the safety of
this procedure.
LSPV
LA LIPV
RA
Figure C9.15
During attempted catheter insertion (Figure C9.15), note

the “tenting” as the operator tried to advance the transsep-
tal system. For patients with small hearts and very pliable
Figure C9.13 intra-atrial septa, the tenting may cross entirely over to the
free wall of the atrium; thus, when advancing through the
In Figure C9.13, the intracardiac echocardiographic probe septum, the left atrial free wall may be perforated simul-
has been placed in the right atrium via the right femoral vein. taneously. Intracardiac ultrasonography is important to
Note the sector of the imaging plane. The initial image would increase awareness of what is on the other side of the tent-
be of blood in the right atrium, followed by the interatrial ing. In other words, should the angle or torque applied
septum, the left atrium, and then the left atrial free wall (pos- while advancing the catheter be changed so the opera-
sibly including the pulmonary veins). tor has more lateral room to maneuver in the left atrium?
Anteriorly, in the region of the left atrial appendage, and
even more anteriorly through the mitral annulus, are spe-
cific areas where torque should be applied while advancing
the catheter, particularly if a patient has a small heart and
pliable septum.
Superior
limbus
Figure C9.14
The echocardiographic image in Figure C9.14 was obtained

from such an orientation. The interatrial septum is clearly
visible. Note the superior limbus and the relatively thin fossa Figure C9.16
ovalis.
In Figure C9.16, the operator is attempting to cross to the
left atrium relatively high and at the level of the superior lim-
bus. Although this can be accomplished and in fact is specifi-
cally attempted in patients with polyethylene terephthalate
patches or atrial septal defect (ASD) closure devices, it is more
difficult to perform and may be more thrombogenic.
Case 9 367
Box C9.1
Efficient Sheath Management
Always have continuous flush (preferably heparinized saline)
through any sheath and catheter system RSPV
Avoid placing empty sheaths in the left-sided circulation, even
for a few minutes
Avoid undersized catheters and sheaths because a layer of
thrombus may form
Heparinize as early as possible; experienced operators should be
comfortable heparinizing before a transseptal puncture
Meticulously avoid air embolization by slow withdrawal of
catheters and by using large sheaths under fluid exchanges
Figure C9.18
Bubbles
Box C9.2 summarizes complications that may arise with
transseptal access. Figure C9.18 shows a transseptal puncture
that was performed too posteriorly and somewhat superiorly.
A dissection of the right superior pulmonary vein was noted.
After that was recognized, the procedure was stopped; the
patient recovered uneventfully.
Figure C9.17
Box C9.1 describes techniques for efficient sheath man-

agement. Figure C9.17 illustrates another cause of bubbles
in the left atrium. The operator was injecting saline through
the transseptal system specifically to determine whether the
septum had been crossed and also to determine the relative
LAA
positions of the transseptal needle tip and the free wall. Thus,
air contrast and ultrasonography were used in an analogous
manner to radiopaque contrast and fluoroscopy.
RAA
Box C9.2
Complications of Transseptal Catheterization
Perforation with a needle into the pericardial space (roof of Figure C9.19 (Adapted from Asirvatham SJ. Cardiac anatomic
left atrium, lateral side of left atrium, atrial appendage, and considerations in pediatric electrophysiology. Indian Pacing
posterior left atrium) Electrophysiol J. 2008 May 1;8[Suppl. 1]:S75–91. Used with permission
Inadvertent entry into the aorta (anterior perforation at the level of Mayo Foundation for Medical Education and Research.)
of the His bundle, superior perforation of the superior vena
cava)
Puncture or catheterization of the coronary sinus Figure C9.19 shows a dissection of an autopsied heart from
Direct catheterization of the right upper pulmonary vein
the superior view (ie, looking from above). This view clearly
Entrance into a cardial vein remnant
illustrates the critical and complex relationships of the aorta
and aortic root with other cardiac structures. Note that the
superior vena cava is immediately adjacent to the posterior
and lateral walls of the ascending aorta. During transseptal without aortic puncture. An important cardiac ganglion is
puncture, the transseptal needle and sheath are often placed also located here.
high in the aorta. If the needle and dilator are not pulled back, Note also the close relationship of the right atrial append-
perforation of the aorta may occur at this site. A small, inter- age and the aorta, the fact that the aortic root is the rightward
vening reflection of the pericardium, termed the aortocaval of the pulmonary outflow tract, and the close relationship of
sinus, is located at this site. Perforation of the aortocaval sinus the posterior and rightward portions of the right ventricular
may also result in pericardial air or eff usion and bleeding, outflow tract with the aortic root.
Table C9.1
Electrophysiologically Relevant Relationships Between the Aortic Root and Coronary Arteries
Relationship Implications
Close relationship of aortic arch and His bundle Left-sided AV node ablation can be performed at the junction of the
right and noncoronary cusps of the aortic valve
Care must be taken not to damage the AV conduction system when
performing left ventricular outflow tract ablation
Anterior puncture during transseptal access may damage the His
bundle or enter the aorta (or both)
Aortic relationship to superior vena cava Left ventricular outflow tract tachycardias with an origin above the
aortic valve can be mapped with a right atrial catheter placed in the
superior vena cava
Inadvertent puncture of the aorta during ablation or transseptal
puncture may occur
Right atrial appendage lies in proximity to the ascending aorta and
right ventricular outflow tract
Signals from the right atrial appendage septum may be surrogates of
far-field ventricular signals; these can help map the origin at these sites
Relationship between the left atrial appendagea and the right A bilobed left atrial appendage sometimes may be inserted between
ventricular outflow tract the 2 outflow tracts
Ventricular tachycardias from the epicardial right ventricular outflow
tract (not usually left ventricular outflow tract) may be mapped or
sometimes ablated via the left atrial appendage
Close relationships between the coronary ostia and the Posterior ablation in the right ventricular outflow tract may damage
posterior right ventricular outflow tract, below the pulmonary the aorta or coronary ostia
valve
Relationship of the transverse sinus of the pericardium, aorta, The transverse sinus is just inferior to the aortic arch; inferior to the
and left atrial appendage transverse sinus is the roof of the left atrial appendage
Direct superior perforations of the left atrial roof may also enter the
aorta via the transverse sinus
a
The left atrial appendage typically has no relationship with the aortic root.
Aortic arch sidedness is defi ned by the bronchus over ascending aorta) is similar, but the arch of the aorta and
which the aorta drapes. In Figure C19.19, the aortic root descending aorta drapes over the right main bronchus.
starts out rightward and then arches left ward and drapes Thus, the relationship of the portion of the aorta relevant to
over the left bronchus (ie, a normal, left-sided aortic arch). transseptal puncture is not affected by aortic arch sidedness
In a right-sided aortic arch, the initial portion (ie, the (Table C9.1).
Case 9 369
SVC
Aorta
Figure C9.20
In Figure C9.20, note that the transseptal needle in the

superior vena cava is butting up against the aorta.
Aorta
Thrombus
Figure C9.21
Figure C9.22
Air embolization into the aorta and cerebral circulation is
associated directly with serious morbidity, including stroke,
Figure C9.22 shows an anatomic dissection and ultra-
and may be fatal. In addition, the presence of air and dis-
sonogram from a patient who had a polyethylene terephtha-
ruption of the endothelium are both highly thrombogenic
late patch closure of an AV canal defect (arrows). Transseptal
(Figure C9.21). Thrombogenic stroke may result.
puncture in this patient could be performed above the patch
and across the superior limbus (Table C9.2).
Table C9.2
Difficult Situations for Transseptal Puncture
Potential Cause of Difficulty Suggested Action
Very pliable atrial septum, with small left atrium Apply slight counterclockwise torque when advancing the needle, such that
after the septum is punctured, the needle will point into the left atrial
appendage or across the mitral annulus
Very thick, nonpliable interatrial septum or fossa ovalis Consider puncturing above the superior limbus and applying slow, steady
pressure
Consider ultrasonography to determine whether the septum has calcification;
if yes, abandon puncture altogether, or puncture above the superior limbus
Very large, dilated aortic root After clear tenting of the fossa ovalis, apply slight clockwise torque on the
catheter while advancing it
Consider intracardiac ultrasound to visualize the dilated aortic root
relationship
Prior polyethylene terephthalate patch or placement of Puncture across superior limbus
patent foramen ovale closure device In the case of a closure device, puncture just posterior to the device is possible
Inability to tent because of poorly formed superior limbus, and Place a strong curve on the Brockenbrough needle and consider using a curved
transseptal needle rises back up to the superior vena cava sheath and applying slight clockwise torque while advancing the catheter
Sheath will not go across the septum, although the Use counterclockwise torque to orient the dilator and needle in the direction
needle is clearly across of the left ventricle; while gently pulling back the needle and dilator, try to
advance the sheath
The maneuver may have to be repeated several times
Care should be taken to advance the needle and dilator only into the
ventricle (not into the atrium)
Right atrium is excluded by a Fontan patch from the Consider a reverse transseptal puncture
original portion of the right atrium; Fontan circuit is not Use a retrograde approach to access the left atrium; puncture the atrial
fenestrated, and prior atrial septal defect is closed septum to access the neo-left atrium
Because of poor sheath support, consider application of radiofrequency energy
with intracardiac ultrasonographic guidance to access this chamber
RAO LAO
Figure C9.23
Case 9 371
An electroanatomic map (Figure C9.23) was obtained close to it) should be mapped to define the entire circuit. In
from a patient with a history of a functional, univentricular Figure C9.23, the purple sites are 130 milliseconds later than
heart (double-inlet, predominantly left ventricle). The patient a reference potential and the red sites are about 139 milli-
had documented atrial flutter (cycle length, 300 milliseconds) seconds earlier. Thus, approximately 40 milliseconds of the
that was easily induced in the electrophysiology laboratory. tachycardia cycle length were not mapped.
The tachyarrhythmia could be entrained and did not show Three possibilities should be considered when the color
overdrive suppression. Right atrial activation is shown in the activation timing does not equal the cycle length of the tachy-
right anterior oblique and left anterior oblique projections. cardia: 1) another chamber requires mapping to define the
entire circuit; 2) there may be electrical conduction that is
Which statement is correct with respect to the electroana-
slow and occurring through the scar (ie, the scar is not really
tomic maps in Figure C9.23?
a scar, it is diseased tissue with low-amplitude potentials and
A. The “red region” should be targeted for ablation
slow conduction); and 3) the tachycardia actually is not reen-
B. An ablation line connecting the gray scar to the supe-
trant. In nonreentrant tachycardias, the cycle length is unre-
rior vena cava will cure the patient’s arrhythmia
lated to the mapped activation sequence because this depends
C. An ablation line connecting the gray scar to the inferior
largely on the intra-atrial conduction characteristics. From
vena cava will cure the patient’s arrhythmia
the observations described above, it becomes clear that some
D. The arrhythmia is likely reentrant, and the circuit
portion of arrhythmogenic tissue, likely outside the right
appears to propagate around the lateral wall scar
atrium, has to be mapped to define the entire circuit and to
choose the sites for further entrainment maneuvers or radio-
frequency ablation.
Several important points should be considered when Several different congenital heart abnormalities may result
interpreting electroanatomic activation maps. First, only in in a functional, univentricular heart that requires surgical
an automatic arrhythmia does the site of early activation have palliation. Surgical palliation consists primarily of right-sided
any meaning. In a reentrant circuit (as was established in this heart bypass (ie, diversion of systemic venous blood flow
patient by the arrhythmia being entrained and by known away from the heart and into the pulmonary circulation).
structural heart disease), there will always be sites of electri- Many different procedures have been devised to address this
cal activity that time earlier than any other site (ie, when con- issue, and even among Fontan conversions, several methods
sidering the atrium as a whole, it shows continual activity). exist. The 2 primary approaches include 1) surgical connec-
Second, the red site has no meaning in a reentrant arrhyth- tion, creating a conduit between the atrial appendage and the
mia, partly because there is no early site and also because pulmonary artery, and 2) a second anastomosis connecting
simply changing the “window” in the mapping settings can the vena cava to the pulmonary circulation via the conduit.
completely change the colors, even though the arrhythmia These procedures can in turn be divided in to fenestrated and
is exactly the same. Third, in a reentrant arrhythmia, the nonfenestrated conduits, depending on whether a connection
entire circuit length should be mapped. If the tachycardia between the cavopulmonary circulation and the pulmonary
cycle length is 300 milliseconds, then 300 milliseconds (or venous circulation was created deliberately.
Univentricular AV connection, another common proce-

dure, is illustrated in Figure C9.25. A previous connection
from the subclavian artery to the right pulmonary artery
has been interrupted. The superior vena cava has been inter-
rupted, and an anastomosis (in an end-to-side fashion) to the
right pulmonary artery is obtained.
Figure C9.24
Figure C9.24 shows a common type of Fontan conversion,

in which the superior vena cava is connected to the right pul-
monary artery in an end-to-side fashion. Thus, the inferior
vena cava empties in to the prior right atrium, and the blood
from here may go into the pulmonary venous circulation if
an ASD is still present or has no meaningful outlet. Figure C9.26
To determine appropriate mapping sites in patients who
have undergone Fontan procedures, a clear understanding of
Figure C9.26 illustrates a fenestrated Fontan procedure,
atrial anatomy is necessary. A catheter placed from the inter-
perhaps among the more common approaches today. A con-
nal jugular vein will enter into a stump of the main pulmonary
duit drains inferior vena caval blood into the pulmonary
artery; interestingly, temporary ventricular capture sometimes
artery, and an end-to-side anastomosis with the superior
can be obtained from this site. This knowledge may be useful
vena cava is made. The previous right atrial circulation and
if pacing is required urgently in the electrophysiology labora-
the pulmonary venous circulation now are in continuity with
tory and transseptal access has not been obtained.
each other.
With this background in mind, what are the likely rea-
sons for the electroanatomically mapped cycle length to be
less than the cycle length of the tachycardia? Consider that
the patient’s cavotricuspid isthmus and right atrium were
transected by the insertion of the Fontan conduit with what
was originally the 2 portions of the right atrium. The map of
the right atrium thus included a portion that was continuous
with the pulmonary venous atrium or left atrium.
Figure C9.25
Case 9 373
RAO LAO
Figure C9.27
illustrates mapping of the complete circuit in surgically cor-

rected congenital heart disease. Note the unusual require-
ment for transseptal access. The original right atrium has a
portion that is excluded by the Fontan conduit. Right atrial
flutters, including typical cavotricuspid isthmus–dependent
flutter, may include part of this myocardium. How can a cath-
Fontan LA Reverse eter be maneuvered to that location?
transseptal
Original RA If a fenestration is present in the Fontan conduit, a cath-
eter can be manipulated through it. A second method is ret-
Mitral rograde access to the ventricle (Figure C9.28). Once in the
Via femoral left (systemic) ventricle, the original right atrium excluded
vein by the Fontan conduit can be accessed by going through a
ventricular septal defect and then through a patent tricuspid
Tricuspid
valve (such as in this patient with a double-inlet left ventricle).
Occasionally, retrograde access to the left atrium does not
allow access to the right atrium because of tricuspid atresia or
other reasons; in such cases, access to the original right atrium
(now excluded by the Fontan conduit) is possible through
retrograde access to the left atrium, followed by crossing a
previous ASD (or an ASD created during surgery). Finally,
Figure C9.28
for patients with tricuspid atresia and no ASD, none of these
approaches are possible. In such cases, a “reverse transseptal”
Figure C9.27 again shows the electroanatomic map from can be performed (ie, transseptal access from the left atrium
the patient with the univentricular heart. Figure C9.28 to right atrium).
RAO LAO
Figure C9.29
Ablation
catheter
Ablation
catheter
RAO LAO
Figure C9.30
The neo-left atrial activation map is shown in Figure access the neo-left atrium (original right atrium). The final
C9.29. In Figure C9.30, the course of the ablation catheter position of the ablation electrode is very similar to the start-
is visible in the fluoroscopic images. Retrograde access had ing point of a traditional ablation line in patients without
been obtained, and the catheter then had been prolapsed back congenital heart disease and cavotricuspid isthmus–depen-
across the mitral valve and through the interatrial septum to dent flutter.
Case 9 375
RAO LAO
Figure C9.31
When both the maps of the neo-left atrium and right AVS, atrioventricular septum [f]
atrium are combined (Figure C9.31), the entire cycle length of L, left [f]
the tachycardia is mapped. Concealed entrainment was found LA, left atrium [f]
on the cavotricuspid isthmus, as well as in the neo-left atrium LAA, left atrial appendage [f]
in the region of the original tricuspid valve. An ablation line, LAO, left anterior oblique [f]
created on both sides of the Fontan conduit, was successful in LAT, lateral view [f]
terminating the flutter (it could no longer be induced). LIPV, left inferior pulmonary vein [f]
Thus, transseptal access occasionally is required in LSPV, left superior pulmonary vein [f]
unusual circumstances. To solve those cases, it is essential to LV, left ventricle [f]
understand the anatomy and relationships of the interatrial RA, right atrium [f]
septum to the great arteries and other structures. RAA, right atrial appendage [f]
RAO, right anterior oblique [f]
RSPV, right superior pulmonary vein [f]
Abbreviations RV, right ventricle [f]
S, superior [f]
ASD, atrial septal defect SVC, superior vena cava [f]
Case 10
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure C10.1
The electrocardiogram in Figure C10.1 was obtained from Considering the electrocardiogram in Figure C10.1, which
a patient with a history of multiple atrial arrhythmias, is an unlikely site of origin for the atrial arrhythmia?
including premature atrial contractions (PACs), nonsus- A. Superior vena cava
tained atrial tachycardia, atrial fibrillation, and atrial flut- B. Azygos vein
ter. Two electrophysiology studies and ablations had been C. Right upper pulmonary vein
performed previously, with possible localization of the D. Left lower pulmonary vein
arrhythmogenic focus in the superior vena cava. The prior E. Crista terminalis
ablation procedure included attempted isolation of the Answer: D—Left lower pulmonary vein.
superior vena cava.
The site of origin of atrial tachycardias or PACs can be
difficult to determine from the surface electrocardiogram
because of fusion of the P wave with the proceeding T wave.
However, carefully compare P waves with the T waves after
Abbreviations are expanded at the end of this chapter. the extrasystolic beats—the P-wave axis is clearly inferior
Terms with “[f]” denote abbreviations that appear in the figures only. (based on the positive, tall P wave in leads II, III, and aVF).
377
This axis suggests a superior origin, which is inconsistent deflection of the P wave in lead V1 is negative because of con-
with an origin in the left lower pulmonary vein. The P-wave duction via the Bachmann bundle to the left atrium, which
morphology in lead V1 can be very helpful in understanding is a posterior structure. If the P wave is completely positive
both the atrium of origin and the anteroposterior location of in lead V1, then a left atrial origin is more likely. In contrast,
the focus. In normal sinus rhythm, an early, positive P wave a completely negative P wave in lead V1 suggests an ante-
is seen in lead V1 because of the origin from the sinus node, rior location within the right atrium such as the right atrial
located posterolaterally in the right atrium. The subsequent appendage.
Figure C10.2
The recording in Figure C10.2 was obtained after inser- the activation pattern recorded by the CS catheter. The fi rst
tion of a circumferential mapping catheter in the left lower beat is with pacing from the coronary sinus, to aid identifi-
pulmonary vein, an HRA catheter near the junction of the cation of pulmonary vein potentials on the circumferential
superior vena cava and right atrium, an HBE and ABL cath- mapping catheter. The second beat is a PAC that precedes
eter placed in the left atrium near the left lower pulmonary the pacemaker spike. Note that with distal coronary sinus
vein, and a CS catheter. pacing, activation in the coronary sinus occurs in a relative
When ectopy is observed, it is important to analyze distal-to-proximal sequence. With a PAC originating in the
the site of earliest activation, the intra-atrial activation superior vena cava or high right atrium, proximal-to-distal
sequence, and the P wave morphology. The site of earli- activation in the coronary sinus is expected. The relatively
est activation is on the HRA catheter. When a catheter in “straight-line” activation pattern suggests an origin in the
this location shows early activation, further mapping of the roof of the left atrium or the right upper pulmonary vein.
superior vena cava, upper portion of the crista terminalis, Th is suggests activation of the entire inferior mitral annular
and right upper pulmonary vein should be performed. Note region at about the same time.
Case 10 379
Figure C10.3
Although the site of earliest activation has been deter- any one interval with a clearly seen P wave. In Figure C10.3,
mined, the intra-atrial activation sequence must be defined the interval between potentials recorded by the HRA catheter
clearly by measuring intra-atrial intervals or the timing of and CS 19,20 was being measured (62 milliseconds).
Figure C10.4
The circumferential mapping catheter was placed in the pulmonary veins. Figure C10.4 shows a spontaneous
right upper pulmonary vein after isolation of the left-sided finding.
Which statement is consistent with the finding? Whenever a particular catheter shows very early activa-
A. The site of origin of the previously observed PACs is in tion, the question of catheter-induced ectopy arises. Thus,
the right upper pulmonary vein it is important to defi ne the intra-atrial activation sequence
B. This finding likely represents catheter-induced ectopy, when spontaneous ectopy is seen early in the procedure,
from the circumferential mapping catheter being before placement of the circumferential mapping catheter.
placed in the right upper pulmonary vein If the circumferential mapping catheter recordings are
C. There is a connection between the proximal coronary visually subtracted, note an identical coronary sinus pat-
sinus and the right superior pulmonary vein tern and a similar timing from the high right atrium to the
D. The superior vena cava is connected with the right coronary sinus, as was seen before placement of the circum-
upper pulmonary vein ferential mapping catheter. Although the P-wave morphol-
Answer: A—The site of origin of the previously observed ogy is difficult to discern, this is strong evidence that the
PACs is in the right upper pulmonary vein. right upper pulmonary vein is activated markedly before
the region of the superior vena cava and right atrium.
Figure C10.5
Note that during this ectopy (Figure C10.5), the timing unchanged (57 milliseconds).
from the high right atrium to the proximal coronary sinus is
Case 10 381
Figure C10.6
RAO LAO
Figure C10.7
Further mapping of the site of origin of the atrial ectopic catheter (in the superior vena cava). This may be because 1) an
beat should be performed (Figure C10.6). In Figure C10.7, the origin for the ectopic beat may exist in the vein with a mus-
circumferential mapping catheter (yellow arrows) is placed cular connection between the vein and either the azygos vein
about 2 cm into the pulmonary vein and the ABL d catheter or superior vena cava; or 2) an origin for the ectopic beat may
(white arrows) is placed close to the ostium of the vein. be deep in the vein, with slow conduction to the ostium of
Note in Figure C10.6 that the signal from the ABL p the vein and a far-field signal being picked up by the HRA
catheter is actually later than the signal seen from the HRA catheter.
Figure C10.8
For the tracing in Figure C10.8, the circumferential map- earlier than previously measured, suggesting an origin very
ping catheter was moved from a relatively ostial (“proximal”) deep in the right upper pulmonary vein. The 69-millisecond
location to a site approximately 5 cm from the ostium of the interval is measured between the early far-field potential
right upper vein (“distal” location). The ablation catheter on LASSO 1,2–2,3 and the potential recorded on the HRA
was about 2 cm into the vein. Here, the activation is even catheter.
Figure C10.9
Case 10 383
During pacing from the high right atrium, the sponta-

neous right upper pulmonary vein ectopy was neither sup-
pressed nor triggered. Unlike in typical atrial pacing or
coronary sinus pacing, the far-field atrial signal is not sep-
arated clearly from the pulmonary vein potential (Figure
C10.9). Yet, the near-field signals are separated from the SVC
far-field signals (arrows), indicating exit delay in the ectopic RA
beats. During atrial pacing, if potentials in the right upper
RSPV RAA
pulmonary vein are seen very close to the pacemaker spike
(no delay), 2 scenarios are possible: 1) far-field capture of
the right upper pulmonary vein musculature from an inap-
Muscular
propriately, posteriorly placed right atrial pacing catheter at connection
high-output pacing or 2) a direct muscular connection from
the superior vena cava or right atrium to the right upper pul-
monary vein. In the tracing in Figure C10.9, however, given
the exit delay that is seen during the ectopic beats, a direct
Figure C10.10
muscular connection is unlikely. Even if one was present, it
is unlikely to alter the method of ablation (ie, circumferential
isolation of the right upper pulmonary vein). Th is is because Figure C10.10 shows an example of a muscular connection
even if unidirectional conduction occurs from the right between the anterior surface of the right upper pulmonary
atrium or superior vena cava into the pulmonary vein, it is vein and the right atrium–superior vena cava junction.
conduction out of the vein that would necessitate more than
just ostial isolation; it would require mapping of the actual
connection and ablation.
Connection
Activation sequence unchanged

= pulmonary vein potential

at high and low output and
independent of pacing site
= connection

at high output only and
“moves” with pacing site
= far-field capture
Figure C10.11
“Paravenous” pacing (Figure C10.11) is another method to connection between the right atrium and the right supe-
determine whether far-field capture or a connection is respon- rior pulmonary vein can be identified. Early pulmonary
sible for the fused signal in Figure C10.9 (pacing spike in the vein activation (deeper in the vein than the ostium) during
right upper pulmonary vein during right atrial pacing). right atrium pacing, regardless of output or pacing location,
By using high and low outputs during paravenous pac- suggests a true connection.
ing and by varying the pacing site in the right atrium, a
High output Intermediate output Low output
Far-field signals
Figure C10.12
In Figure C10.12, the pacing output was gradually site of high-output pacing in the posterior high right atrium.
decreased. Note that the far-field potential to pulmonary vein Both findings suggest that the cause of this phenomenon is
potential delays with low-output pacing, with little change in far-field capture of the pulmonary vein muscle, rather than a
the intra-atrial activation sequence. Further, the site of ear- true connection.
liest activation within the pulmonary vein varied with the
Figure C10.13
Case 10 385
During circumferential ablation of the atrial tissue just Note that the frequency of ectopic beats is not markedly
proximal to the right upper pulmonary vein ostium, the fol- changed and that during atrial pacing with capture, con-
lowing tracing was obtained (Figure C10.13). duction continues into the pulmonary vein (no entrance
block). Also note that the previously conducting pulmo-
Which of the following is most likely shown in Figure C10.13? nary vein ectopy is now blocked (exit block). Entrance block
A. Entrance block into the pulmonary vein may potentially occur with further ablation (worsening
B. Exit block from the pulmonary vein as a result of cir- source-sink mismatch), rather than exit block, because of
cumferential ablation the relatively small amount of pulmonary vein musculature
C. Ectopy continuing as before, with no effect of ablation compared with the rest of the atrial myocardium. We can-
D. Changing intra-atrial activation sequence not be certain of entrance block in this instance, however,
Answer: B—Exit block from the pulmonary vein as a result because atrial pacing with entrance into the vein may be
of circumferential ablation. promoting exit block.
Figure C10.14
With further ablation (Figure C10.14), note that exit block pulmonary vein potential and continued presence of the
and entrance block are both seen, with disappearance of the far-field right and left atrial signals on the last 2 paced beats.
Figure C10.15
With the use of isoproterenol at low doses, a persis- junctional rhythm, a dissociated rhythm in the pulmonary
tent junctional rhythm is seen (Figure C10.15). During vein is noted (arrow).
Figure C10.16
With increasing doses of isoproterenol (Figure C10.16), complete exit block and dissociation from the underly-
more complex ectopy and runs of nonsustained tachy- ing junctional rhythm (now faster with the higher dose of
cardia from the pulmonary vein are seen. Note the isoproterenol).
Case 10 387
Figure C10.17
With rapid pacing (not shown), the ectopy was not (Figure C10.17). Note that ectopy within the vein is completely
suppressed. Eventually, typical atrial flutter was induced dissociated from the atrial flutter elsewhere in the atria.
Figure C10.18
The atrial flutter disorganized to an atrial fibrillation vein (no suppression of the ectopic rhythm) and the dissocia-
(Figure C10.18). Note the lack of evidence of entrance into the tion of the pulmonary vein and the fibrillating atrium.
Figure C10.19
The tracing in Figure C10.19 was obtained 90 minutes pulmonary vein rhythm continued.
after administering isoproterenol (6 mcg/min). Dissociated
Figure C10.20
Case 10 389
Because typical atrial flutter was easily induced and sus- During coronary sinus ostial pacing, a catheter on the
tained, it was targeted for ablation. During ablation of the cavotricuspid isthmus that is placed as described above should
cavotricuspid isthmus, the multilead electrode catheter was show either distal-to-proximal activation (earliest in pole 1,
placed (Figure C10.20) with distal IS 1,2 electrodes at the latest in pole 20) if conduction occurs in the medial-to-lateral
ostium of the coronary sinus and proximal IS 19,20 electrodes direction across the cavotricuspid isthmus or a reversal of
in the superolateral right atrium. During proximal coronary activation lateral to the line of block after the ablation line
sinus pacing, the tracing in Figure C10.20 was obtained. is complete. Yet the tracing in Figure C10.20 shows neither
of these findings. In fact, it shows a paradoxic finding of a
Which statement is an unlikely explanation for this
reversed activation sequence, with lateral-to-medial conduc-
finding?
tion in the more distal electrodes and the appearance of con-
A. The catheter position is abnormal, with portions of the
tinued conduction in the more proximal (laterally placed)
catheter being behind the eustachian ridge
electrodes.
B. There is conduction block across the cavotri-
When encountering such a finding, first check the catheter
cuspid ablation line, but the appearance of con-
position fluoroscopically or with intracardiac ultrasonogra-
tinued conduction is attributable to lower-loop
phy (or both) to determine whether the distal electrodes
conduction
have migrated posterior to the eustachian ridge. In this situ-
C. There is longitudinal dissociation within the cavotri-
ation, more proximally and laterally placed electrodes show
cuspid isthmus
true conduction occurring across the isthmus, and a block
D. There is continued conduction in the medial-to-lateral
appears more medially on the distal electrodes because they
direction, but the appearance of block is attributable to
are placed behind a physiologic line of block (the eustachian
lower-loop conduction
ridge). If this is fluoroscopically shown not to be the case,
Answer: D—There is continued conduction in the other considerations include block across the isthmus from
medial-to-lateral direction, but the appearance of block is ablation but with rapid conduction posteriorly around the
attributable to lower-loop conduction. inferior vena cava (lower-loop conduction).
Crista terminalis
Lower-loop reentry
TV
IVC Typical
flutter
CS CS
Pacing Pacing
site site
IVC IVC
Pseudoconduction Pseudoblock
Figure C10.21
Figure C10.21 shows propagation of the wave front in the to the lower-loop phenomenon. If pseudoconduction is rec-
medial-to-lateral direction (caudal to cephalad) on the lateral ognized, no further ablation is required. Th is situation can
wall. Th is is sometimes termed pseudoconduction because be determined either by point-to-point mapping of the lower
the appearance of conduction despite a block is attributable loop, circumferential catheter mapping of the lower loop, or
differential pacing with a change in timing of the potentials fibrosed pectinate muscles, or a Chiari malformation. A por-
across the ablation line being observed, depending on the tion of the cavotricuspid isthmus may be blocked, but another
pacing site. For example, with proximal coronary sinus pac- portion (perhaps more anteriorly) may have conduction. If a
ing, the timing between the potentials just medial to and multilead electrode catheter is placed such that some of the
lateral to the ablation line will be longer than pacing from electrodes are in the blocked portion, a reverse sequence will
the mid coronary sinus or high right atrium; this is attribut- be seen. Additional information on how unilateral block and
able to the relatively more rapid conduction across the lower other complex conduction-related phenomena occur is pro-
loop from pacing at these sites. If true conduction across vided in the appendix of Chapter 7.
the isthmus is present, there would be no change in timing,
provided that the activation sequence is similar between the Abbreviations
potentials on either side of the ablation line (this interval
is determined by the continued slow conduction across the CS, coronary sinus [f]
ablation line). IVC, inferior vena cava [f]
Sometimes, conduction actually occurs across the abla- LAO, left anterior oblique [f]
tion line. However, lower-loop conduction (Figure C10.21) is PAC, premature atrial contraction
rapid, which results in a fused activation sequence along the RA, right atrium [f]
cavotricuspid isthmus catheter (distal electrodes). However, RAA, right atrial appendage [f]
in this example, there was no evidence of fusion—a clear RAO, right anterior oblique [f]
reversal of activation was observed. Finally, rare instances RSPV, right superior pulmonary vein [f]
of longitudinal dissociation along the cavotricuspid isthmus SVC, superior vena cava [f]
have been reported. This may be due to previous ablation, TV, tricuspid valve [f]
Case 11
Figure C11.1
The electrocardiogram in Figure C11.1 was obtained from C. Atrioventricular (AV) nodal conduction is likely to be
a patient with a history of paroxysmal palpitations. He had intact
been told during childhood that he had an abnormal electro- D. Multiple pathways are present
cardiogram consistent with preexcitation. E. The pathway does not conduct in a retrograde manner
Which of the following can be deduced from the Answer: C—AV nodal conduction is likely to be intact.
electrocardiogram? Analysis of the 12-lead electrocardiogram before ablation
A. The pathway is likely to be on the left side is of critical importance. Several features need to be scruti-
B. The pathway is likely to be posteriorly located nized carefully. First, when preexcitation is present, the likely
pathway location must be deduced as accurately as possible.
Abbreviations are expanded at the end of this chapter. Based on the Arruda-Jackman criteria (Circulation. 1995 Apr
Terms with “[f]” denote abbreviations that appear in the figures only. 15;91[8]:2264–73), pathway sidedness must be determined first.
391
Note the positive delta wave in lead I and how the amplitude present (that is, to assess whether the potential is maxi-
of the R wave is less than that of the S wave in lead V1. Both mally preexcited). Th is is particularly important in patients
features strongly suggest a right-sided accessory pathway. The with prior ablation because the AV node may have been
delta wave is positive in leads II, III, and aVF, suggesting that inadvertently ablated and a pacemaker could be required
the accessory pathway is in an anterior location. Next, deter- if the accessory pathway is subsequently ablated. In Figure
mining the location of the pathway on the septum or on the C11.1, note the arrow showing a premature atrial contrac-
free wall just off the septum is important because this preproce- tion. With this premature contraction, the degree of pre-
dure information allows appropriate counseling of the patient excitation increases because of further decrement in the
regarding the risk of AV block. For true septal pathways, the AV node; this suggests that AV nodal conduction is still
delta wave is negative in V1 and becomes positive in V2. In this intact.
tracing, a small positive delta wave in lead V1 (assuming correct Third, when preexcitation increases with the premature
lead positioning) suggests that the pathway is off the septum; atrial contraction, only minimal changes in the pattern of
thus, the risk of requiring a pacemaker is low. preexcitation are seen in lead V6 and perhaps aVR. A marked
Second, the electrocardiogram should be analyzed to change in the pattern and degree of preexcitation would sug-
determine whether underlying AV nodal conduction is gest that more than 1 accessory pathway is present.
Figure C11.2
In Figure C11.2, the intracardiac tracing shows that distal coronary sinus appears to be activated earlier than
during ventricular pacing, the fi rst 2 paced beats result the mid–coronary sinus. In some situations, this fi nding
in retrograde conduction to the atrium. Following this, may suggest the presence of a second accessory pathway in
intermittent conduction (white arrows) and intermittent the free wall of the left atrium. Alternatively, the coronary
retrograde block (yellow arrows) occur with ensuing sinus sinus catheter may have been placed deep into the coronary
beats. Note that for beats displaying ventriculoatrial (VA) sinus such that the distal electrode is in the vicinity of the
conduction, the earliest atrial potential is seen on the HBE4 anterior interventricular vein. The latter explanation is
catheter; this is best noted by comparing one potential in likely to be correct in this case because a similar coronary
a beat without VA conduction with that of a conducted sinus pattern occurs with the sinus beats (white arrows)
beat. The coronary sinus activation is unusual in that the that occurred after VA block.
Case 11 393
Figure C11.3
In Figure C11.3, note the ventricular signal on the part of the diagnostic portion of the electrophysiology
coronary sinus shows a similar “bowed” pattern dur- study in this case will involve correct elucidation of
ing sinus rhythm with preexcitation. The potentials on the origin of each of the components of this complex
the HBE3 catheter are highly complex (arrows). A major signal.
Figure C11.4
The phenomenon in Figure C11.4 was observed during incremental atrial pacing.
What is (are) the likely origin(s) of the potential indicated D. Pathway potential
by the arrow? E. A or B is possible
F. C or D is possible
A. His bundle potential
B. Atrial potential Answer: F—It may be a ventricular or pathway potential.
C. Ventricular potential
Figure C11.5
A key portion of the procedure with anteroseptal path- with that of the preexcited beat, the His bundle potential
way ablation is accurate identification of the component sig- can be identified (“H” in Figure C11.5). The remaining 2
nals. Here, during atrial pacing, the second and fourth beats large potentials may represent 2 components of a complex
show atrial capture with no conduction to the ventricle, the ventricular signal or a pathway potential plus a ventricular
fi rst and third beats show atrial capture with conduction to potential.
the ventricle through the AV node and His bundle system, Pathway potentials rarely have the large amplitude seen
and the fi ft h and sixth beats show atrial capture with con- in Figure C11.5. Also, in the beat conducted without preex-
duction via an accessory pathway, resulting in preexcited citation, a complex ventricular signal is noted (albeit with
QRS complexes. Because atrial capture is common to all the near- and far-field components reversed when compared
these beats, the atrial signal on the distal His electrogram with the preexcited beat). The “?” arrow thus likely points to
is easily identified. When conduction without preexcitation a component of a complex ventricular signal; however, an
occurs, a clear His bundle deflection is noted. By compar- unusually prominent pathway potential cannot be excluded
ing the near-field nature and morphology of this signal (see Case 1).
Case 11 395
Figure C11.6
In Figure C11.6, note that the first atrial stimulus conducts because of AV block with the previous beat, or it may represent
to the next QRS complex. The second stimulus occurs at about continued block in the AV node with retrograde activation of
the same time as the His bundle potential. Thus, this stimulus the His bundle occurring after ventricular activation through
cannot be responsible for the QRS complex (upper arrow). The the accessory pathway. In other words, the His bundle poten-
second stimulus is either blocked or may be conducting with tial may represent either antegrade or retrograde conduction.
a very long atrial-His (AH) interval to the next QRS complex. However, with continued decremental pacing, the His bundle
Eventually, after a blocked beat, preexcitation returns. signals occur progressively later, allowing clear visualization
Carefully examine the relationship between the His bundle of the complex ventricular signal (lower arrow). With nondec-
potential, the pacing stimulus, and the captured atrial poten- remental pathways, the AH interval would increase with fur-
tial. Note that the AH interval prolongs with initial pacing, ther decremental pacing only if the His potential was caused
consistent with rapid decremental atrial pacing. After preex- by conduction through the compact AV node.
citation occurs, the AH interval shortens, but with continued It can be difficult to know whether a recorded His bundle
pacing, the AH interval slightly lengthens (in a later paced beat, signal is caused by antegrade or retrograde conduction. Some
it is 140 milliseconds). The initial shortening of the AH inter- of the important differentiating features are discussed below
val may be due to more rapid conduction through the AV node and summarized in Table C11.1.
Table C11.1
Characteristics of His Potentials During Antegrade and Retrograde Conduction
Characteristic Antegrade Retrograde
AH interval AH prolongation continues with shorter atrial coupling No further change is seen in the AH interval with
intervals progressive shortening of the AA interval, except in
Mahaim or other decremental pathways
Activation With a multielectrode catheter located at the His bundle and Direction of activation is from distal to proximal
direction right bundle, activation proceeds from proximal to distal Proximal-to-distal activation occurs only if the catheter
(His potential is earlier than right bundle potential) has been placed too distally and there is retrograde
right bundle branch block, with antegrade activation of
the right bundle and retrograde activation of the Hisa
Preexcitation When the AH interval increases and then a block occurs, His bundle potential is not seen when preexcitation is no
preexcitation increases and reaches a maximal value longer seen (block in pathway)
Abbreviations: AA, atrial-atrial; AH, atrial-His.
a
See Chapter 6.
Examine Figures C11.7 through C11.10, which show elec- with progressively shorter coupling intervals. Duration of
trocardiograms recorded during atrial extrastimulus testing AH intervals are shown on each figure.
Figure C11.7
Figure C11.8
Case 11 397
Figure C11.9
Figure C11.10
Changes in AH Interval During Atrial

Extrastimulus Pacing
350
150
AH Interval, msec
150
150
150
100
50
0
200 250 300 350 400
AA Interval, msec
Figure C11.11
The changes in the AH interval, with progressive to retrograde via the accessory pathway and ventricular
shortening of the atrial-atrial (AA) interval, are shown myocardium. After the plateau, an abrupt increase in the
in Figure C11.11. Note the initial gradual prolongation of AH interval is seen. This coincides with loss of preexci-
the AH interval as the AA coupling intervals get shorter. tation and either unmasking of a poorly conducting slow
A plateau appears, signifying that activation of the His pathway to the AV node or, more likely, an escape junc-
bundle has now switched from antegrade via the AV node tional beat.
Figure C11.12
Case 11 399
In Figure C11.12, when preexcitation is lost, the His bundle activation was dependent on preexcitation (retro-
bundle signal is no longer seen. Th is suggests that the His grade His).
Figure C11.13
The graph in Figure C11.11 illustrates that decrement AV interval has changed markedly and retrograde activation
(mild upslope before the plateau) may occur even in a regu- of the atrium is seen, in a pattern consistent with AV nodal
lar accessory pathway (ie, not a Mahaim pathway). In Figure conduction. This represents a single beat of antidromic reen-
C11.13, note that preexcitation is unchanged; however, the try or ectopy from the accessory pathway with AV block.
Antegrade His Activation Retrograde His Activation
His catheter position

RB catheter position
Figure C11.14
475 continued and progressive increase in the intervals between

Respective Interval, msec
Stimulus-His the stimulus to His, stimulus to right bundle, and stimulus to

Stimulus-RB ventricular potentials. Regardless of whether the His bundle
375 Stimulus-V
QRS Width
is being activated antegrade or retrograde, it is activated via
a decrementally conducting structure (AV node or Mahaim
275 fiber).
Examine the echo beat (last beat) in Figure C11.13. How
175 can one determine whether that beat represents an antidro-
mic echo (retrograde conduction via the AV node), antegrade
conduction via the accessory pathway, an AV nodal reen-
75
trant echo beat with a bystander decrementally conducting
0
0
38
40
42
44
46
48
50
52
54
56
58
60
pathway (antegrade conduction via both the pathway and

Atrial-Atrial Interval, msec AV node and retrograde conduction occurring as a reentrant
echo from the AV node), or ectopy from the pathway? This
Figure C11.15 can be very difficult to differentiate accurately. However, close
analysis of the His-atrial (HA) interval can sometimes allow
Figure C11.14 shows a patient with a Mahaim-type path- the correct diagnosis. Generally, the VA interval is not as use-
way (antegrade, decrementally conducting pathway). Because ful as the HA interval because the VA interval is affected by
of the accessory pathway plus the AV node decrement, the more variables, including the exact site of pacing and intra-
classic “plateau” associated with decremental atrial pacing ventricular conduction. When determining the length of
and accessory pathways may not be seen when retrograde His the HA interval, the time between the end of the His bundle
activation occurs. As shown in Figure C11.15, the QRS width potential and the beginning of the earliest atrial potential
(degree of preexcitation) shows only minimal changes with should be measured.
Case 11 401
Figure C11.16
In Figure C11.16, the HA interval is relatively short with a than the coronary sinus, distal His bundle, and atrial potentials.
junctional beat. The proximal His bundle atrial potential is earlier This suggests retrograde conduction via the fast pathway.
Figure C11.17
In Figure C11.17, the HA interval is longer with a reen- precedes the proximal His bundle atrial potential (arrow)
trant echo beat. Here, the distal His bundle atrial potential and others.
The reason for this activation sequence change on the His Because AV nodal conduction can exit to the atrium through
bundle electrogram is worth consideration. With antegrade the fast pathway located even more posteriorly (“behind” the
AV nodal conduction, the distal ventricle is activated before tendon of Todaro), the proximal His bundle electrodes are
the proximal ventricle because of the insulation on the His activated before the distal electrodes. In contrast, when ret-
and proximal right bundles. Conduction breaks out to the ven- rograde conduction occurs through an accessory pathway,
tricle more distally. Similarly, the compact AV node is located the atrial myocardium at the annulus is the first to be excited.
closer to the annulus than the pathway’s exit to the atrium. Thus, the distal His atrial potential precedes other potentials.
IVC LA
Eustachaian valve
“Pouch”
CS
Thebesian valve
Figure C11.18
The anatomy dissection in Figure C11.18 shows why coro- pathway. Activation, either via the retrograde fast pathway or
nary sinus activation generally is earlier when the atrium the retrograde slow pathway, is earlier because of the septal
is activated via the AV node versus an anterior accessory location of the AV node.
124 msec
Figure C11.19
During orthodromic reciprocating tachycardia (Figure shows a relatively late potential (arrow) with retrograde acti-
C11.19), note that the HA interval is relatively long (124 mil- vation via the accessory pathway.
liseconds). Again, the proximal coronary sinus (CS 19,20)
Case 11 403
Figure C11.20
During ventricular pacing with retrograde atrial activa- simultaneously) via the right bundle to the His bundle and
tion via the accessory pathway (determined by parahisian also to the atrium via the accessory pathway. Therefore, the
pacing [not shown]), a very short HA interval is seen (Figure HA interval with ventricular pacing is considerably shorter
C11.20). Th is is because when VA conduction is through an than the HA interval during reciprocating tachycardia,
accessory pathway, the HA interval is a pseudointerval (not a without changing the retrograde atrial activation sequence.
true conduction interval but rather a measure of relative con- Now study the interesting “echo” beat in Figure C11.21.
duction time from a common point to 2 structures). Thus, In this beat, the atrial activation sequence occurs much
the ventricle activation proceeds simultaneously (or nearly earlier than the His potential; the activation sequence was
Figure C11.21
identical to that observed with retrograde conduction via common turnaround point close to the AV node, conduction
the AV node (Figure C11.16 and C11.17). The HA interval proceeds simultaneously (or nearly simultaneously) toward
with AV node conduction tends to be shorter during tachy- the His bundle in an antegrade fashion and to the atrium via
cardia or AV node reentrant beats. In fact, it may be nega- the fast pathway (typical AV nodal reentry tachycardia) in
tive when compared with the HA interval with ventricular a retrograde fashion. The characteristics of the HA interval
pacing. Th is is because with AV node reentry, the HA inter- during ventricular pacing and tachycardia are summarized
val during tachycardia is a pseudointerval. That is, from a in Table C11.2.
Table C11.2
Comparison of HA Interval Characteristics During Pacing and Tachycardia
Tachycardia HA Interval HA Interval HA Delta
During Pacing During Tachycardia (Tachycardia – Pacing)
AVNRT (general) Represents a true interval Represents a pseudointerval Often negative

Always a positive number Number may be positive,
negative, or 0
Typical AVNRT As above; tends to be short because As above; tends to be a positive Usually slightly positive (~10
of the 180° orientation of the fast number because of the 90° msec)
pathway and minimal involvement orientation for the wave front
of the compact AV node between the slow pathway and
retrograde fast pathway
Atypical AVNRT As above; tends to be a longer interval As above; often shorter and Almost always a negative
because it is a true conduction time sometimes very negative number
and because of the 90° orientation because of a lower common
between the His bundle and the pathway (proximal
retrograde slow pathway turnaround) and 180 °
orientation between right- and
left-sided slow pathways
AVRT (retrograde accessory Represents a pseudointerval Represents a true interval because Positive number
pathway) May be positive, negative, or 0, the His is stimulated before
depending on site of pathway, site of the ventricle, which in turn is
ventricular pacing, and infrahisian stimulated before the accessory
conduction pathway and atrium
Usually greater than 80 msec
Mahaim (antidromic Usually short; represents a true interval Usually greater than 80 msec Typically 0, unless retrograde
tachycardia) because retrograde conduction is with the atrial potential always right bundle branch
only through the AV node occurring after the His because block occurred during
See also comments for AVNRT conduction is retrograde tachycardia (then would be
through the AV node positive)
HA interval will be similar
to that observed during
ventricular pacing
Permanent junctional Because of decremental conduction The His potential occurs even Positive number
reciprocating tachycardia through the pathway, the HA earlier than the atrial potential
interval tends to be a large number because this represents a true
(>110 msec) HA conduction interval
See also comments for AVRT HA interval will be very long,
(retrograde accessory pathway) longer than the HA interval in
pacing
See also comments for AVRT
(retrograde accessory pathway)
Abbreviations: AV, atrioventricular; AVNRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reentrant tachycardia; HA, His-atrial.
Case 11 405
Figure C11.22
Identification of the retrograde His bundle potential can the tachycardia. The identical activation sequence confi rms
be useful when attempting to reset the tachycardia from the the diagnosis of orthodromic AV reentrant tachycardia.
ventricle (see Chapter 6). In Figure C11.23, His extrasystoles are observed (arrow).
In Figure C11.22, a premature ventricular contraction, His extrasystoles can be very useful during an electrophysiol-
which clearly does not affect the His bundle potential, resets ogy study for ablation of accessory pathways. First, as the His
Figure C11.23
Figure C11.24
signal is dissociated from the other signals, it becomes easier A pseudointerval is an interval between 2 potentials that is
to know which of the complex signals was the His potential. caused by activation of a common site that propagates to
Second, in a His extrasystole, a complete loss of preexcita- activate sites that are responsible for each of the potentials;
tion should be expected. If preexcitation persists with the His it does not result from conduction between the site respon-
extrasystole, the presence of a fasciculoventricular tract should sible for 1 potential to the site responsible for the other
be considered. If a right bundle morphology is seen with His potential.
extrasystoles (or during orthodromic AV reentrant tachycar- For example, in the fascicular tachycardia shown in
dia) and a left bundle morphology from preexcitation is seen Figures C11.24 and C11.25, a prepotential (Figures C11.24
in sinus rhythm, an Ebstein anomaly with a right-sided acces- and C11.25, arrows) is often used to diagnose a fascicular
sory pathway should be suspected (nearly all patients with origin to the arrhythmia. However, the interval between
Ebstein anomaly have underlying right bundle branch block). the fascicular potential and local ventricular potential may
The concept of a pseudointerval is useful in supraventric- represent a pseudointerval, with an unidentified early site
ular tachycardia and also in certain ventricular arrhythmias. elsewhere in the fascicular system that simultaneously (or
Figure C11.25
Case 11 407
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure C11.26
nearly simultaneously) activates the fascicle; it is this poten- tachycardia. The typical tachycardia shown in Figure C11.26
tial that is recorded by the mapping catheter and appears is a left bundle branch morphology tachycardia with a very
in the QRS complex and ventricular electrograms. short R-P interval. This can be mistaken for AV node reentry
One can be more certain that the recorded fascicular (the VA and HA interval tends to be longer in orthodromic AV
potential is in fact the culprit fascicle only when the interval reentrant tachycardia compared with AV node reentry). The
from the fascicular potential to the local ventricular poten- reason for the very short HA interval is because the Mahaim
tial or QRS is similar during sinus rhythm and spontaneous fibers often are inserted directly into the right bundle.
arrhythmia (see Chapter 6). Thus, the right bundle is activated early, even before the
Understanding pseudointervals and the possible reasons local right ventricular myocardium; then retrograde acti-
for short R-P intervals during tachycardia are also impor- vation to the His occurs from the right bundle, followed by
tant in the analysis of Mahaim fiber–related antidromic conduction to the AV node (Figure C11.27; part B, arrows
A B
I
II
V1
315 350
RA
CS
A A
HBp
H
HBm
H
HBd
RB RB
RVMSp
RB
RVMSd
RB RB
RVA
215 105 190 160

A RB A A RB A
Figure C11.27 (Adapted from McClelland JH, Wang X, Beckman KJ, Hazlitt HA, Prior MI, Nakagawa H, et al. Radiofrequency catheter
ablation of right atriofascicular (Mahaim) accessory pathways guided by accessory pathway activation potentials. Circulation. 1994
Jun;89[6]:2655–66. Used with permission.)
200 ms
Figure C11.28
point to a local ventricular potential). In fact, very short VA An eccentric sequence in the coronary sinus atrial sig-
intervals are typical in Mahaim fiber–related tachycardia nals usually indicates that a left-sided accessory pathway
and provide a clue to this pathology. Some patients may have is responsible for retrograde conduction. However, in the
retrograde right bundle branch block develop during tachy- third beat of Figure C11.28 (ventricular extrastimulus), the
cardia (see Chapter 6). As previously discussed, when retro- VA interval abruptly lengthens without a change in the ret-
grade right bundle branch block occurs, either an antidromic rograde atrial activation sequence. Some accessory path-
tachycardia with a pathway in the right ventricle or pacing ways may have decremental conduction; in such cases, a
from the right ventricle will prolong the ventriculo-His inter- longer VA interval is still consistent with an accessory path-
val and thus the VA interval. In fact, a long or moderate VA way. However, the key fi nding is that with the ventricular
interval with a Mahaim tachycardia strongly suggests either extrastimulus, a retrograde His bundle activation (arrow)
a retrograde right bundle branch block or retrograde conduc- is clearly seen. Thus, the lengthening of the VA interval is
tion occurring through another accessory pathway and not primarily from prolonged conduction time from the pacing
the AV node. site to the His bundle as a result of retrograde right bun-
Recognition and occasionally purposeful induction of dle branch block. If an accessory pathway was present, one
retrograde right bundle branch block can elucidate the would expect either no change in the VA interval with the
mechanism of retrograde conduction during antidromic increase in the ventriculo-His interval (pathway conduction
tachycardia (as mentioned above), and it can also distinguish not dependent on the infrahisian conduction system) or a
between retrograde AV nodal conduction and accessory block in the accessory pathway that causes a change in the
pathway conduction. Figure C11.28 shows ventricular extra- retrograde atrial activation sequence. Retrograde AV nodal
stimulation. The first 2 beats are ventricular pacing from near conduction is shown by atrial potentials occurring later
the right ventricular apex. The third beat is a closely coupled when conduction time to the His bundle during ventricu-
extrastimulus, delivered from the same site. The last beat is lar pacing is lengthened without a change in the atrial acti-
a junctional escape beat. Note that in all the paced beats, the vation sequence. Although the coronary sinus activation
coronary sinus atrial activation sequence appears to be eccen- sequence is eccentric, the potential on the HIS p electrode is
tric, with the atrial potentials in the distal coronary sinus (CS actually the earliest atrial signal. Thus, retrograde conduc-
1,2) preceding the atrial potentials in the proximal coronary tion is via the AV node and through the fast pathway, but as
sinus (CS 17,18 and CS 19,20). With biplane fluoroscopy, using detailed in the electrophysiology maneuvers in Chapter 4,
the right and left anterior oblique projections (see Chapter 1), the coronary sinus is being activated from the fast pathway
the coronary sinus electrodes were found to be well seated via the intra-atrial septum, left atrium, and a connection
into the coronary sinus, with electrodes CS 17,18 around the between the relatively distal left atrium to the coronary
ostium. sinus musculature.
Case 11 409
The last beat in the tracing (junctional escape) has an Abbreviations

intriguing retrograde atrial activation sequence. We note
that the coronary sinus activation is now concentric (poten- AA, atrial-atrial
tials on CS 19,20 preceding the atrial potential on CS 1,2). The AH, atrial-His
atrial potential, however, continues to be early on the HIS p AV, atrioventricular
electrodes. This is likely because of simultaneous retrograde AVN, atrioventricular node [f]
activation from the AV node via the fast pathway and the CS, coronary sinus [f]
slow pathway (proximal coronary sinus musculature). This HA, His-atrial
finding is not uncommon during retrograde VA conduction, HBd, His bundle distal [f]
particularly when ventricular activation occurs at a cycle HBm, His bundle mid [f]
length close to the refractory period of either the fast or slow HBp, His bundle proximal [f]
pathways. IVC, inferior vena cava [f]
Important considerations when trying to determine LA, left atrium [f]
whether an accessory pathway is present (and if so, its location) RA, right atrium [f]
are summarized in Box C11.1 RB, right bundle [f]
RVA, right ventricular apex [f]
RVMSd, right ventricular mid septum distal [f]
Box C11.1 RVMSp, right ventricular mid septum proximal [f]
Points To Remember V, ventricle [f]
• Careful analysis of the electrocardiogram is necessary before VA, ventriculoatrial
placing catheters during accessory pathway ablation
• An attempt should be made to localize the pathway by study-
ing the 12-lead electrocardiogram, regardless of the presence
or absence of atrioventricular nodal conduction or multiple
pathways
• When fragmented (multicomponent) signals are seen on
electrodes placed near the site of an accessory pathway, pac-
ing maneuvers should be performed and carefully interpreted
to determine the nature of each component of these complex
signals (see Chapter 4).
• It is useful to have a thorough understanding of how to
distinguish between antegrade and retrograde His bundle
activation in patients with antegrade accessory pathway
conduction
• The concept of pseudointervals and the effect of induced or
spontaneous retrograde right bundle branch block should be
clearly understood because they can help elucidate the mech-
anism of complex arrhythmias with a wide QRS complex.
Case 12
Figure C12.1
Which of the following diagnoses is least likely, consider- this electrophysiologic tracing is consistent with several
ing the tracing in Figure C12.1? diagnoses. As discussed previously (see Chapter 4), the VA
A. Typical atrioventricular node reentrant tachycardia interval is not a reliable sole criterion to distinguish between
(AVNRT) typical and atypical atrioventricular (AV) node reentry. This
B. Atypical AVNRT is because the VA interval is a pseudointerval in AV node
C. AVNRT using an accessory bypass tract reentry, and it represents the relative ease of reaching the
D. Junctional tachycardia atrium vs the ventricle from the turnaround point (with or
E. Atrial tachycardia without a lower common pathway). Sometimes, the shortest
F. All of the above VA intervals are seen in atypical AV node reentry.
Answer: C—AVNRT using an accessory bypass tract. The only reliable method that distinguishes between these
2 forms of AVNRT is analysis of the atrial activation sequence.
A cursory evaluation of this tracing could result in the If the arrhythmia shown in Figure C12.1 already is established
quick diagnosis of typical AVNRT, on the basis of the very as a form of AV node reentry, the type of AVNRT present can
short ventriculoatrial (VA) or His-atrial interval. However, be distinguished by determining whether the atrial potential
on the proximal His bundle catheter precedes the atrial poten-
tial in the proximal coronary sinus catheter (typical AVNRT)
Abbreviations are expanded at the end of this chapter. or succeeds the atrial potential in the proximal coronary
411
sinus (atypical AVNRT). The true fast-pathway exit from the fast-pathway location likely is the earliest and the arrhythmia
AV node is not at the proximal His bundle region but behind is typical AVNRT. With atypical AVNRT, because a catheter
the tendon of Todaro, which may need to be mapped specifi- usually is positioned at the proximal coronary sinus (the site
cally to make an accurate distinction. As a rule of thumb, if it of exit of the slow pathway), the atrial potential on the proxi-
is difficult to determine which atrial potential comes earlier mal CS catheter usually will clearly precede that of the proxi-
(proximal His vs proximal CS catheters), the unmapped, true mal His catheter.
Table C12.1
Distinguishing AVNRT from Junctional Tachycardia
Characteristic AVNRT Junctional Tachycardia
Clinical features Multiple age groups Often seen in pediatrics patients

Usually no obvious triggering factor Often occurs after cardiac surgery
Always sudden onset and offset Onset may be more gradual
Regularity Almost always regular May be irregular
Earliest atrial Retrograde fast pathway behind the tendon of Todaro in typical Earliest atrial potential might be in
potential AVNRT the fast- or slow-pathway region,
Retrograde earliest atrial potential in the proximal coronary sinus in depending on the mode of retrograde
atypical AVNRT conduction from the junctional focus
Dissociation from May occur with retrograde upper common pathway block (rare) May be dissociated from the atrium or
the atrium ventricle (or both)
Dissociation from Sometimes spontaneous; often seen during ventricular pacing with Relatively common to have dissociation
the ventricle infrahisian block from the ventricle, particularly in
Infrahisian block more likely to occur in patients with preexisting older patients after cardiac surgery
bundle branch block (eg, older patients)
Suprahisian block may occur with lower common pathway block (rare)
Excitable gap Relatively narrow and difficult to penetrate the circuit and/or reset Wide “excitable” gap easily resets and/or
with premature atrial contractions unless coupled very early. advances with late, coupled, premature
atrial contractions
Effect of PVCs PVCs reset the tachycardia only by resetting (advancing) the PVCs may advance to His bundle
retrograde His bundle potential potential in junctional tachycardia, but
In typical AVNRT, tachycardia can be reset by advancing a the tachycardia typically will be reset
retrograde His bundle potential by as little as 10 msec, but
preexcitation of the His bundle by 30 msec or more is required to
reset atypical AVNRT
Successful Slow-pathway ablation, 4–5 cm away from the His bundle potential, Slow-pathway ablation less commonly
ablation site almost always successfully eliminates the arrhythmia eliminates the arrhythmia successfully
(compared with AVNRT)
Abbreviations: AVNRT, atrioventricular nodal reentrant tachycardia; PVC, premature ventricular contraction.
Table C12.2
Differential Diagnosis of Tachycardia with a Very Short VA Interval
Arrhythmia Cause of the Short VA Comparison of VA and HA Characteristics of the HA Distinguishing Characteristics
Interval Intervals Interval During Tachycardia
and Ventricular Pacing
Typical The VA interval is a Usually, the VA interval The HA interval during Earliest atrial potential is at a
(slow-fast) pseudointerval and is shorter than the HA tachycardia is slightly fast-pathway site
AVNRT represents a “race” from interval (see Chapter 4) longer (5–10 msec) than PVCs reset the tachycardia only
a turnaround point of the HA interval during by advancing the
the circuit to the atrium ventricular pacing retrograde His
and ventricle Entrainment from the atrium
There is no actual VA only with a long AH interval
conduction
(continued)
Case 12 413
Table C12.2
(Continued)
Arrhythmia Cause of the Short VA Comparison of VA and HA Characteristics of the HA Distinguishing Characteristics
Interval Intervals Interval During Tachycardia
and Ventricular Pacing
Atypical As above, the VA interval Usually, the VA interval The HA interval during Earliest atrial potential is at
(retrograde is a pseudointerval is shorter than the pacing is longer than the proximal coronary sinus
slow) representing HA interval during the HA interval during region
AVNRT near-simultaneous tachycardia tachycardia (lower PVCs can reset the tachycardia
activation of the atrium common pathway) only by advancing the
and ventricle from a retrograde His bundle
lower common pathway deflections by at least 20 msec
(see Chapter 4) Difficult to reset the tachycardia
from the atrium
Atrial The VA interval is a Variable No predictable relationship With close analysis during
tachycardia pseudointerval with no initiation and termination
actual VA conduction of the tachycardia, it will
When the cycle length be apparent that the atrial
of the tachycardia potential that is simultaneous
approximates the AV with 1 ventricular potential
interval with antegrade results in antegrade
conduction, the conduction to the next
atrial and ventricular ventricular potential
potentials are When the tachycardia
simultaneous “wobbles,” changes in
the atrial cycle length are
predictive of subsequent
changes in the HH and
ventricular cycle length
Junctional Pseudointerval with The VA interval typically The HA interval in Earliest atrial potential may
tachycardia simultaneous activation is shorter than the tachycardia is very be at the fast-pathway or
of the atrium and HA interval during similar to the HA proximal coronary sinus site
ventricle from the tachycardia interval during Tachycardia is easily reset from
junctional focus ventricular pacing the atrium with a normal AH
interval
Ventricular If a long VA interval The VA interval typically HA intervals are very Changes in the ventricular
tachycardia approximates the is longer than the HA similar during cycle length when the circuit
tachycardia cycle length, interval tachycardia and “wobbles” predict subsequent
there will be near– ventricular pacing changes in the HH and AA
simultaneous ventricular intervals
and atrial potentials Atrium and His bundle can
recorded be dissociated from the
tachycardia
With fascicular tachycardia,
simultaneous activation
can occur from the
bundle branch exit to the
ventricle and retrograde
via the AV node to the
atrium
Similar pseudointervals are
seen with bundle branch
reentrant tachycardia
Abbreviations: AA, atrial to atrial; AH, atrial-His; AVNRT, atrioventricular node reentrant tachycardia; HA, His-atrial; HH, His to His; PVC, premature ventricular
contraction; VA, ventriculoatrial.
Could this tracing be consistent with junctional tachycardia? resulting long VA interval may approximate the cycle length
Any electrophysiologic tracing of AVNRT will have features of the tachycardia; however, this is only an impression of a
consistent with some form of junctional tachycardia (and vice short VA tachycardia. The reason that this is not a true VA
versa), so it is impossible to know which diagnosis is correct from interval is because several other unusual features must be
a single tracing (Table C12.1). One must consider the clinical present to produce a truly short or simultaneous ventricular
history, method of induction, and outcomes of various electro- and atrial activation. Thus, even if the retrograde conduc-
physiologic maneuvers (Table C12.2) to make this distinction. tion limb of the orthodromic reciprocating tachycardia cir-
Could this tracing be consistent with atrial tachycardia? cuit is very long, antegrade conduction still needs to occur
In atrial tachycardia, the VA interval is also a pseudointer- via the AV node. Th is results in a fi nite AV interval that does
val because no VA conduction is actually occurring. Atrial not allow the atrial potential to occur simultaneously or just
and ventricular activation may occur simultaneously if the after the ventricular or His bundle potential, as shown with
atrial-His (AH) interval approximates the cycle length of the the tachycardia in Figure C12.1. Very rarely, however, the
tachycardia. This is more likely to occur in older patients with true earliest atrial potential may not be recorded on the left
poor AV nodal conduction or when antegrade conduction mid-septal or left anterior region. In these circumstances
occurs via a slow pathway. (eg, earliest activation in the left mid-septal region), the AV
Could this tracing be consistent with an accessory path- node may have direct, left-sided input (left-sided fast path-
way? This is the least likely of all the possibilities described. way), and the earliest right-sided atrial potential recorded
However, a seemingly very short VA interval can occur, albeit may appear to be simultaneous with the His bundle poten-
rarely, with a retrograde accessory pathway that conducts very tial. Clearly, such a coalescence of unusual circumstances
slowly; in other words, the VA interval approximates the cycle would be extremely rare. Thus, for the purpose of routine
length of the tachycardia. This phenomenon is sometimes electrophysiology practice (or the electrophysiology board
seen in persistent junctional reciprocating tachycardia. examinations), a very short VA interval excludes ortho-
Theoretically, if the retrograde pathway conducts very dromic AV reciprocating tachycardia as a mechanism of
slowly during orthodromic AV reentrant tachycardia, the tachycardia.
Earliest atrial potential near fast-pathway exit
Figure C12.2
In the tracing in Figure C12.2, note that ventricular pacing potential. However, upon cessation of ventricular pacing,
makes it easy to separate the ventricular and atrial potentials, the right atrial potential occurs nearly simultaneously with
and it is clear that the proximal His-atrial potential is earliest, the retrograde His bundle potential. What could be the
consistent with typical AV node reentry. Further maneuvers reason for this?
were performed that were relatively conclusive for AVNRT. A. A right lateral accessory pathway is likely present
Premature ventricular contractions (PVCs) could reset the B. It is common for the atrial appendage to be early in
tachycardia without a change in the atrial activation sequence AVNRT
by advancing the retrograde His by about 15 milliseconds. C. The arrhythmia was a junctional tachycardia
D. Atrial tachycardia was the primary (initially observed)
Careful analysis of Figures C12.1 and C12.2 shows an
arrhythmia
unusual phenomenon. During tachycardia (Figure C12.1)
and ventricular pacing (Figure C12.2), the His bundle
atrial potential is far ahead of the right atrial appendage Answer: E—None of the above.
Case 12 415
A change in the atrial activation sequence without a sequence. Such a short His-atrial (or VA) interval suggests
change in the cycle length of the tachycardia is a very unusual a pseudointerval, which means the patient has either some
fi nding for a patient with AV node reentry. A bystander AV form of AVNRT with the fast-pathway exit in the high right
accessory pathway should be considered, although it is highly atrium (possible but very rare [see Case 20]) or atrial tachy-
unlikely because of the very short His-to-atrial activation cardia is simultaneous with continued AV node reentry.
Figure C12.3
With continued observation of the arrhythmia (Figure paced beat in Figure C12.2 shows that retrograde conduc-
C12.3), the cycle length of the tachycardia does not change (as tion to the atrium may not only have re-induced AVNRT
determined by the His bundle and ventricular potentials) and but also induced another atrial tachycardia with a rate that is
the atrial potentials “march right through” the arrhythmia. just slightly faster than the AVNRT. Although dissociation of
This strongly suggests an atrial tachycardia that is simulta- AVNRT from the atrium is rare, a junctional tachycardia and
neous with continued AV node reentry. The last ventricular atrial tachycardia can occur simultaneously.
Figure C12.4
However, notice that in Figure C12.4, the tachycardia is nei- tachycardia occurring relatively early in the cycle of AVNRT
ther reset nor terminated for a long period, despite the atrial (equivalent of early coupled premature atrial contractions).
Eventually, the phase shift between these arrhythmias is suf- with early activation in the region of the high right atrium or
ficient that a very early atrial tachycardia beat likely terminates atrial appendage. Therefore, although atrial tachycardia was
the AVNRT. The subsequent pattern is an atrial tachycardia also present, the initially observed arrhythmia was AVNRT.
Figure C12.5
Note the unusual termination of the tachycardia (Figure contraction terminated the atrial tachycardia, and by being
C12.5). At first glance, the atrial tachycardia appears to ter- early, it prolonged the subsequent AH interval.
minate with a prolongation in the AH interval. This would be Although the electrophysiology board examinations use
highly unusual for atrial tachycardia, being the equivalent of relatively straightforward tracings (in which termination
termination with an “A” (atrial activation). For this to occur in with AV node dependence will almost always mean either AV
atrial tachycardia, there would have to be a sudden and seren- node reentry or AV reentry), in actual practice, close scru-
dipitous cessation of the atrial focus and a block or delay in the tiny of the electrograms and activation sequence is neces-
AV node. Note the slight change in atrial activation sequence sary before concluding where and how to ablate or map the
in the last beat of arrhythmia. It is likely that a premature atrial arrhythmia.
Figure C12.6
Case 12 417
Figure C12.6 shows initiation of AV node reentry. With show a left bundle branch block type of aberration. With left
atrial pacing, the AH interval increases at the start of a tachy- bundle branch block aberration and AV dissociation, infra-
cardia; the first beat is narrow complex and subsequent beats hisian block also may be expected.
Figure C12.7
Figure C12.7 shows continuation of the AV node reentry. the circuit is conduction from the fast-pathway exit site to the
However, there are more ventricular potentials than atrial (as slow-pathway entrance site in the region within or adjacent
described in the case illustrated by Figures C12.1-C12.5), and to the eustachian ridge. If such conduction forms the upper
the atrium may be completely dissociated from the AVNRT limb of the circuit, the connection from the retrograde fast to
circuit. In that case, an atrial tachycardia was responsible for the antegrade slow pathways may be within a protected isth-
the entire atrial activation sequence recorded by the catheters, mus, with a discrete exit from this upper limb of the circuit
even though AVNRT continued. In this case, an upper com- to the remainder of the atrium. This discrete exit from the
mon pathway block has occurred and no atrial activation is circuit to the atrium is termed the upper common pathway.
observed, despite continuation of what was otherwise docu- Thus, if the upper common pathway has a block, AV node
mented to be AV node reentry. reentry continues without atrial potentials.
How can the atrium be dissociated from the AV node reen- Now that atrial dissociation can be separated from AVNRT,
try circuit? In the early days of electrophysiology, this was an it is relatively straightforward to picture how AVNRT can
easy question to answer because the circuit for AVNRT (or coexist with various atrial arrhythmias. With an upper com-
the focus, as suggested by some) was thought to be within mon pathway block, atrial tachycardia, atrial flutter, and even
the compact AV node. Therefore, just as junctional tachycar- atrial fibrillation can occur in the atrial myocardium without
dia may have retrograde block to the atrium, it was simple affecting the AVNRT circuits (and vice versa). An intrigu-
to understand dissociation from the atrium during AVNRT. ing possibility in this case is that the atrial tachycardia focus
However, with the present understanding that AVNRT is in may have penetrated the upper common pathway in an ante-
fact largely an atrial reentrant arrhythmia (the major por- grade manner and created or maintained retrograde block
tions of the fast and slow pathway input to the AV node are in through the upper common pathway, facilitating dissociation
fact part of and continuous with the atrial myocardium), how of AVNRT from the atrial tachycardia itself.
can dissociation from the atrium be explained? Although dissociation of AVNRT from the atrium is very
The answer to this question is in the “upper limb” of the rare, the electrophysiologist should remain mindful about the
AVNRT circuit. For example, in slow-fast AVNRT, antegrade fact that a tachycardia like AVNRT with atrial dissociation
slow-pathway conduction reaches the AV node from this often is misdiagnosed as junctional tachycardia (with such
turnaround point, but as conduction proceeds to the ventri- a diagnosis, ablation is not performed for fear of AV block
cle, the atrium has retrograde activation via the fast pathway. or other reasons). This may result in failure to recognize that
Now consider how the wavefront proceeds from this exit site slow-pathway ablation could be curative. The electrophysiol-
back down through the antegrade slow pathway. Various cir- ogy board examinations commonly include questions per-
cuits are possible—these may involve the right atrium only, taining to AVNRT with atrial and ventricular dissociation or
portions of the left atrium, etc. One potential upper limb of relative block.
Figure C12.8
What arrhythmia is suggested by the electrocardiogram The finding of a P wave that is narrow and negative in
shown in Figure C12.8? leads II, III, and aVF, with a small, narrow, positive deflection
A. Ventricular tachycardia in V1, strongly suggests retrograde fast-pathway activation.
B. Junctional tachycardia Because this characteristic P wave is seen between 2 QRS
C. AVNRT with 2:1 AV block complexes, it raises the possibility of (typical) AVNRT with
D. AVRT 2:1 AV block.
Answer: C—AVNRT with 2:1 AV block.
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Figure C12.9
A closer view in Figure C12.9 shows the typical fast-pathway

P wave.
Case 12 419
I
aVF
V1
V6
hRA
HIS p
HIS d
CS 1,2
CS 3,4
CS 5,6
CS 7,8
RVa
ABL d
ABL p
Stim 1
Figure C12.10
With catheters in place (Figure C12.10), note the early His typical AV node reentry.
bundle atrial activation precedes the P wave, consistent with
I
aVF
V1
V6
hRA
HIS p
HIS d
CS 1,2
CS 3,4
CS 5,6
CS 7,8
RVa
ABL d
ABL p
Stim 1
Figure C12.11
With continued observation, the 2:1 conduction is no lon- may be completely dissociated from the circuit, but in other
ger seen and the tracing shows characteristic AV node reentry instances, either suprahisian or infrahisian block may occur,
(Figure C12.11). Thus, in AV node reentry, atrial activation dissociating the arrhythmia from ventricular activation.
Box C12.1
Features of Dissociated AVNRTa
Not all arrhythmias with block to the atrium or ventricle (or both) are junctional tachycardias
When there are more atrial than ventricular potentials in AVNRT, infrahisian block is most common, but suprahisian block (lower common
pathway block) may also occur
Suspect 2:1 AVNRT when the typical P-wave morphology, consistent with retrograde fast-pathway activation, is seen between 2 QRS
complexes
For the electrophysiology board examinations, as well as in clinical practice, any arrhythmia that shows unusual atrial and ventricular
conduction patterns should include AVNRT in the differential diagnosis; one should not give up on the case without attempting
slow-pathway ablation
Abbreviation: AVNRT, atrioventricular nodal reentrant tachycardia.

a
Questions pertaining to these aspects of AVNRT often are included in board examinations.
Figure C12.12
In Figure C12.12, during AVRT with a far lateral acces- large far-field potential is advanced, but the near-field poten-
sory pathway (note the eccentric coronary sinus activation tial in the center of the complex signal remains unchanged.
sequence), a PVC is placed (Box C12.1). Although PVCs are This patient had a prior ablation that was inadvertently placed
placed during supraventricular tachycardia for various rea- too far into the ventricle; thus, the ventricular signal was
sons, including defining the mechanism of the tachycardia, highly fragmented but the (very early) atrial potential was
they can also be very useful in understanding the potential amidst this far-field fractionated ventricular signal. The PVC
recorded by a mapping catheter. Note on the MAP d catheter, that was placed changed the ventricular potential, allowing
a highly complex signal is seen, with multiple far-field signals identification of an excellent site for ablation.
but 1 sharp potential (arrow). When the PVC is placed, the
Case 12 421
Tachycardia terminates during ablation
Figure C12.13
Ablation was performed with underlying ventricular pac- B. The pathway has been successfully ablated and now ret-
ing (Figure C12.13), a common maneuver to avoid sudden rograde conduction is via the AV node
catheter movement when the tachycardia terminates. Note C. Cannot say from the information provided
that the tachycardia terminates and a different ventricular Answer: C—Cannot say from the information provided.
activation sequence is shown.
Clearly, VA activation has changed and the VA interval
What is your diagnosis? is very short, which raises the possibility of a second acces-
A. A lateral pathway has been successfully ablated and sory pathway. This possibility must be considered seriously
now a more septal pathway is seen because up to 10% of patients with an accessory pathway
actually have multiple pathways.
Figure C12.14
However, in Figure C12.14, note that VA conduction retrograde conduction is through a “slick” AV node and ret-
shows early atrial activation in the region of the fast pathway. rograde fast pathway or through an anteroseptal accessory
Thus, the electrophysiologist must now determine whether pathway.
His
Figure C12.15
Parahisan pacing should be performed to make this block to the atrium, despite continued AVNRT, in the case
distinction; however, note in Figure C12.15 that a clear shown in Figures C12.8 through C12.10.
retrograde His bundle potential (arrow) is seen during ven- The patient described later in this section (Figure
tricular extrastimulus testing. This is because of the induc- C12.12) demonstrated the concept of association. After
tion of retrograde right bundle branch block. The ventricular ablation of the arrhythmia, an unusual activation sequence
paced activation now has to travel to the left ventricle, go with a short VA interval was seen. However, when a placed
up the left bundle, and then reach the His bundle. Thus, the premature ventricular extrastimulus induced retrograde
ventriculo-His interval and the VA interval have lengthened, right bundle branch block, activation of the atrium was
although the atrial activation sequence has not changed (see delayed without changing the retrograde atrial activation
Chapter 4). An accessory pathway would not depend on sequence. The association among the ventricle, retrograde
whether the ventriculo-His interval increased (retrograde His bundle, and atrium (ie, delay in the ventriculo-His
right bundle branch block), and thus, this maneuver is diag- interval resulted in an equivalent delay in the VA interval)
nostic of retrograde conduction via an AV node–dependent proved that retrograde activation was via the AV node (see
process (ie, the fast pathway). Chapter 4).
The patients described in Case 12 illustrate the importance Electrophysiologists must be constantly aware of the usual
of knowing which potentials are necessarily associated with pattern of association between potentials and the common
each other during certain arrhythmias and which may be dis- causes of supraventricular tachycardia. Yet they also must be
sociated from the primary circuit in other arrhythmias. alert to less common situations in which one or more cardiac
In the case described in Figures C12.1 through C12.5, the chambers may be dissociated from the primary tachycardia
atrium clearly can be dissociated from the AVNRT circuits. circuits.
This is particularly surprising, given our present understand-
ing of the importance of the atrial myocardium to the AVNRT
circuit. In fact, some electrophysiologists describe AVNRT as Abbreviations
an atrial tachycardia that happens to have the turnaround
point (low zone) close to or within the compact AV node. The AH, atrial-His
concept of the upper common pathway and how block in that AV, atrioventricular
pathway can result in atrial dissociation from AVNRT was AVNRT, atrioventricular node reentrant tachycardia
described above. This dissociation took the form of a simul- PVC, premature ventricular contraction
taneous atrial tachycardia (Figure C12.1-C12.5) and with a VA, ventriculoatrial
Case 13
Figure C13.1
The electrocardiogram in Figure C13.1 was obtained from Which statement about the electrocardiogram in Figure
a patient with symptomatic palpitations, documented ven- C13.1 is true?
tricular tachycardia, and syncope. Right ventricular outflow A. The R wave in lead V1 is diagnostic of a left ventricular
tract (RVOT) tachycardia was diagnosed, and treatment with origin
β-blockers followed by sotalol was ineffective. The patient B. QS complex waves in leads aVR and aVL cannot occur
previously had undergone 3 radiofrequency ablation proce- and signify improper lead placement
dures, with lesions placed in the RVOT and left ventricle, but C. The S waves in leads I and aVL are diagnostic of a left
the symptoms persisted. ventricular origin
D. The R waves in leads II, III, and aVF are diagnostic of an
outflow tract focus
Abbreviations are expanded at the end of this chapter. E. An origin near the His bundle is unlikely
Terms with “[f]” denote abbreviations that appear in the figures only. Answer: E—An origin near the His bundle is unlikely.
423
Right ventricular outflow

tract tachycardia Box C13.1
Left bundle/inferior axis Causes of Difficulty in Ablating Outflow Tract
Idiopathic posterior Tachycardia
left ventricular tachycardia
Right bundle/left axis 1. Inability to induce tachycardia in the electrophysiology
laboratory
2. Origin in the left ventricle
3. Supravalvular focus
4. Epicardial coronary vein or artery–related focus
5. Association with right ventricular dysplasia
6. Inducible but hemodynamically unstable ventricular
tachycardia
7. Varying fusion with sinus rhythm or other premature ven-
tricular contractions, making mapping unreliable
8. Origin in the conduction system
Along with RVOT tachycardia, bundle branch reentrant

ventricular tachycardia and idiopathic fascicular ventricular
tachycardias are considered curable disorders. At times, how-
ever, outflow tract tachycardia can be very difficult to ablate
Bundle branch reentrant (Box C13.1), with multiple recurrences that require repeated
ventricular tachycardia
procedures. The electrocardiogram must be carefully ana-
Left bundle/left axis
lyzed (in both difficult and straightforward situations) for
Figure C13.2 clues that may reveal the cause of difficulty with ablation.
In general, outflow tract tachycardias are readily ame-

nable to radiofrequency ablation. The schematic in Figure
C13.2 shows ventricular tachycardias that can be readily
ablated.
Case 13 425
Figure C13.3
In this patient, tachycardia was readily inducible and signifies a right-sided origin, QS complexes are found nearly
hemodynamically welltolerated at all prior electrophysiol- universally in both leads in outflow tract tachycardias. This
ogy studies, which allowed extensive mapping. Figure C13.3 is because the axis for leads aVR and aVL are not only right-
shows a schematic and the classic electrocardiogram pattern ward and left ward but also are superior leads. Thus, in the
of RVOT tachycardia. Carefully note the following 5 points. fairly wide arc between the vectors for leads aVR and aVL, all
First, there is no R wave in lead V1 (ie, it is a complete nega- superiorly originating tachycardias will be negative in both
tive deflection), which suggests an anterior location such as leads and apically originating rhythms will be positive in
the RVOT. both leads.
Second, there is an inferior axis (ie, deflections in leads II, Fourth, a negative deflection in lead I (QS complex) by no
III, and aVF are all positive). This is seen in virtually all cases means signifies a left ventricular origin. In fact, as explained
of outflow tract tachycardia. However, a similar pattern can below, the RVOT is more left ward in the heart than the left
also occur in tachycardias that originate in the anterior por- ventricular outflow tract (LVOT).
tion of the mitral annulus or the anterior inflow portion of Fift h, lead aVL will be either slightly positive or isoelectric
the right ventricle. Thus, an inferior axis is not diagnostic of when the origin is located near the His bundle because the
an outflow tract origin. His bundle is located in the most rightward and inferior part
Third, although a negative deflection in aVL usually signi- of the RVOT. In fact, it is the only location in the RVOT where
fies a left-sided origin and a negative deflection in lead aVR the deflection in aVL is not completely negative. Thus, in the
electrocardiogram in Figure C13.1, the possibility of requir- difficulty. For example, if the tachycardia was difficult to
ing ablation near the His bundle can be safely excluded. induce and only a few beats were available for mapping, or
The electrophysiology study was repeated in this patient if hemodynamic instability occurred, then noncontact map-
with a plan to address the remaining potential causes of ping would need to be considered.
His
prox
His dist
Lateral
Earliest site
of activation
Septal
1. Define geometry 2. Record map 3. Guide catheter to critical

map site
Figure C13.4
With noncontact mapping (Figure C13.4), a multielectrode on the far-field potential picked up by the intracavitary array
array catheter is placed in the RVOT. The geometry of the catheter). Points A through D indicate the pattern of activa-
chamber is defined with point-to-point movement of a con- tion. The earliest site of activation is then targeted, either for
tact catheter (any electrophysiologic catheter). Next, a map of further mapping with a contact catheter or for radiofrequency
virtual potentials is created (potentials are calculated based ablation (see Chapter 3).
Pulmonary valve
Figure C13.5
Figure C13.5 shows an example from another patient; sometimes exit to multiple locations around the pulmonary
here, a noncontact map showed an origin for the tachycardia annulus and be difficult to map until the true earliest site of
above the pulmonary valve. Suprapulmonary valve foci can origin is located.
Case 13 427
(A)
Figure C13.6
The autopsied heart in Figure C13.6 shows the pulmo- (B)

nary valve and a myocardial sleeve that extends into the
pulmonary artery. For some patients, a sleeve can extend
several centimeters into the pulmonary artery, whereas for
others, it terminates abruptly at the level of the pulmonary
valve.
Figure C13.7
It can be very difficult to know where the RVOT ends

and the pulmonary valve and arterial tissue begin. A com-
monly used maneuver is to advance the mapping catheter
until potentials are no longer seen. However, this can be mis-
leading because potentials will continue to be seen as long
as myocardium is present and, as noted above, myocardial
tissue can extend above the valve. Figure C13.7A shows a lin-
ear, phased-array, intracardiac echocardiogram, with a probe
placed at the ostium of the RVOT (Figure C13.7B) to examine
the pulmonary valves. Note that one valve leaflet has myocar-
dium that extends into the pulmonary artery but the other
does not.
RVOT
Cardiac
vein
Ao PA
LCX
LAD
LVOT retrograde
approach
RV
LAO
Figure C13.8 LV
Tachycardia was induced in the electrophysiology labo-

ratory and the outflow tract was mapped extensively. Note
the complex anatomy of this region in this fluoroscopic
image (Figure C13.8). Catheters were placed in the RVOT,
the LVOT, the anterior intraventricular vein, and the His
bundle region. Note in this left anterior oblique projec- Anterior view
tion that the His bundle is the most rightward location of
the outflow tract, and thus lead aVL has a positive deflec- PA: anterior to aorta, to left shoulder
tion when tachycardia originates in this site. The intimate Ascending Ao: posterior to PA, to right shoulder
relationship of the coronary arterial system with both
Ao-PA angle, 60-90 degrees
the RVOT and LVOT is apparent from this angiographic
image.
Figure C13.9 (Courtesy of W. D. Edwards, MD, Mayo Clinic,
To understand the anatomy of this region (Figure C13.9),

remember that the RVOT is anterior and mostly left ward of
the LVOT in a normal heart. In other words, sites close to
the pulmonary artery are toward the left side of the body,
relative to many sites in the supravalvular portion of the
LVOT. The angle formed between these outflow tracts is
variable (as great as 90°). When mapping the RVOT, it is a
common misperception that the origin may be in the LVOT
if the earliest sites are left ward and far-field potentials are
seen at the earliest map sites. Th is is not true, as shown
in Figure C13.9. The coronary venous system (epicardial
RVOT) and the mitral annulus are left of the RVOT. The
LVOT is posterior to and slightly rightward of the RVOT.
Thus, when earliest sites with far-field potentials are noted
posteriorly in the RVOT, it may be indicative of an LVOT
origin.
Case 13 429
RVOT
Ao
LV
LA
Long-axis view
Figure C13.10
The long-axis pathologic and echocardiographic images aortic valve. Fourth, the left main coronary artery is closer
in Figure C13.10 clearly demonstrate the anterior-posterior to the posterior subvalvular RVOT than it is to the subval-
orientation of the RVOT, left ventricular–aortic tract, and vular or supravalvular LVOT. Fift h, myocardial tissue nor-
aorta. Several anatomic points important for ablation should mally is not found between the aortic valve and mitral valve
be noted. First, the anterior-most structure is the free wall or (aortic mitral continuity). Sixth, the noncoronary cusp of the
anterior portion of the RVOT. Thus, foci originating in this aortic valve has a functional shared wall with a portion of
region will be associated with a sharp and completely nega- the left atrium. Thus, early sites of atrial tachycardia can be
tive deflection in lead V1. Second, note that the anterior wall mapped from this site, and far-field ventricular signals can
of the supravalvular portion of the aorta is adjacent to the be obtained in the left atrium and possibly ablated from the
posterior wall of the RVOT (they share a common functional left atrium if ventricular tachycardia originates in the non-
wall). Third, note that the pulmonary valve is cephalad to the coronary cusp.
Figure C13.12
Figure C13.11
Figure C13.11 illustrates the aortic mitral continuity and the aortic valves. Figure C13.12 illustrates the anatomic loca-
potential for myocardial sleeves to occur above the plane of tions of the 2 valves relative to the RVOT.
Figure C13.13
Figure C13.14
The subsequent discussion pertains to Figures C13.13 and left anterior descending artery and left main coronary artery
C13.14. The anatomic section illustrates the coronary arter- (arrow); they are posterior and below the level of the pulmo-
ies. Note the relation between the RVOT and the proximal nary valve.
Case 13 431
Figure C13.15
When analyzing the cause of a positive deflection in lead true origin in the left ventricle (the posterior ventricle) will
V1, several factors must be considered. First, a right ven- almost always have a positive R wave, most often with no
tricular tachycardia originating in the posterior wall adja- S wave, in lead V1. Fourth, the origin of a premature ven-
cent to the aorta will have an initial vector that is positive in tricular contraction (PVC) or tachycardia from the aortic
lead V1. Second, a supravalvular origin in the RVOT that is mitral continuity will have a prominent R wave in lead V1.
in a very left ward location above the pulmonary valve will However, by being at the geometric center of the heart, the
also have a vector going toward lead V1 (left to right), which axis will also have a vector moving away from V1, which will
gives rise to a positive deflection (Figure C13.15). Th ird, a give rise to an S wave.
Figure C13.16
Analysis of the electrocardiogram in terms of the frontal ventricular tachycardia (still possible for the origin to be in
axis and limb lead axis is also highly useful (Figure C13.16). the RVOT but closer to the free wall or valvular location), the
As noted above, the origin for arrhythmia in the arc between R wave will be more positive in lead III than in lead II.
aVR and aVL will give rise to QS complexes in both these For example, in Figure C13.15, a very small R wave can
leads. However, if the QS complex in lead aVL is relatively been seen in lead V1. This should raise suspicion of a possible
more negative than that in lead aVR, a left ward origin (per- origin in the posterior RVOT or sites closer to the pulmonary
haps supravalvular in the RVOT) should be considered. valve. Note that aVR and aVL are both negative but that aVL
Similarly, analysis of the inferior leads II, III, and aVF can is more negative, which again suggests a left ward origin, more
also be useful to better understand the precise origin of out- likely to originate from the RVOT closer to the pulmonary
flow tachycardias. Although leads II, III, and aVF are all infe- valve. The same conclusion can be reached by noting that the
rior leads, lead III is a relatively rightward lead and lead II R wave is more positive in lead III than in lead II and that lead
is a relatively left ward lead. Thus, in “left ward” outflow tract I has a predominant negative deflection.
Case 13 433
Figure C13.17
In Figure C13.17 (going back to the original patient), note or whether tachycardia originates within or in proximity of
the distinct variation in QRS width and cycle length of the the conduction system. In this case, there is no clear evidence
arrhythmia. This finding can be important to recognize for the of conducted sinus beats giving rise to capture and fusion, and
successful ablation of certain outflow tract tachycardias. One the overall axis for the narrow and wide beats are so similar
needs to consider 3 options: whether more than one arrhyth- that 2 different foci with varying degrees of fusion is unlikely.
mia is occurring, whether fusion with sinus beats is occurring, That leaves the third option for consideration.
Inlet-outlet ring around
Right AV junction Outflow tracts
Left AV junction
Dead-end tract
Compact node
Primary Penetrating bundle
septum
Trabecular
Left Dead-end tract
component of right
ventricle
ventricle
Ventricular bundle
branches on apical
AV AV
trabecular septum
groove Right groove
ventricle
Branching bundle
and bundle branches
Figure C13.18
The embryologic form of the conduction system is depicted outflow tracts; these are known by various names such as right
in Figure C13.18. The primitive atrial ventricular junction and left superior fascicles, dead-end tracts, and Lancisi fibers.
(conduction) tissue has remnants that can extend into the When these conduction elements are found, they may be the
origin for an arrhythmia with varying degrees of conduction tachycardia to simultaneously activate other myocardial sites,
block, or they may be a “roadway” used by a muscular-origin giving rise to subtle yet distinct changes in QRS morphology.
(B)
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure C13.19
This very important possibility must be kept in mind, Ablation at this site was successful and permanently elimi-
especially when pace-mapping is used to pick an ablation site. nated the patient’s arrhythmia.
The electrocardiogram in Figure C13.19A was obtained when Pace-mapping is a method commonly used to estimate
pacing at the cycle length of tachycardia, just at the capture where automatic tachycardias can be ablated, but it has impor-
threshold. tant limitations. First, pace-mapping at high output may
The near-identical pace map (Figure C13.19B) was obtained capture myocardium of a contralateral chamber and result
by pacing above the level of the anterior pulmonary valve. in spurious findings. Second, for a true identical pace map,
Note that with slight variation in the pacing output (close every deflection (eg, notches, QRS width, etc) must be iden-
to threshold), narrower and wider beats could be obtained. tical. Third, when tachycardias originate in the conduction
Case 13 435
system, the pace map at the site of origin (within the conduc- myocardium. Fourth, high- and low-output pacing should be
tion system) may be completely different from the ventricular considered, especially when the tachycardia shows spontane-
tachycardia QRS morphology because of concomitant capture ous variation in QRS duration or when multiple early sites are
of the surrounding myocardium near the conduction tissue, noted when mapping with a 3-dimensional system (see Case
whereas during tachycardia, the exit is at a distal site into the 14 and Chapter 6).
Figure C13.20
Figure C13.21
Figures C13.20 and C13.21 illustrate another cause of spu- illustrated also may occur during pace mapping for ventricu-
rious results with pace-mapping (marked variation in the QRS lar tachycardia ablation.
with high- and low-output pacing). Although this example This patient had a left ventricular lead placed as part of
is taken from a patient with a pacemaker, the phenomenon a biventricular pacing system. The lead had not changed
position, and left ventricular capture is seen in both figures. the output changing, particularly when the anode is consider-
With high-output pacing (Figure C13.20), a strong inferior axis ably larger than the cathode; this may also occur with the more
is noted that is not seen at lower-output pacing (Figure C13.21). commonly used anode-to-cathode ratios of electrophysiology
This illustrates the phenomenon of anodal stimulation. The catheters. Here again, slight changes in the wave front can give
vector or wave front of pacing stimulation can vary without rise to incorrect interpretation of pace-mapping results.
Figure C13.22
The electrocardiogram in Figure C13.22 was obtained D. An origin in the LVOT should be suspected because
from a patient who had undergone several previous abla- the deflection in lead III is more positive than that of
tion attempts for outflow tract tachycardia associated with lead II.
degeneration to polymorphic tachycardia and ventricular Answer: B—An origin in the LVOT should be suspected
fibrillation. because of the completely positive R wave in lead V1.
Which of the following can be deduced from this electro- As explained above, the RVOT is toward the left side of the
cardiogram (Figure C13.22)? body, and thus a negative deflection in lead I, strongly nega-
A. An origin in the LVOT should be suspected because the tive deflection in lead aVL, and strongly positive deflection
deflection in lead I is negative. in lead III can all be seen with a RVOT origin. However, it is
B. An origin in the LVOT should be suspected because of unlikely that RVOT tachycardia, even from the posterior wall,
the completely positive R wave in lead V1. will have a completely positive R wave in lead V1. Thus, a left
C. An origin in the LVOT should be suspected because ventricular origin should be suspected. Because this patient
the deflection in lead aVL is more negative than that of had undergone multiple procedures previously, detailed map-
lead aVR. ping of both chambers was planned.
Case 13 437
Figure C13.23
A noncontact map (see Chapter 3) of the RVOT was cre- virtual electrograms was not significantly ahead of the QRS
ated (Figure C13.23). Note that the earliest deflection in the complex in the 12-lead electrocardiogram.
Figure C13.24
Contact mapping with the ABL catheter was performed deflection was seen earlier than the QRS complex (Figure
in the supravalvular pulmonary outflow tract. Again, no C13.24).
Figure C13.25
The LVOT was then mapped and again, there was no truly fusion should be mapped. Otherwise, one is simultaneously
early site. Note also in Figure C13.25 that the potential for mapping the usual exit for a normal sinus beat. Figure C13.25
sinus beats to cause varying degrees of fusion is an impor- shows varying atrioventricular intervals between the sinus
tant cause for failure when mapping PVCs with any mapping activation of the atrium and the PVCs. Every effort should be
system. Only PVCs with a fi xed degree of fusion or minimal taken to map only nonfi xed beats.
RAO LAO
Figure C13.26
The fluoroscopic image in Figure C13.26 shows the com- placed in the epicardium via a subxyphoid pericardial
plex catheter positions that now include a catheter (arrows) axis.
Case 13 439
Figure C13.27
Although mapping of the epicardium is important, when- Figure C13.28 shows the superior view of the outflow
ever a true early site cannot be found endocardially, the electro- tract. The region between the RVOT and LVOT is very diffi-
physiologist needs to understand which sites of the outflow tract cult to access using a pericardial approach. Other approaches
are not easily accessible with a pericardial approach. In Figure that should be considered include mapping from the left
C13.27, the earliest epicardial site (Epi 3,4) was also not much atrial appendage for epicardial RVOT tachycardia sites (but
ahead of the QRS complex. Thus, even after extensive mapping not LVOT sites). Sometimes, a second lobe of the left atrial
of the RVOT, LVOT, and the epicardium, no local activation appendage (ie, a bifid appendage) may be found between the
site earlier than the start of the surface QRS was found. 2 outflow tracts, which can be used for mapping. Note that
the supravalvular aortic region is in very close proximity to
the right atrial appendage and superior vena cava (Figure
C13.28); in fact, it can be mapped from these sites. The distal
coronary venous system and anterior ventricular veins (yel-
low arrow) also can be used to map epicardial left ward loca-
tions in the RVOT.
SVC
Aortic root
Figure C13.28
(A) (B)
I
I
II
III II
aVR III
aVR
aVL
aVL
aVF
aVF
V1
V1
V2
V2
V3
V3
V4
V4
V5
V5
V6 V6
Distal coronary sinus pacing Baseline premature ventricular contractions

Figure C13.29
Figure C13.29 shows a pace map obtained when pacing from map was nearly identical to one showing baseline PVCs (Figure
the distal coronary sinus at the junction of the great cardiac C13.29B). This site is very close to the aortic mitral continuity,
vein and anterior interventricular vein (Figure C13.29A); the left main coronary artery, and supravalvular aortic annulus.
RAO LAO
Figure C13.30
Case 13 441
Superior (A)
Right Left
Aorta
Inferior
Ao
LPA
LPA
Lasso in
SVC
SVC RPA
RPA aortic root
Transverse
sinus
Recess
Recess
Ao
Recess
Recess
Figure C13.31
The arrows in Figure C13.30 show the ablation catheter

in the transverse pericardial sinus. Pericardial access can be
obtained for this complex region, located behind the RVOT
and alongside the supravalvular aortic annulus (Figure (B)
C13.31). The catheter is not placed above the RVOT; rather,
access is obtained by entering the transverse sinus of the
pericardium superior to the roof of the left atrium and going
around the RVOT. Note that the transverse sinus (Figure
C13.31) can also be used to map the region between the aorta
and superior vena cava (aortocaval sinus).
Signals above the aortic valve
Figure C13.32
A circumferential mapping catheter with widely spaced

electrodes was placed in the supravalvular aortic region
(Figure C13.32A). Very early, fascicle-like signals (sharp,
near-field potentials) were observed (Figure C13.32B).
Figure C13.33
Note that the signals from the circumferential mapping Myocardium has depth
catheter were found even during sinus rhythm and, at times,
were completely isolated from both sinus rhythm and PVCs
(Figure C13.33). However, when PVCs occurred, they always
had a fi xed interval between the spikes and the onset of the
QRS complex. Successful ablation was performed in this case
by near-circumferential ablation at the aortic root, which iso- Endocardium
lated these potentials and prevented further ectopy.
Focus
Epicardium
Figure C13.34
Although an epicardial origin always must be considered

for reentrant and automatic arrhythmias, epicardial origins
are more common with the inflow portion of the ventricles
(particularly the left ventricle) than it is with the outflow por-
tion. This is because one inflow portion of the LV is thicker
(Figure C13.34), thereby making the epicardium difficult to
map (and ablate) using an endocardial approach.
Case 13 443
(A)
RVOT
(anterior) LVOT
(posterior)
Figure C13.35
(B)
As illustrated in this electroanatomic image with the Epicardial mapping catheter
RVOT and LVOT mapped (Figure C13.35), the epicardial sur-
face of the posterior RVOT is the supravalvular portion of the
LVOT, and the epicardial anterior portion of the LVOT is the
posterior RVOT. Thus, very careful mapping of the posterior
RVOT and anterior LVOT (particularly the supravalvular
portion) is required to define the actual chamber of origin.
Figure C13.36
Rarely, true epicardial foci occur in the RVOT. In an

unusual case, mapping is performed with an epicardial cath-
eter (Figure C13.36A and C13.36B, arrow) along with stan-
dard endocardial mapping. The earliest site of activation was
epicardial. This patient had an unusual fistula from the right
coronary artery conus branch to the right ventricle that may
have been the reason for the unusual epicardial origin of
arrhythmia.
Figure C13.37
The 12-lead electrocardiogram in Figure C13.37 was Computed tomography and magnetic resonance imaging
obtained from another patient with RVOT tachycardia that may be used in the evaluation of right ventricular dysplasia.
was very difficult to ablate. The electrocardiogram was highly Characteristic abnormalities found in this patient (Figure
suggestive of right ventricular dysplasia. Note the negative C13.38) were in the free wall of the outflow tract, distal
T waves in leads V1, V2, and V3 (arrows), consistent with a intraventricular septum, and the free wall of the right ven-
persistent juvenile T-wave pattern. Note also the wider QRS tricle inflow portion (arrows). Although tachycardia from the
complex in leads V1 and V2 compared with that in leads V5 inflow right ventricular portion will have a distinctly differ-
and V6. ent QRS axis than outflow tract tachycardia when dysplasia
involves the RVOT, the QRS morphology is very similar to
commonly observed RVOT morphologies.

Case 13 445
Table C13.1
Criteria for Diagnosis of RV Dysplasia
Defect Major Criteria Minor Criteria
Global or regional dysfunction Severe dilatation and decreased RV ejection fraction Mild global RV dilatation or decreased ejection
and structural alterationsa Localized RV (akinetic or dyskinetic areas with fraction (or both)
diastolic bulging) Mild segmental dilatation
Severe RV segmental dilatation Regional RV hypokinesia
Abnormal tissue in walls Fibrofatty replacement of myocardium on biopsy ...
Repolarization abnormalities ... Inverted T waves in right precordial leads
(V2 and V3)
Depolarization or conduction Epsilon waves or localized QRS prolongation Late potentials (single-averaged
abnormalities (>110 msec) in leads V1, V2, and V3 electrocardiogram)
Arrhythmias ... Left bundle branch–type ventricular tachycardia
Frequent ventricular premature complexes
(>1,000 per 24 h; Holter monitoring)
Family history Familial disease confirmed at necropsy or surgery Familial history of premature sudden cardiac
death (age <35 y) due to arrhythmogenic right
ventricular dysplasia
Other relevant family history
Abbreviation: RV, right ventricular.
a
Detected by echocardiography, angiography, magnetic resonance imaging, or radionuclide scintigraphy.
A biopsy (Figure C13.39), although difficult to perform, Box C13.2 describes features of outflow tract tachycar-
can help with the diagnosis; however, it is not necessary to dias. Dysplasia complicates the long-term management of
establish the diagnosis in patients with suspected dysplasia. a patient with outflow tract ventricular tachycardia, and it
Criteria for diagnosis are enumerated in Table C13.1. also completely alters invasive electrophysiologic manage-
ment. Th is is because RVOT tachycardia, like any other
focal-source tachycardia, requires “simple” point-to-point
Box C13.2. mapping to fi nd the earliest site of activation; the activa-
Salient Points for Outflow Tract Tachycardias
tion site is then targeted for ablation. However, in the cases
• Understanding the relative anatomy of the 2 outflow tracts discussed in this series, there may be difficulties with actu-
is essential ally determining the ideal site for ablation. The procedure
• The anatomic relationships of the appendages, coronary
is still relatively straightforward compared with ablation of
sinus, superior vena cava, and coronary arterial and venous
system should be appreciated reentrant ventricular (or atrial) tachycardia (see Case 14).
• Right ventricular dysplasia, supravalvular origins, and Arrhythmogenic right ventricular dysplasia is associated
anatomic abnormalities (including remnant conduction tissue) with multiple reentrant circuits because fatty infi ltration
should be considered in the differential diagnosis of a patient and fibrosis causes electrophysiologic behavior similar to
with outflow tract tachycardia that is difficult to ablate
multiple scars.
Table C13.2
Causes of Difficulty for “Readily Ablatable” Ventricular Tachycardia
Type of Tachycardia Why it is Readily Ablatable When it is not Readily Ablatable
Location Comments
Right ventricular Point-source tachycardia Posterior wall origin R wave in lead V1, difficulty with contact
outflow tract Right ventricular Proximity to His bundle Isoelectric or small R wave in lead aVL
tachycardia myocardium is not very Consider cryoablation
thick and energy delivery Proximity to conduction system ...
is straightforward Possible proximity to coronary Posterior subpulmonic valve location
Minimal risk for stroke or artery Consider cryoablation
valvular damage Coronary arteriography with
intravascular ultrasonography to
visualize anatomy
Epicardial origin Very rare because the ventricular wall is
too thin to cause difficulties
Consider dysplasia or AV malformation
Left ventricular outflow Point-source tachycardia Supra-aortic valve location Multiple exit sites
tract tachycardia Usually accurate mapping Multiple morphologies
and ablation at the mapped Possible polymorphic ventricular
site is curative because tachycardia
myocardium is fairly thin Proximity to coronary arteries Intracardiac ultrasonography and
in the outflow tract angiography to visualize anatomy
Consider isolation of the aortic root
Aortic mitral continuity site Poor catheter stability makes mapping
difficult
Exit sites may vary
Exact supravalvular and infravalvular
maps are required
Proximity to conduction system Medial proximal aortic root tachycardias
may be close to the compact
atrioventricular node
The His bundle should be mapped before
energy delivery
Consider cryoablation
Fascicular tachycardia Structurally normal heart Arrhythmogenic fascicle may As discussed in Chapter 6, pace at high
Usually single-source for exit at a distant site and low output; low-output pacing will
tachycardia Multiple bystander fascicular reproduce a tachycardia morphology
potentials may be seen; these with a stimulus-to-QRS interval that is
do not need to be targeted for similar to the local fascicular signal-to-
ablation QRS interval during tachycardia
Can be difficult to distinguish
from interfascicular
tachycardia
This series has explored the primary, readily ablatable Interventional management of ventricular tachyarrhyth-
tachycardias, with emphasis on outflow tract ventricular mia perhaps has the greatest need (compared with other
tachycardia. The variations that should alert an electrophysi- electrophysiologic situations) for an exact understanding of
ologist to potential difficulty include an R wave in lead V1, an fluoroscopic anatomy, correlation with electrocardiographic
abnormal resting electrocardiogram, and variation in the QRS findings, and correlation with anatomic variants. In Case 14,
width or cycle length during tachycardia. The importance of this need for exact understanding is taken one step further by
completely analyzing the electrocardiogram and understand- examining multiple reentrant circuits, which require famil-
ing the limitations of pace-mapping were explained during iarity with methods to define the circuit and identify critical
these case discussions. The causes and methods to overcome zones that should be targeted for ablation.
difficulty with the “readily ablatable” ventricular tachycardias
are outlined in Table C13.2.
Case 13 447
Abbreviations LVOT, left ventricular outflow tract

MCL, mid chest lead [f]
Ao, aorta [f] PA, pulmonary artery [f]
AV, atrioventricular [f] PVC, premature ventricular contraction
LA, left atrium [f] RA, right atrium [f]
LAD, left anterior descending artery [f] RAO, right anterior oblique [f]
LAO, left anterior oblique [f] RPA, right pulmonary artery [f]
LCX, left circumflex artery [f] RV, right ventricle [f]
LPA, left pulmonary artery [f] RVOT, right ventricular outflow tract
LV, left ventricle [f] SVC, superior vena cava [f]
Case 14
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure C14.1
The electrocardiogram in Figure C14.1 was obtained from D. Reentrant tachycardia from the right ventricular free
an elderly man with a history of myocardial infarction that wall is present
involved the inferior and inferolateral left ventricular walls. E. The successful ablation site may be located in the left
ventricle
Which statement about this electrocardiogram is true?
A. Supraventricular tachycardia with left bundle branch Answer: E—The successful ablation site may be located in
block aberrancy is present the left ventricle.
B. Automatic tachycardia arising from the right ventricu- The differential diagnosis for this wide complex tachy-
lar outflow tract is present cardia includes supraventricular tachycardia (with aber-
C. Automatic tachycardia from the right ventricular free rancy or preexcitation) and ventricular tachycardia. Note the
wall is present narrow-looking QRS complex in lead aVR. At times, portions
of the QRS complex may be isoelectric in one lead, giving a
false impression of a narrow QRS rhythm.
Abbreviations are expanded at the end of this chapter. A supraventricular tachycardia with left bundle branch
Terms with “[f]” denote abbreviations that appear in the figures only. block could be present, given the information in this
449
electrocardiogram (Figure C14.1). However, the completely atrioventricular accessory pathways exit close to the base of
negative QS complexes in leads III and aVF make this unlikely the ventricle, typically with positive concordance in leads
because when the left bundle branch is blocked, the exit for a V1 through V6 (excitation proceeding toward the apex). An
supraventricular rhythm is from the right bundle branch. The exception, however, is antidromic tachycardia associated with
right bundle branch exit is located anteriorly and in the mid a Mahaim fiber. This is because these bypass tracts may insert
portion of the right ventricular septum. Thus, it is unusual to into the right bundle system and produce a nearly typical left
not have at least a small R wave in leads III and aVF when the bundle branch block pattern. For the same reasons explained
exit is from the right bundle branch. above, a completely negative QRS complex in leads III and
Supraventricular tachycardia with preexcitation is another aVF (in the absence of precordial concordance) is not usually
possibility. However, most antidromic tachycardias with seen with these bypass tracts.
Table C14.1
Distinguishing Between Automatic and Reentrant Mechanisms for Tachycardia
Mapping Technique Automatic Tachycardia Reentrant Tachycardia
Activation sequence Spread of activation from a focal source Highly variable, dependent on location of circuit and scars
in the remaining myocardium
Earliest site of Usually an excellent target for ablation No true early site exists because continuous electrical
activation Exceptions are an epicardial or other-chamber origin, activity is present throughout the cardiac cycle
when mapping was not performed at the true site of
origin
Pace mapping Low-output pacing usually approximates the earliest Pace-mapping site that reproduces the surface
site of activation electrocardiogram pattern may identify the exit site for
Exceptions include a fascicular origin or origin in an the tachycardia
intracavitary source such as the papillary muscles
Electroanatomic When a complete map is created, the red area The red area has no electrophysiologic significance and is
map represents the site of earliest activation and is the dependent on the window taken for the activation map
target for ablation
Early site indicates the origin of the tachycardia There is no early site in reentrant tachycardia
The pattern of activation rarely identifies the circuit (where
“head meets tail”)
More importantly, the timing for the activation map
(earliest to latest site) should approximate the
tachycardia cycle length; if this does not occur, then
parts of the circuit have not been mapped (eg, other
ventricle, epicardium, surgically excluded chamber, etc)
Noncontact White area represents earliest site of activation and White area represents a likely exit from the circuit,
mapping will correlate with onset of the earliest virtual especially if seen after an apparent isoelectric period
potential
If wider fi lter settings are used and a bluish (far-field)
earlier site is noted, suspect an epicardial or
other-chamber origin
This patient’s history of previous myocardial infarction is supported by the left bundle branch block pattern (sug-
and a structurally abnormal heart greatly increases the like- gestive of a right ventricular origin), negative deflections
lihood that this arrhythmia is a ventricular tachycardia. If in leads III and aVF (posterior), and a positive deflection
the arrhythmia is ventricular tachycardia, then whether the in lead I and a negative deflection in lead aVR (free wall).
tachycardia is automatic or reentrant cannot be determined In contrast, if this was known to be a reentrant ventricular
by a 12-lead electrocardiogram (nor, for that matter, can it be tachycardia, a similar conclusion could be reached regard-
determined by intracardiac electrograms or activation maps ing the exit site of the reentrant circuit responsible for the
rendered via an automated system). Only pacing maneuvers tachycardia.
(specifically, entrainment mapping) can identify the mecha- Occasionally, a ventricular tachycardia with a left bundle
nism of an arrhythmia (Table C14.1). branch block pattern may be ablated successfully from the
If this arrhythmia was known to be an automatic ven- left ventricle. This can occur in a tachycardia arising from
tricular tachycardia, an origin in the posterior right ven- the conduction system, for example, from the proximal left
tricle would be suspected, probably on the free wall. Th is bundle branch with antegrade left bundle branch block and
Case 14 451
retrograde conduction to an exit site in the right bundle. After catheters are placed, it is fairly easy for an invasive
Another scenario is the so-called mitral isthmus ventricu- electrophysiologist to distinguish ventricular tachycardia
lar tachycardia; in this tachycardia, successful ablation is from supraventricular tachycardia with aberrancy (excep-
performed by targeting a region of slow conduction in the tions include tachycardias due to Mahaim fibers or those
inferior wall of the left ventricle. Mitral isthmus ventricu- arising from the conduction system itself). After ventricu-
lar tachycardia should be suspected in this patient, who has lar tachycardia is confi rmed, the most important step is to
a previous inferior wall myocardial infarction and a wide establish whether a reentrant tachycardia is present and,
QRS tachycardia with a left bundle branch block pattern and if so, to design an approach to determine the tachycardia
left-axis deviation. circuit.
VT ablation
Less difficult More difficult
Outflow tract Fascicular Anatomic target Have to map
Mitral
LV ARVD Purkinje Scars System
valve
Valvular Reentry Sarcoid, etc Entrainment
Imaging Lesion creation
Electrophysiology Anatomy
Figure C14.2
The more difficult ventricular tachycardia ablations an origin of tachycardia near a semilunar valve. The best
involve reentrant arrhythmias such as those associated chance for successful ablation in reentrant arrhythmias
with ischemic cardiomyopathy, prior ventriculotomy, and is supported by a thorough knowledge of entrainment, an
congenital heart disease (Figure C14.2). If a nonreentrant understanding of the anatomic location of scars and inert
arrhythmia is undoubtedly present, the ablation procedure valvular structures, and the adjunct use of intracardiac
is generally simpler. Even automatic tachycardias can some- ultrasonography to determine catheter contact and ana-
times be challenging, such as with a fascicular origin or tomic details.
Slow zone
QRS onset
Scar
Figure C14.3 (Adapted from Gersh BJ, Gibbons RJ. Abstracts of original contributions: 41st annual scientific session [abstract no.
960–111]. J Am Coll Cardiol. 1992 Mar;19[3] Suppl 1:18A-395A. Used with permission.)
With a reentrant circuit in ventricular tachycardia (Figure 12-lead surface electrocardiogram. The exit site from the scar
C14.3) if a discrete scarred area is found and the rest of the determines the morphology of the QRS complex on the elec-
myocardium is relatively normal, then the electrical activa- trocardiogram. The exit site in this situation is analogous to
tion within the circuit (in the scar) will not be evident on the the site of origin in an automatic tachycardia.
Septal
Lateral
I, aVL
II, III, aVF
Figure C14.4
The QRS morphology can be analyzed to get a general positive, then activation likely originates in the anterior
idea of the location of the ventricular tachycardia exit site. wall and proceeds toward the inferior leads. Similar con-
For example, if the lateral leads I and aVL show mostly nega- siderations, used to assess the origin of an automatic tachy-
tive QS complexes, a lateral or left ventricular free wall exit cardia, can be helpful in identifying a reentrant tachycardia
is likely (Figure C14.4). If leads II, III, and aVF are mostly exit site.
Case 14 453
(A) Cross-section (B) RAO/LAO

Anterior
12:00
Base
Septal Lateral E
9:00 3:00 D
C
B
Posterior A
6:00
Apex
Figure C14.5
Similarly, the exit site can be further localized to assess and E being the level of the annulus (base of the heart). Leads
the apex-to-base location and the “clock-face” location in V4 and aVR are the primary electrocardiographic leads used
the left anterior oblique projection (Figure C14.5A). The to identify the apex-to-base orientation. If V4 is negative and
cross-sectional clock face is a commonly used location aVR is positive, then the tachycardia has a relatively apical
nomenclature, with 12:00 as anterior, 3:00 as the left lateral exit (location A). If aVR (a basal lead) is negative and most of
wall, etc. The apex-to-base orientation is often lettered from the apical leads (V4, V5, and V6) are positive, then the tachy-
A to E (Figure C14.5B), with A being the left ventricular apex cardia has a basal exit (location E).
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure C14.6
Box C14.1
Approach to Ventricular Tachycardia Ablation
1. Determine the mechanism of tachycardia (automatic or reentrant). Th is is accomplished by pacing faster than the tachycardia to see if
the tachycardia is overdrive suppressed (suggesting automaticity) or entrained (suggesting reentry).
2. If reentry is diagnosed, entrainment mapping is performed to identify the chamber housing the circuit (right vs left ventricle).
3. Further entrainment is performed to identify whether the pacing catheter is within the culprit circuit (postpacing interval equal to
tachycardia cycle length).
4. Further entrainment is performed to identify the entrance and exit sites for the tachycardia.
5. Further entrainment is performed to identify the culprit slow zone for the circuit (concealed entrainment with capture latency approxi-
mately 30% of the tachycardia cycle length).
6. In addition to entrainment maneuvers, mapping of the tachycardia and mapping of the substrate (scarred areas, areas of low amplitude
and slow conduction, etc) should be performed.
7. The slow zone (located by entrainment mapping) should match an area of fragmented potentials between scars or between a scar and an
anatomic obstacle (eg, mitral valve).
8. When all information (activation mapping, scar mapping, and entrainment mapping) suggest the same target for ablation, ablation
should proceed.
9. If ablation at the site is unsuccessful, then consider a mid-myocardial or epicardial slow zone. However, other possibilities include a mis-
diagnosis, poor catheter contact, incomplete mapping of the reentrant tachycardia circuit (because of congenital heart disease, surgery,
etc), or inadequate energy delivery.
Thus, in the electrocardiogram in Figure C14.6, an exit site circuit with an unusual exit). Thus, the ablationist should
in the inferior right ventricle could be suspected. However, have a systematic approach for deciding the ablation location.
the successful ablation site could be anywhere from the right A suggested approach to ablation of ventricular tachycardia is
ventricular free wall (if it is an automatic mechanism) to summarized in Box C14.1.
the inferoposterior mitral annular region (if it is a reentrant
Case 14 455
II
V1
380 380 380 400 400
V6
RV prox
HRA
HIS pro
HIS dis
PPI=435 VTCL=400
6:00 E
stim−QRS=350 egm−QRS=315
CS 7,8
CS 1,2
Figure C14.7
Box C14.2
Simplified Scheme for Entrainment Mapping
1. Demonstrate continuous resetting of the reentrant circuit.

2. Demonstrate constant fusion at a given pacing rate.
3. Demonstrate that the tachycardia continues after pacing is stopped.
4. Demonstrate that the last entrained beat is not fused.
5. Demonstrate that the postpacing interval on the pacing catheter approximates the tachycardia cycle length.
6. If a site with a postpacing interval equal to the tachycardia cycle length is found (with no evidence of fusion [concealed entrainment]),
then the site is either in the slow zone or at the exit site of the tachycardia.
7. The stimulus-to-QRS interval should be similar to the local potential-to-QRS interval during tachycardia.
8. If the duration of the stimulus-to-QRS interval is greater than 70% of the tachycardia cycle length, then the catheter is either at an
entrance location (usually not concealed entrainment) or at a bystander site.
9. If the stimulus-to-QRS duration is 30% to 50% of the tachycardia cycle length and concealed entrainment is noted, the catheter likely is
located in the slow zone, which is an excellent target for ablation.
The introductory chapter on entrainment (Chapter 5) QRS morphology and because tachycardia during pacing
details the principles of entrainment mapping. Consider occurred at the rate of pacing. After capture is documented,
Figure C14.7 as an example that illustrates the approach to analyze the last beat that occurs at the pacing cycle length. In
entrainment (pacing into ventricular tachycardia at 6:00 E) this instance, it was the fourth QRS complex (arrow). Note
(Box C14.2). Ventricular pacing was performed during ven- that this beat, although entrained and thus occurring at the
tricular tachycardia. The first 3 beats were paced, and upon pacing cycle length, showed a QRS morphology that was
cessation of pacing, the tachycardia continued. The first step identical to the tachycardia (ie, there was no fusion).
with entrainment mapping is to pace the ventricle about 20 At this point, the patient appeared to have a reentrant
milliseconds shorter than the tachycardia cycle length and arrhythmia. The next step was to determine whether the
then ascertain whether capture is occurring. In this example, pacing electrode (6:00 E) was located within the tachycardia
capture was easy to identify because of clear changes in the circuit. To do this, the postpacing interval (the interval on
the pacing catheter, from the captured potential to the return circuit. However, the electrode likely was close to the ven-
potential) was compared with the ventricular tachycardia tricular tachycardia circuit or its exit because the difference
cycle length. Note that the postpacing interval exceeded the between the postpacing interval and tachycardia cycle length
ventricular tachycardia cycle length by 35 milliseconds. This was fairly small and the fused QRS complexes were not very
suggests that the pacing site was not within the tachycardia different from the tachycardia QRS complexes.
II
V1
V6
370 370 450 405 405
RV
stim−QRS=430 egm−QRS=+30
HRA
HIS pro
PPI=450 VTCL=405
HIS dis
CS 7,8
CS 1,2
Figure C14.8
When pacing from the right ventricular apex, the electro- Answer: A—The right ventricular apex is not in the tachy-
gram in Figure C14.8 was obtained. Which statement cor- cardia circuit.
rectly assesses the outcome of this maneuver?
A. The right ventricular apex is not in the tachycardia The steps in Box C14.2 were followed to interpret entrain-
circuit ment mapping. First, capture and continuous resetting of
B. The tachycardia originates in the left ventricle the tachycardia were documented. Second, the postpacing
C. The slow zone for the tachycardia is not in the right interval markedly exceeded the ventricular tachycardia
ventricle cycle length. Thus, the pacing site (right ventricular apex)
D. The pace map during right ventricular apical pacing is was not located in the tachycardia circuit. Th ird, no further
somewhat similar to the tachycardia; thus, the success- conclusions could be made at this point about whether the
ful ablation site will be in the right ventricle slow zone was located in the right or left ventricle.
Case 14 457
II
V1
370 370 370 370 395 395
V6
RV prox
HRA
HIS pro
HIS dis
6:00 E
PPI=395 VTCL=395
st−QRS=265 egm−QRS=295
CS 7,8
CS 1,2
Figure C14.9
Figure C14.9 shows pacing performed close to the base of because the tachycardia sped up to the pacing cycle length.
the inferior left ventricle (6:00 E). Which statement is now The absence of fusion suggested that the pacing catheter was
true? located either in the circuit (slow zone or exit site) or in a
A. Ablation at this site will terminate the tachycardia cul-de-sac (bystander site). Pacing from a bystander site will
B. The absence of fusion suggests that capture is not show many features of an excellent ablation site, including
occurring concealed entrainment and sometimes a postpacing inter-
C. The pacing catheter is located within the tachycardia val nearly equal to the tachycardia cycle length because of
circuit, not the slow zone the inability to exit to the myocardium except through the
D. The pacing catheter is located in a bystander pathway tachycardia circuit. However, the distinguishing feature of
from where conduction enters the circuit a bystander site is an inordinately long stimulus-to-QRS
interval and the failure to approximate the stimulus-to-QRS
Answer: D—The pacing catheter is located in a bystander
interval with the local potential-to-QRS interval (the latter
pathway from where conduction enters the circuit.
interval is shorter). Ablation at bystander sites is rarely suc-
Although fusion was not seen during pacing, capture and cessful and is one of the most common types of misapplied
continuous resetting of the tachycardia clearly was occurring ablation.
25
30
22 C
15 10
33 1
3 8
E 6
391 391 356 391

ECG
S
193 299
Site C
391 250 497 391
Postpacing
interval
Figure C14.10 (Adapted from Stevenson WG, Khan H, Sager P, Saxon LA, Middlekauff HR, Natterson PD, et al. Identification of reentry
circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circulation.
1993 Oct;88[4 Pt 1]:1647–70. Used with permission.)
In Figure C14.10, when pacing from site C, the stimulus will Activation progresses simultaneously to the bystander site
have to exit to the primary circuit and then exit from there to the and in the circuit toward the exit, giving rise to a shortened
rest of the myocardium, giving rise to the long stimulus-to-QRS potential-to-QRS interval compared with the stimulus-to-QRS
interval. Note that a pseudointerval exists during tachycardia. interval when pacing from the bystander site.
25
30
22 C
15 10
33 1
3 8
E 6
ECG 391 391 369 391
S
EG−QRS S−QRS
248 248
Site 15 391 370 391 391
Postpacing
interval
ECG 350 350 350 391 391
S−QRS
S S S 248 248
Site 15
391
Postpacing
interval
Figure C14.11 (Adapted from Stevenson WG, Khan H, Sager P, Saxon LA, Middlekauff HR, Natterson PD, et al. Identification of reentry
circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circulation.
1993 Oct;88[4 Pt 1]:1647–70. Used with permission.)
Case 14 459
In comparison, when pacing from the slow zone of the the tachycardia cycle length) from the pacing stimulus to the
tachycardia (Figure C14.11, site 15), the potential-to-QRS captured QRS is absent. Such areas are excellent targets for
interval is nearly identical to the pacing stimulus-to-QRS radiofrequency ablation.
interval. Further, the inordinate delay (greater than 50% of
(A) (B)
Voltage map Activation map
Figure C14.12
With electroanatomic mapping (Figure C14.12), comple- sites not in the tachycardia circuit. For example, if the tachy-
mentary information is obtained from the voltage map and the cardia exits in an apical location, then passive activation with
activation map. When these maps are analyzed correctly, they varying delays will occur along the annulus, and several colors
provide important information that adds to that determined of activation (representing pseudointervals) may be in close
by entrainment mapping. In an activation map, the colors proximity, giving the mistaken impression of slow conduction.
represent an activation interval (for example, 30 millisec- Therefore, analysis of conduction timing from the activation
onds of conduction). If multiple colors are seen within a short map is best performed after entrainment shows that the site is
myocardial space (see the red, yellow, green areas located very in the circuit. In the map shown in Figure C14.12, knowledge
close to each other at the septum), then conduction at that site that the perimitral annular region is in the circuit will allow
is very slow. For example, conduction through 1 cm of myo- assessment for conduction delay as explained above.
cardial tissue with 4 color zones takes about 120 milliseconds. Second, even when entrainment, activation sequence
If a large area (eg, 3 cm wide) consists of a single color (Figure analysis, and voltage suggest a site of likely successful abla-
C14.12B, dark blue area [arrows]), then it takes only about 30 tion, the ablation lesion often needs to be anchored to a scar,
milliseconds to cover this large distance of myocardium, sug- an electrically inert structure (eg, mitral annulus), or both.
gesting that conduction is rapid at these sites. This is because even if a discrete slow zone is ablated, con-
Thus, from this activation map, an area of slow conduc- duction may proceed in a slightly different manner through
tion may be suspected septally, near the mitral annulus. The nearly equally diseased myocardial tissue and give rise to a
voltage map supports this interpretation because it shows a similar tachycardia with a slightly different cycle length.
small-amplitude bipolar potential at the septal mitral annu- Third, for the voltage map to give meaningful information,
lus. Given that concealed entrainment was shown when catheter contact at the site of interest must be assured. If the
pacing from the septal mitral annulus, the postpacing catheter is not making contact with the tissue, the site may be
interval approximated the tachycardia cycle length, and the diagnosed mistakenly as a site of poor myocardial potentials.
stimulus-to-QRS interval approximated the local potential-to- Additionally, if the catheter is in contact with an overlying
QRS interval, this site should be targeted for ablation. papillary muscle and not the posterior wall of the myocar-
The following 3 points are important caveats to be kept in dium, the posterior site may be mistakenly viewed as having
mind. First, activation mapping may show conduction delay at a normal potential.
MV
MV
MV
MV
ABL ABL
Beginning drag lesion End drag lesion

Figure C14.13
In Figure C14.13 (right anterior oblique view), note posterior, septal, mitral annular location between an inferior
the ablation catheter is performing a linear ablation in the wall scar and the mitral valve.
CS
CS
ABL
ABL
Beginning drag lesion End drag lesion

Figure C14.14
Upon completion of this linear lesion (when the mitral longer inducible (Figure C14.14 shows the left anterior oblique
annulus was reached), tachycardia terminated and was no view).
Case 14 461
II
V1
36 sec
V6
RV prox
HRA
HIS pro
HIS dis
6:00 E
CS 7,8
CS 1,2
Figure C14.15
The case illustrated in Figures C14.15 and C14.16 is an

example of a mitral isthmus ventricular tachycardia. This
case also was described by Wilber et al (Circulation. 1995
Dec 15;92:3481–9). Depending on the direction of the cir-
LBBB-LAD cuit through this perimitral annular tissue, either a pattern
of right bundle branch block and right-axis deviation or, as
1 in this instance, a pattern of left bundle branch block and
4 3 left-axis deviation is seen.
2
RBBB-RAD
Figure C14.16 (Adapted from Wilber DJ, Kopp DE, Glascock

DN, Kinder CA, Kall JG. Catheter ablation of the mitral isthmus
for ventricular tachycardia associated with inferior infarction.
Circulation. 1995 Dec 15;92[12]:3481–9. Used with permission.)
VT-1 VT-2
I
350 420
II
III Anterior
aVR Basal
Inferior
aVL
aVF
V1
V2
V3
V4
V5
V6
Figure C14.17 (Courtesy of D. J. Wilber, MD, Loyola University Medical Center, Maywood, Illinois. Used with permission.)
Figure C14.17 illustrates multiple QRS morphologies of entrainment was found. In addition, the postpacing inter-
ventricular tachycardia seen in a patient with an inferior wall val was equal to the tachycardia cycle length, and the local
myocardial infarction. Two dramatically different ventricular potential-to-QRS during tachycardia was equal to the pac-
tachycardia morphologies arise from a circuit and slow zone ing stimulus-to-QRS interval. Radiofrequency ablation was
located in a single region between the mitral annulus and the performed at this site, achieving a temperature of 60°C and
inferior wall myocardial infarction scar. power of 50 watts. Yet despite multiple ablations at this site,
During mapping of a ventricular tachycardia in a patient the tachycardia continued.
with prior myocardial infarction, a site with concealed
Case 14 463
Which statement describes a possible explanation for the C. The ablation lesion may not be anchored appropriately
failure to terminate tachycardia when ablating at this D. All of the above
location? Answer: D—All explanations are applicable in this
A. The slow zone may have an epicardial location situation.
B. Saturation from pacing may have obscured the true
local potential, resulting in a miscalculated postpacing
interval
LV
Endocardium
Focus
Epicardium
Figure C14.18
The ventricular myocardium has depth (Figure C14.18). appears appropriate, it may not be sufficient to completely
Just as the focus of automatic tachycardias may be located in ablate the culprit slow zone. Intracardiac ultrasonography
a mid myocardial or epicardial location, so also may a slow can be useful to assess the depth of lesion formation, particu-
zone be responsible for maintaining a reentrant tachycar- larly in the basal regions of the heart. Because immediate suc-
dia. Even when the amount of energy delivered to the lesion cess with ablation is not always expected, even with correct
identification of the arrhythmogenic substrate, it is impor- pericardial access or ablation through the venous system can
tant to thoroughly identify the target for ablation. Thus, if be performed at that site. However, if the mechanism and the
the culprit site in the myocardium is identified unequivo- slow zone location are uncertain, then the patient may have
cally and the problem is failure to ablate the epicardium, then
I
II
III
640
V1
640
V6
550 550
Abl 1,2
520
Abl 2,3
Abl 3,4
Figure C14.19 (Courtesy of D. J. Wilber, MD, Loyola University Medical Center, Maywood, Illinois. Used with permission.)
to undergo another invasive (epicardial access) procedure ablation catheter electrode can be saturated and difficult to
unnecessarily. assess. As shown in Figure C14.19, the potential from a nearby
Another common cause of difficulty with entrainment catheter (usually ABL 2,3 prox) can be used to determine the
mapping is the fact that the local potential on the distal
VT VP VT VP
RV
LAO
LV
Figure C14.20
Case 14 465
postpacing interval after correcting for the timing between house multiple reentrant circuits, and the resultant ventricu-
this electrogram and the distal electrogram. lar tachycardia may have numerous morphologies. Detailed
Another problem may arise if highly diseased tissue is entrainment mapping of each circuit is impractical and may
mistaken as a scar (Figure C14.20). This diseased tissue may
2 mV
0.05 mV
Scars
Scars
Double
potentials Potential
circuits
Figure C14.21
actually compromise the patient’s hemodynamic and clinical Abbreviations

status.
For patients with multiple tachycardias that are inducible, ABL, ablation catheter [f]
another approach applies the concept of channel detection and ARVD, arrhythmogenic right ventricular dysplasia [f]
ablation (Figure C14.21). Here, a detailed voltage map is cre- CS, coronary sinus [f]
ated, often by obtaining more than 300 discrete points during ECG, electrocardiogram [f]
mapping (endocardial regions possibly combined with epi- EG or egm, electrogram (potential) [f]
cardial regions). True scar tissue is identified by the absence LAD, left-axis deviation [f]
of local potentials and the inability to capture the underlying LAO, left anterior oblique [f]
tissue, and it is further confirmed by intracardiac ultrasonog- LBBB, left bundle branch block [f]
raphy. Other sites of poor or fragmented electrograms are not LV, left ventricle [f]
considered scar tissue, and they are included in the voltage MV, mitral annulus [f]
map. The premise here is that poor voltage is indicative of PPI, postpacing interval [f]
slow conduction, and these slow zones represent channels for RAD, right-axis deviation [f]
ventricular tachycardia circuits. The areas between true scar RAO, right anterior oblique [f]
tissue or between scar and the mitral annulus (ie, channels RBBB, right bundle branch block [f]
with slow conduction) are all targeted for ablation, with the RV, right ventricle [f]
aim of eliminating all potential tachycardia circuits. S or stim, stimulus [f]
VP, ventricular-paced morphology [f]
VT, ventricular tachycardia [f]
VTCL, ventricular tachycardia cycle length [f]
Case 15
Figure C15.1
A 34-year-old woman with a history of congenital tricus- Which is the most likely diagnosis?
pid atresia and a single ventricle presented with tachypal- A. Ebstein anomaly with an accessory pathway
pitations. At age 10 months, the patient underwent a right B. Automatic atrial tachycardia
Blalock-Taussig shunt procedure. At age 11 years, she had C. Atrioventricular (AV) node reentry
a modified Fontan procedure (atriopulmonary anastomo- D. Atrial flutter
sis) and atrioseptal defect patch closure. At age 24 years, the E. Atrial fibrillation
patient had episodic atrial arrhythmia. At age 28 years, she
had atrial fibrillation that required multiple direct current Answer: D—Atrial flutter.
cardioversion procedures. Figure C15.1 is an electrocardio- Although the possibility of an AV reentrant tachycardia
gram obtained during a typical episode of tachypalpitation. or an automatic atrial tachycardia cannot be excluded by this
electrocardiogram, the most common cause of a narrow com-
plex tachycardia with a single P-wave morphology is mac-
Abbreviations are expanded at the end of this chapter. roreentrant tachycardia (atrial flutter), probably attributable
Terms with “[f]” denote abbreviations that appear in the figures only. to scarred atrial tissue.
467
Table C15.1 Table C15.2

Surgical Procedures That May Be Associated With Medication Efficacy for Atrial Flutter in Patients With
Arrhythmia for Patients With Repaired Congenital Heart Congenital Heart Disease (N=347)a,b
Disease
Medication Patients Effectively
Procedure Patients with Postoperative Treated, %
Arrhythmia, %
Any medication (N=347) 58
Fontan procedure (1,2) 29 Amiodarone (n=9) 78
Mustard or Senning repair (3,4) 27 Digoxin (n=105) 53
Tetralogy of Fallot repair (5,6) 23
Digoxin + class I agent (n=235) 44
Secundum atrioseptal defect (7) 18
Tricuspid valve procedure (6)a 17 Digoxin + propranolol + class I agent (n=14) 43
a
Class I agent (n=25) 36
Fift y percent of patients had prior atrial arrhythmias.
References: Propranolol (n=18) 33
1. Gelatt M, Hamilton RM, McCrindle BW, Gow RM, Williams WG, Trusler GA, Digoxin + diltiazem (n=7) 28
et al. Risk factors for atrial tachyarrhythmias after the Fontan operation. J Am
Coll Cardiol. 1994 Dec;24(7):1735–41.
Digoxin + propranolol (n=56) 21
2. Driscoll DJ, Offord KP, Feldt RH, Schaff HV, Puga FJ, Danielson GK. a
Congenital heart defects included D-transposition (21%), complex lesions (18%),
Five- to fi fteen-year follow-up after Fontan operation. Circulation. 1992 atrioseptal defects (12%), tetralogy of Fallot (8%), and other defects (40%).
Feb;85(2):469–96. b
Sixty percent of patients had repaired defects; 13% had palliated defects.
3. Gelatt M, Hamilton RM, McCrindle BW, Connelly M, Davis A, Harris L, et al. Data from Garson A Jr, Bink-Boelkens M, Hesslein PS, Hordof AJ, Keane JF,
Arrhythmia and mortality after the Mustard procedure: a 30-year single-center Neches WH, et al. Atrial flutter in the young: a collaborative study of 380 cases.
experience. J Am Coll Cardiol. 1997 Jan;29(1):194–201. J Am Coll Cardiol. 1985 Oct;6(4):871–8.
4. Bink-Boelkens MT, Velvis H, van der Heide JJ, Eygelaar A, Hardjowijono RA.
Dysrhythmias after atrial surgery in children. Am Heart J. 1983 Jul;106(1 Pt
1):125–30. Unfortunately, drug therapy is only somewhat efficacious
5. Roos-Hesselink J, Perlroth MG, McGhie J, Spitaels S. Atrial arrhythmias in for recurrent atrial arrhythmia if a patient has congenital
adults after repair of tetralogy of Fallot: correlations with clinical, exercise, and heart disease (Table C15.2). The recurrence rate of arrhythmia
echocardiographic fi ndings. Circulation. 1995 Apr 15;91(8):2214–9.
6. Overgaard CB, Harrison DA, Siu SC, Williams WG, Webb GD, Harris within a year after drug therapy is 50% to 60%. Amiodarone
L. Outcome of previous tricuspid valve operation and arrhythmias in generally is associated with the highest chance of maintain-
adult patients with congenital heart disease. Ann Thorac Surg. 1999 ing sinus rhythm, but it has clinically significant long-term
Dec;68(6):2158–63.
7. Bink-Boelkens MT, Meuzelaar KJ, Eygelaar A. Arrhythmias after repair of and cumulative organ toxicity.
secundum atrial septal defect: the influence of surgical modification. Am Heart Special considerations must be given to medical treatment
J. 1988 Mar;115(3):629–33. of patients with congenital heart disease. Drug therapy is par-
Atrial arrhythmias often occur after surgical repair of ticularly difficult in this population because patients may have
congenital heart disease. The Fontan procedure is commonly proarrhythmia (from hypertrophy or dilatation), underlying
associated with the late sequela of recurrent atrial arrhyth- sinus node dysfunction, conduction system defects, 1:1 con-
mia. Table C15.1 lists other common surgical repairs for duction in drug-organized atrial flutter, impairment of ven-
which patients subsequently may seek therapy for palpitation. tricular function, or altered drug metabolism because of renal
A combination of factors such as atrial stretch, surgical scars, or hepatic abnormalities or protein-losing enteropathy. In addi-
and altered hemodynamics may also contribute to the recur- tion, the negative inotropic effects of drugs such as quinidine or
rence of arrhythmia. sotalol may limit their use in patients with advanced disease.
This patient underwent a hemodynamic catheterization,
Which medication will most likely control the patient’s which showed no evidence of Fontan obstruction. The patient
symptoms? was offered a procedure that included a Fontan conversion
A. Amiodarone and surgical maze, but she preferred a trial of drug therapy.
B. Sotalol Amiodarone was initiated, but atypical atrial flutters recurred
C. β-Blocker with digoxin and early amiodarone lung toxicity was observed.
D. Calcium-channel blocker with digoxin
E. Digoxin alone
Answer: A—Amiodarone. Box C15.1
Mechanisms of Atrial Arrhythmia in Patients With
Repaired Congenital Heart Defects
1. Natural anatomic obstacles
2. Congenital defects
3. Atriotomy or cannulation site scars
4. Functional reentry
5. Dispersion of refractoriness or conduction delay
6. High wall stress or hypertrophy (ectopic sites)
7. Junctional ectopic tachycardias (postoperative)
8. Interruption of normal blood supply
Case 15 469
Because of the severity of the patient’s symptoms and fail- In this patient, which scar is most likely to be the associated
ure of medical therapy, she was referred for an electrophysi- substrate for the flutter?
ology study and an ablation procedure. Box C15.1 lists the A. Cannulation scar
mechanisms of atrial arrhythmia that an ablationist needs B. Atriotomy scar
to consider when designing an approach for electrophysiol- C. Septal patch–related scar
ogy study and ablation in a patient with repaired congenital D. Cavotricuspid annulus
heart disease. A thorough knowledge of these mechanisms E. The atrium as a whole may be scarred
will allow a targeted approach to selecting electrophysiologic F. All of the above
maneuvers (entrainment) and designing appropriate ablation Answer: F—All of the above.
lines.
Atriotomy
RAA
SVC
SVC
TA
TA
CT Patch
RV
CS
IVC
IVC
TA
Incisional reentry Septal patch reentry

Figure C15.2 (Adapted from Kalman JM, VanHare GF, Olgin JE, Saxon LA, Stark SI, Lesh MD. Ablation of ‘incisional’ reentrant atrial
tachycardia complicating surgery for congenital heart disease: use of entrainment to define a critical isthmus of conduction. Circulation.
1996 Feb 1;93[3]:502–12. Used with permission.)
The traditional view is that reentrant circuits are most disease has strongly suggested that typical cavotricuspid isth-
likely associated with atriotomy scars and septal patches mus flutter is common, as are flutters associated with cannu-
(Figure C15.2). However, increasing experience in ablat- lation sites. Flutter around a septal patch is less common than
ing arrhythmias of patients with repaired congenital heart these other circuits.
Table C15.3
Flutters Induced During Electrophysiologic Stimulation
Flutter Cycle Length, msec Surface Leads Coronary Sinus Site
II, III, aVF aVL V1 aVR
1 440 − + +/− + Proximal to distal Low medial RA

2 320 + +/− − − Distal to proximal LA
3 240 − + + +/− Proximal to distal RA
4 240 − + − +/− Proximal to distal Septal
5 230 ... ... ... ... ... ...
6 260 + +/− − +/− Distal to proximal LA
7 180 − + +/− + ... ...
Abbreviations: LA, left atrium; RA, right atrium.
It is often difficult to map and ablate a number of these atrium, as a whole, produces abnormal electrograms and has
arrhythmias because entrainment maneuvers often cause poor conduction and can be regarded as a large heterogenous
degeneration of one arrhythmia into another or sometimes scar. Frequently, multiple flutters can be induced during elec-
into atrial fibrillation. Perhaps the most important lesson trophysiologic stimulation. In this patient, the induced flut-
from the past decade has been the understanding that the ters are summarized in Table C15.3.
Figure C15.3
For this patient, when a tachycardia with flutter wave A left anterior oblique view with electroanatomic mapping
morphology that was similar to the clinically documented of the clinical atrial flutter is shown in Figure C15.4.
arrhythmia was found, electroanatomic mapping and
In this map (Figure C15.4), what is demonstrated in the
entrainment were performed (Figure C15.3).
region by the arrow?
A. The origin of the arrhythmia
B. Likely successful ablation site
C. Area of relatively rapid conduction
D. Area of relatively slow conduction
E. Likely site of scarring
Answer: C—Area of relatively rapid conduction.
When analyzing an electroanatomic map, the following
4 points must be remembered. First, in a reentrant circuit,
there is no early site or origin of the arrhythmia as such. The
colors represent the timing relative to a reference potential;
by themselves, they are meaningless, and the temptation to
focus on the “red areas” (as is done in automatic arrhythmia)
should be resisted. By simply shifting the frame of reference
(window), the colors can be shifted.
Second, it is sometimes possible to visualize the circuit,
although this may be fraught with several hazards. The entire
tachycardia cycle length must be accounted for; this can be
verified by analyzing the color progression that supposedly
explains the culprit circuit. Typically, this should include an
area where late activation merges with early activation (red
meeting purple). In patients with highly diseased atria, areas
of early merging with late may appear at many dead-end or
bystander conduction sites in the atrium.
Figure C15.4
Case 15 471
Third, it may be possible to estimate the conduction veloc- periods) are needed for conduction through a relatively small
ity in various areas of the atrium. Because the colors represent anatomic area. Likewise, a large area shown as a single color
conduction intervals, multiple colors in close proximity (ie, (ie, a single interval) suggests rapid conduction and relatively
thin rims of colors) are suggestive of slow conduction in this healthy tissue.
region; the map indicates that multiple intervals (ie, longer
Activation during
atrial flutter
Figure C15.5
Fourth, it may be difficult to draw the ablation line based points have been taken in this region. The system-programmed
on information provided by the activation map alone. Ideally, extrapolation of data creates the misleading appearance of
knowledge of the activation map, anatomic obstacles, and rapid conduction (see Case 14). To attempt ablation in these
entrainment mapping results (to identify slow zones of con- difficult cases, high-density mapping is required to identify
duction) and analysis of the bipolar electrogram map (to scar tissue and assess zones of slow conduction. In some
assess scarred regions) must be considered before ablation. cases, greater than 300 discrete points are required to yield a
Caution is necessary when interpreting conduction veloci- meaningful map.
ties from a single map. For example, Figure C15.5 shows acti- Analysis of the multiple views shown in Figure C15.5 sug-
vation in posterior and lateral wall views during flutter; from gests that a conduction wave front travels in the direction noted
this map, the posterolateral wall may appear normal (exhibit- by the arrows. A slow conduction region near the coronary
ing rapid conduction). However, note that very few mapping sinus suggests a culprit slow zone for the tachycardia circuit.
However, this map must be compared with the voltage map to A cavotricuspid isthmus ablation was performed to linearly
see if the assumed slow zone site also shows fragmented and ablate across the diagnosed slow zone of conduction for the
low-amplitude potentials. At this point, entrainment map- mapped flutter (Figure C15.6). Ablation was performed after
ping is the next step; if it too suggests that the circuit has been entrainment maneuvers and after assessment of anatomic
identified and a slow zone documented, then ablation along obstacles (using voltage maps and echocardiographic images).
this line should be performed. Some ablationists will perform The cavotricuspid isthmus remains an important arrhyth-
discrete point ablations in small slow zones, but most of the mogenic substrate for flutters in patients with repaired con-
time, ablation points must be anchored either to anatomic genital heart disease, despite the multiple scars that may be
obstacles (eg, heart valve) or to scar tissue. present. Nevertheless, considerable difficulties may be encoun-
tered when attempting ablation to obtain a line of block across
the cavotricuspid isthmus in these patients (Box C15.2).
Right and left atrial activation

during atrial flutter
Isthmus ablation for cavotricuspid Figure C15.7
isthmus−dependent atrial flutter
Figure C15.6
Atrial flutter is being mapped in a patient with congenital
heart disease (Figure C15.7). In which scenario should the
left atrium also be mapped?
Box C15.2
A. The earliest site of activation is by the crista terminalis
Causes of Difficulty in Ablating the Cavotricuspid
B. The circuit mapped in the right atrium is at least 50
Isthmus in Patients With Repaired Congenital Heart
Disease
milliseconds shorter than the tachycardia cycle length
C. The earliest site of activation is on the septum
1. The tricuspid valve may be inaccessible because of a patch
D. The cycle length of the mapped tachycardia is greater
2. The tricuspid valve may be absent and the relevant isthmus
may be between the mitral valve and the inferior vena cava than the tachycardia cycle length by 50 milliseconds
3. The Fontan conduit or patch may separate the cavotricuspid Answer: B—The circuit mapped in the right atrium is at
isthmus into 2 portions; typically, one is accessible only least 50 milliseconds shorter than the tachycardia cycle
from the right atrial chamber and the other is excluded
from catheter access by the conduit or patch
length.
4. It is difficult to test for bidirectional block because it may
not be possible to place multielectrode catheters across the
ablation line
5. The potentials may be so fragmented in the isthmus (especially
near a surgical patch sutured onto the isthmus) that end
points for ablation at a given site may be difficult to assess
Case 15 473
RAO LAO
Figure C15.8
Again, the site of early activation means little in the setting

of macroreentrant arrhythmia because a relatively “earlier”
site in the atrium can always be found. If the mapped cycle
length (red to purple intervals) is less than the tachycardia
cycle length by at least 50 milliseconds, a large portion of
the circuit has not been mapped and is likely in the neo-left
atrium or left atrium. (These chambers may be difficult to
access. Figure C15.8 shows right and left anterior oblique
images of transseptal puncture to access the left atrium.) A
mapped tachycardia cycle length on electroanatomic map-
ping that exceeds the cycle length of the clinical tachycardia
is suggestive of either a problem in the electrograms used for
mapping (inappropriate annotation) or the presence of mul-
tiple, slowly conducting bystander sites.
Figure C15.9
For patients with repaired congenital heart disease, one of

the most important parts of the electrophysiology study and
ablation procedure is analysis of scarred areas. The bipolar
voltage map in Figure C15.9 shows regions of very small–
amplitude signals (red areas), areas of double potentials (blue
dots), and areas of fragmented signals (white dots). The volt- No ablation approach is so standardized that it can be used
age map settings are configured to focus on areas of poor sig- in all patients with multiple flutters or fibrillation and repaired
nals; in this case, anything with an amplitude greater than 0.5 congenital heart disease. The standard right atrial maze line
to 1 volt (purple areas) is considered relatively healthy tissue. cannot be assumed to effectively treat all flutters. As detailed
In general, areas that are not scarred (inability to stimulate, above, accurate knowledge of the given patient’s scars, slow
no consistent electrogram) are not arrhythmogenic per se, zones, and anatomic obstacles must be obtained before the
but culprit sites are often areas with low-amplitude potentials ablation line is designed. Some ablationists will create stan-
but no scar tissue. dard maze lines, in addition to mapping an ablation of the
recognized flutter; this substrate modification is most com-
monly performed to address the persistent atrial fibrillation
that can be seen in patients with advanced disease.
Interventional atrial
incision from baffle
to RAVV annulus
RAA
ASD
Cryoablation
IVC
SVC
Fenestrated
baffle
Figure C15.11 (Adapted from Collins KK, Rhee EK, Delucca JM,
Alexander ME, Bevilacqua LM, Berul CI, et al. Modification to
the Fontan procedure for the prophylaxis of intra-atrial reentrant
tachycardia: short-term results of a prospective randomized
blinded trial. J Thorac Cardiovasc Surg. 2004 Mar;127[3]:721–9.
Figure C15.10
Because of the high degree of difficulty in treating these

In Figure C15.10, the red dots represent ablation points.
complex flutters, ablationists should confer with their surgi-
They follow a line from the superior vena cava to the inferior
cal colleagues to develop a combined approach to preventing
vena cava.
and treating these flutters. One possible approach is a modi-
What is the reason for creating this intercaval ablation fied Fontan procedure to prevent intra-atrial tachycardias
line? (Figure C15.11). Essentially, the aim is to prevent circuits
A. To treat (eliminate) the mapped flutter around scars; thus, necessary incisions are anchored to ana-
B. To treat flutters associated with the cannulation site tomic obstacles or to each other. Adjunct cryoablation is per-
C. To treat atrial fibrillation formed to further anchor these lesions.
D. To treat flutters associated with the neo-left atrium
E. To treat flutters associated with a lateral atriotomy scar
Answer: C—To treat atrial fibrillation.
Case 15 475
Transect SVC or IVC,

excise RA wall Isthmus ablation
Atrioseptal rim
to RAA
Extracardiac
conduit
Antitachycardia
pacemaker
Atrioseptal rim
to RA wall
Figure C15.12 (Adapted from Mavroudis C, Backer CL, Deal BJ, Stewart RD, Franklin WH, Tsao S, et al. Evolving anatomic and
electrophysiologic considerations associated with Fontan conversion. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu. 2007:136–45.
In some patients, Fontan conversion is combined with

arrhythmia surgery in an attempt to cure multiple atrial flut- Box C15.3
Fontan Circulation Factors to Consider Before
ters (Figure C15.12). In addition, an antitachycardia pace-
Ablation
maker may be placed. It is worthwhile to note that unless the
arrhythmias are targeted, the efficacy of Fontan conversion 1. Exact type of Fontan connection
alone in treating reentrant tachycardia is poor. • Right atrial appendage to pulmonary artery
For the ablationist, the lesson from the surgical experience • Cavopulmonary anastomosis
is that high-density mapping must be performed and a com- • Identify any fenestrations in the conduit
• Extracardiac conduit
plete understanding attained of the slow zones responsible 2. Is the coronary sinus accessible from the right atrium?
for the mapped tachycardia (and those that could contribute 3. Is the cavotricuspid isthmus excluded from the right atrium,
to future tachycardias) before deciding the target for abla- and if so, how can it be accessed?
tion. Before starting the ablation procedure, the electrophysi- • Fenestration
ologist must be certain of details of the Fontan circulation • Transseptal puncture
• Retrograde access via a ventriculoseptal defect
(Box C15.3). • Retrograde access via an atrioseptal defect or patent fora-
men ovale
(A)
Fontan LA Reverse
transseptal
Original RA
Via
femoral vein Mitral
Tricuspid
Figure C15.14
(B)
However, if a fenestration is not present, then mapping the

entire circuit requires retrograde aortic access and either hav-
ing the catheters cross the intraventricular septum (to access
Small the supravalvar tricuspid region) or prolapsing the catheter
“residual” into the left atrium and through an atrioseptal defect or pat-
ASD ent foramen ovale into the new left atrium (Figure C15.14).
(right-to-left
shunt)
Figure C15.13
It is said that there are as many Fontan procedures as there

are surgeons who perform them. The mapping ablations and
likely slow-zone regions are very different if a patient has an
extracardiac Fontan conduit (Figure C15.13A) or a fenestrated
Fontan circulation with a small residual atrioseptal defect
(Figure C15.13B). Generally, fenestrations facilitate access to
the entire atrium (as shown in Figure C15.8).
Case 15 477
Figure C15.15
Figure C15.15 shows electrograms recorded during an Because of the combined occurrence of atrial fibrillation
induced atrial flutter. A circumferential mapping catheter and atrial flutter in patients with advanced disease after sur-
(LASSO) was placed in the left superior pulmonary vein. gery for congenital heart defects, the pulmonary vein may
Other catheters were in the high right atrium (hRA), His require mapping. Note that during atrial flutter, pulmonary
bundle region (HBE), and coronary sinus (CS). The ABL cath- vein activation, with 2 distinct potentials, is seen in both the
eter was placed in the left lower pulmonary vein. upper and lower veins (LASSO and ABL). In both instances,
a 1:1 relationship is seen between the venous activation and
Which statement regarding the atrial arrhythmia is true?
the atrial flutter electrograms in the coronary sinus. However,
A. The arrhythmia originates in the left upper pulmonary
the near-field pulmonary vein potential in the upper and
vein
lower left-sided veins occurs after the far-field left atrial acti-
B. The arrhythmia originates in the left lower pulmonary
vation. This strongly suggests that activation into the vein is
vein
passive. Nevertheless, because arrhythmogenic pulmonary
C. The atrial flutter likely is left sided
vein potentials were identified, pulmonary vein isolation may
D. The atrial flutter possibly activates the pulmonary
be undertaken if atrial fibrillation is also documented as a
veins
clinical arrhythmia (as it was for the patient described here).
E. Atrial fibrillation is present
Sometimes, atrial flutter is present, but a rapid pulmonary
Answer: D—The atrial flutter possibly activates the pulmo- vein tachycardia may be responsible for inducing and possi-
nary veins. bly entraining the flutter (see Case 16).
Figure C15.16
The arrhythmia seen in Figure C15.16 occurred during an

electrophysiology study of a patient who had undergone a
Fontan procedure. Which statement is true?
A. The arrhythmia is likely a junctional tachycardia
B. The arrhythmia may be AV nodal reentrant
tachycardia
C. The arrhythmia is an atrial tachycardia
D. Atrial flutter is likely
E. A and B are true
Answer: E—A and B are true.
In Figure C15.16, the first arrow points to the atrial poten-
tial; the second arrow points to the anticipated timing of the
atrial potential for that beat. Junctional tachycardia some-
times occurs in patients with repaired congenital heart dis-
ease, especially in the postoperative state. Note that the His
bundle potential precedes both ventricular and atrial activa-
tion. AV node reentry is also seen somewhat more frequently
in patients with scarred atria, probably because of slow
intra-atrial conduction that promotes the arrhythmia. The
termination of the tachycardia in this case, however, suggests
AV node reentry. Termination occurs when there is a block
from the His bundle to the atrium. Nevertheless, junctional
tachycardia cannot be excluded on the basis of this one trac-
ing, and given its relative frequency in this patient popula-
tion, it should still be considered a possible diagnosis. Atrial
tachycardia and atrial flutter are highly unlikely because of Right atrium, right lateral-caudal
the very short atrial-His interval (pseudointerval). Figure C15.17
Case 15 479
In the electroanatomic map shown in Figure 15.17, an septal atrial tachycardia or junctional tachycardia (as was the
apparent reentrant arrhythmia around a scar in the lateral case in this patient) to be the primary mechanism, with pas-
wall is seen. The patient was a 56-year-old with atrial tachy- sive conduction around a scar (or scars) giving the impression
cardia and tetralogy of Fallot that was “completely” repaired of a reentrant circuit. Entrainment attempts will reveal fea-
at age 22 years. However, without entrainment maneuvers tures of automaticity, including the absence of fusion during
proving this to be a reentrant tachycardia, it is possible for a pacing and overdrive suppression of the arrhythmia.
Figure C15.18
Another important manifestation of junctional tachycar- tachycardia (His bundle tachycardia) that either induces
dia in patients with congenital heart disease is the induction atrial fibrillation or is associated with fibrillatory conduc-
of atrial fibrillation. In fact, atrial fibrillation is sometimes tion in the diseased atrium (Figure C15.18). Note that in the
an underrecognized arrhythmia in this population because coronary sinus electrograms, a pattern of atrial fibrillation is
the clinical focus tends to be on macroreentrant flutters. induced by an otherwise regular tachycardia arising from the
One cause of atrial fibrillation may be a rapid junctional His bundle.
Right superior LA PVP

pulmonary vein Left superior
pulmonary vein
SVC
Ostial delay
Ostium
RA LA
Left inferior
IVC Right inferior pulmonary vein
pulmonary vein
Figure C15.19
Pulmonary vein tachycardia may also induce atrial fibril- atrial fibrillation should not be assumed. A primary focus
lation in patients with repaired congenital heart disease or (eg, in a pulmonary vein) could possibly give rise to atrial
patients with paroxysmal atrial fibrillation. If atrial fibrilla- fibrillation and various atrial flutters (Figure C15.19) (see
tion has been documented, degeneration of atrial flutter to Case 16).
Figure C15.20
For this patient, rapid paroxysms of tachycardia arose from of atrial fibrillation (Figure C15.20).
the His bundle and, when sustained, created the appearance
Case 15 481
Figure C15.21
Figure C15.21 shows evidence of a single His extrasystole D. Atrial fibrillation may arise from a rapid junctional
with conduction to the atrium, delayed conduction to the tachycardia
ventricle, and concealed (block to atrium and ventricle) His E. All of the above
extrasystoles. (Arrows indicate His bundle potentials.) Answer: E—All of the above.
Which statement is true about atrial fibrillation in patients As described above and elsewhere in this textbook, atrial
with repaired congenital heart disease? fibrillation may occur with an accessory pathway in some
A. Atrial fibrillation may be associated with preexcitation congenital heart diseases such as Ebstein anomaly. For this
B. Atrial fibrillation may be associated with complete and other reasons, including poor hemodynamic status, atrial
heart block arrhythmias can be lethal in patients with repaired congenital
C. Atrial fibrillation may arise from the pulmonary veins heart disease.
Figure C15.22
Atrial fibrillation may also occur with complete heart block is seen in an elderly patient with an acute myocardial infarc-
in patients with conduction disease, which often accompanies tion in the inferior wall. The regularization (regular R-R
other congenital malformations. In Figure C15.22, another intervals), despite continued atrial fibrillation, is diagnostic
common cause of atrial fibrillation with complete heart block of complete AV block.
Figure C15.23
Case 15 483
Which diagnosis is compatible with the findings from the Because of the propensity for conduction abnormalities and
intracardiac electrograms shown in Figure C15.23? the marked variation in anatomy and location of the AV node
A. Ventricular tachycardia with variable retrograde in certain congenital heart diseases (corrected transposition of
conduction the great vessels), great care must be used when ablating at or
B. Junctional rhythm near the septum. In this patient, complete heart block is seen
C. Isorhythmic AV dissociation during ablation. The higher rate of atrial potentials compared
D. Complete heart block with an escape from the right with the ventricular escape potentials exclude AV dissocia-
bundle branch tion and is diagnostic of AV block. The escape rhythm has a
E. Complete heart block with an escape from the left bun- left bundle branch block morphology, suggesting an origin in
dle branch the right bundle branch system or possibly the mid-to-apical
Answer: D—Complete heart block with an escape from the right ventricular region. A left bundle branch block origin for
right bundle branch. an escape rhythm would appear on the electrocardiogram to
have a right bundle branch block pattern.
Figure C15.24
During continued complete heart block, an unusual pat- conduction, with varying AV intervals. Note the early activa-
tern was seen (Figure C15.24). The escape rhythm now had a tion in the distal His bundle catheter (arrow). There appeared
right bundle branch block pattern, and although not appar- to be a block and reversal of conduction on the proximal His
ent in this single tracing, there clearly was no evidence of bundle electrograms.
Figure C15.25
Figure C15.25 shows alternating bundle branch block Figure C15.26 shows 2 areas of scar (black arrows) with a
escapes, and in the middle beat (arrow), isolated His bundle small isthmus or channel between them; slow conduction was
potentials from a right bundle escape and blocks to the ven- evident, and concealed entrainment between the 2 scars was
tricle were noted. Near-simultaneous escape depolarization noted. (White arrows emphasize the pattern of activation.)
was occurring from the right and left bundles. A similar The 40-year-old patient’s history included a double-outlet
approach to ablating atrial flutters can be taken for patients right ventricle and severe pulmonary stenosis, with a primary
who have undergone surgery (other than a Fontan procedure) repair performed at age 5 years. Here, point ablation of the
for congenital heart disease. channel between the 2 scars likely is sufficient to terminate
the arrhythmia and prevent recurrence. Some ablationists,
SVC
however, will further ablate between other scars and will
anchor these scars, in turn, to anatomic obstacles such as the
superior or inferior vena cava or the tricuspid valve.
Tricuspid
valve
IVC
Figure C15.26
Case 15 485
Transposition of great arteries IVC and pulmonary veins SVC

Figure C15.27
Unique challenges for the ablationist arise when treating When atrial flutters arise in patients who have undergone
patients with transposition of the great arteries who have the Mustard procedure for transposition of the great arteries,
undergone an atrial switch procedure (Figure C15.27 shows potential circuits that must be sought include those around
rerouted venous pathways). Sometimes, pacemakers must the pulmonary veins, between the pulmonary veins and the
be placed; this may be done by placing the wire through the baffle, around the AV valve, and between the baffle and the
baffle and then through the mitral valve into the morphologic AV valves (Figure C15.28).
left ventricle.
Which is the most common cause of palpitation in patients
who have had surgical repair for tetralogy of Fallot?
A. Atrial tachycardia (automatic)
B. Atrial tachycardia (reentrant)
SVC C. Ventricular tachycardia
D. Junctional tachycardia
Answer: B—Atrial tachycardia (reentrant).
Pulmonary Baffle Similar to patients who have undergone a Fontan pro-
veins Tricuspid cedure, the most common arrhythmia for patients with
valve
repaired tetralogy of Fallot is atrial flutter. However, unlike
the Fontan patients, ventricular tachycardia is also of clear
clinical significance and should be considered as a possible
mechanism. Ventricular tachycardia is a particular concern
for patients with corrected tetralogy of Fallot because of ven-
tricular scars.
IVC
Figure C15.28 (Adapted from Sokoloski MC, Pennington JC

3rd, Winton GJ, Marchlinski FE. Use of multisite electroanatomic
mapping to facilitate ablation of intra-atrial reentry following
the Mustard procedure. J Cardiovasc Electrophysiol. 2000
Aug;11[8]:927–30. Used with permission.)
Figure C15.29
The electrocardiographic pattern of the ventricular tachy- tetralogy of Fallot. However, because of the scar from surgery,
cardia may seem similar to that of a right ventricular outflow reentrant arrhythmias should be considered primarily, par-
tract tachycardia (Figure C15.29), and automatic atrial tachy- ticularly if the patient has a diseased, dilated, or fibrotic right
cardias in this location may in fact be seen in a patient with ventricle.
Tetralogy of Fallot • Ventriculoseptal defect patch

• Pulmonary valvectomy
• Right ventricular outflow tract and
main pulmonary artery patch
Figure C15.30
Case 15 487
should be placed at the time of ablation; thus, ablation is a

Box C15.4
palliative procedure thought to improve quality of life and
Causes of Ventricular Arrhythmias in Patients With
prevent frequent shocks from the defibrillator.
Tetralogy of Fallot
1. Around ventriculoseptal defect patch
2. Ventriculotomy site reentry Abbreviations
3. Right ventricular outflow tract patch site
4. Right ventricular fibrosis or myofiber disarray
5. Reentry around area of functional block ASD, atrioseptal defect [f]
ATC, atrial tachycardia mapped [f]
Detailed mapping must be performed around sites of ana- CS, coronary sinus [f]
tomic obstacles or scar, including the ventriculoseptal defect CT, crista terminalis [f]
patch, pulmonary valvectomy site, and right ventricular FC, fragmented complexes [f]
outflow tract patch (Figure C15.30). Also, a search must be IVC, inferior vena cava [f]
undertaken for an atrial arrhythmia. Box C15.4 details the LA, left atrium [f]
causes of ventricular arrhythmias in patients with tetralogy LAO, left anterior oblique [f]
of Fallot. PVP, pulmonary vein potential [f]
Programmed stimulation will usually induce tachyar- RA, right atrium, right atrial [f]
rhythmia. Entrainment should be targeted around the ven- RAA, right atrial appendage [f]
triculoseptal defect patch, ventriculotomy sites, and the right RAO, right anterior oblique [f]
ventricular outflow tract patch. In patients with markedly RAVV, right atrioventricular valve [f]
enlarged ventricles and multiple arrhythmias, a defibrillator RV, right ventricle [f]
SVC, superior vena cava [f]
TA, tricuspid annulus [f]
Case 16
Figure C16.1
A 41-year-old woman began experiencing palpitations. The electrocardiogram (Figure C16.1) is consistent with
Initially, the palpitations were paroxysmal but then became which diagnosis?
persistent. Her evaluation showed a structurally normal heart A. Counterclockwise, cavotricuspid isthmus–dependent
with no evidence of ventricular dysfunction or coronary flutter
artery disease. A 12-lead electrocardiogram was obtained B. An automatic atrial tachycardia arising close to the
during typical symptoms (Figure C16.1). coronary sinus ostium
C. Lower-loop reentrant tachycardia
D. Lateral atriotomy-related reentrant tachycardia
Abbreviations are expanded at the end of this chapter. E. All of the above
Terms with “[f]” denote abbreviations that appear in the figures only. Answer: E—All of the above.
489
500 ms
If the flutter waves are typical for counterclockwise flut-
I ter, why should other diagnoses be considered? An ectopic
50 mm/s
II atrial tachycardia that arises from near the usual exit of a
III cavotricuspid isthmus flutter produces a clinically indis-
aVF tinguishable electrocardiogram pattern. However, patients
aVR will often have clinical features suggestive of an automatic
aVL tachycardia (ie, paroxysmal palpitations with warm-up and
V1 more rapid rates with exercise, etc). An automatic tachy-
cardia may also induce an atrial flutter or entrain an atrial
V2
flutter. Lateral atriotomy or septal scar-related flutters may
V3
also have very similar exits on the cavotricuspid isthmus, as
V4
does classic isthmus-dependent flutter. Finally, the entity of
V5 lower-loop reentry may produce an electrocardiogram mor-
V6 phology that is difficult to distinguish from typical atrial
flutter (Box C16.1).
Figure C16.2
The patient initially was treated with β-blockers to achieve
better rate control. However, she still had clinically signifi-
Remember that a reentrant vs automatic mechanism for a cant symptoms with exercise, including Holter-documented
tachycardia cannot be discerned from a single 12-lead electro- heart rates of up to 180 beats/minute with minimal exertion.
cardiogram. The P-wave morphology can indicate only the site Because of this, she was referred to the electrophysiology lab-
of exit from a reentrant circuit or the origin of an automatic oratory for radiofrequency ablation.
tachycardia. Although the electrocardiogram shows a classic
counterclockwise, cavotricuspid isthmus–dependent flutter,
other possibilities should be considered (Figure C16.2).
(A)
What are the classic features of cavotricuspid isthmus– T 19,20
dependent flutter? The first and perhaps most important char-
A Fossa
acteristic is the finding of a terminal-positive P wave in lead V1.
ovalis
Thus, if a caliper is placed at the start of the flutter wave in any
Crista
of the other leads, then the last portion of the flutter wave corre- terminalis
sponds to a positive deflection in lead V1. This is the pattern most
commonly seen when the critical zone for the tachycardia is in T 1,2
the cavotricuspid isthmus. Next, determine whether the flutter
waves appear positive or negative in the inferior leads (II, III, IS 1,2
IS 19,20 B
aVF). Flutter wave morphology is largely dependent on activa-
tion of the left atrium. In counterclockwise isthmus-dependent Coronary
atrial flutter activation, after exit through the slow zone on the Isthmus sinus
isthmus, the axis is away from the inferior leads (caudal to cra- catheter
nial), and thus, negative flutter waves are seen. In clockwise
isthmus-dependent atrial flutter, the left atrium is largely acti-
vated in a cranial-to-caudal pattern, and thus the flutter waves
(B)
tend to be positive in leads II, III, and aVF.
Box C16.1
Electrocardiographic Manifestations of Atrial Flutter T 19,20
1. Terminal positive P waves in lead V1 suggest an
isthmus-dependent flutter circuit
2. With the pattern described in #1, if the flutter waves are
positive in leads II, III, and aVF, clockwise activation of the
cavotricuspid isthmus is suggested
3. If the P-wave morphology is as described in #1 and the T 1,2
flutter waves are negative in the inferior leads, then a
IS 19,20 IS 1,2
counterclockwise isthmus-dependent flutter is suggested
4. If the P wave in lead V1 is either positive throughout the
period of the flutter waves seen in other leads, or all negative, Isthmus catheter
or the terminal portion is negative, either an atypical flutter
or other atrial tachycardia is suggested
Figure C16.3
Case 16 491
Figure C16.3A illustrates the catheter position sometimes crista terminalis (T 1,2), is also in the atrial tissue behind the
used during ablation of typical atrial flutter. Note that 2 mul- tricuspid annulus. Wave front “A” represents counterclock-
tielectrode catheters are placed on the atrial myocardium, just wise activation around the tricuspid annular atrium, and wave
behind the tricuspid annulus. The distal poles of the isthmus front “B” shows clockwise activation. Figure C16.3B shows a
catheter (IS 1,2) engage the ostium of the coronary sinus. The fluoroscopic image with typical catheter position in a patient
second multielectrode catheter, placed just anterior to the who also had a previously placed dual-chamber pacemaker.
Figure C16.4
The activation sequence along the cavotricuspid isthmus, with bundle atrial electrogram (His-A), the proximal coronary
the catheter positions as described above, is illustrated in Figure sinus atrial electrogram (coronary sinus-A), and a right atrial
C16.4A. In Figure C16.4B, note that activation proceeds from electrogram (RA-A) from a laterally placed atrial catheter
the proximal electrodes (T 19,20) toward the distal electrodes of can yield similar information. The counterclockwise activa-
the IS catheter (IS 1,2) engaging the coronary sinus ostium. This tion sequence of His-A is followed by lateral RA-A, and then
pattern shows counterclockwise activation along the cavotricus- after a considerable delay, the coronary sinus-A is seen. With
pid annulus. Figure C16.4C shows the opposite sequence, with clockwise isthmus-dependent flutter, the coronary sinus-A,
clockwise activation along the cavotricuspid isthmus. Note that after a considerable delay, is followed by the lateral RA-A and
even with the intracardiac electrodes in place, the mechanism then the His-A.
of the tachycardia cannot be defined. For example, a tachycar- For the sake of clarity, the next 3 tracings (Figures
dia originating from the coronary sinus ostium could produce C16.5–C16.7) are taken from a patient with slow ventricular
either of these patterns on the cavotricuspid isthmus, depending (paced) rates during atrial flutter; these figures more clearly
on the conduction characteristics of the right atrium. illustrate the atrial activation sequence and P waves dur-
If multiple catheters are not used during a flutter abla- ing flutter. We will then get back to our initially described
tion, quick examination of activation sequences in the His patient.
Figure C16.5
With the catheter position as described above (Figure atrial free wall. To demonstrate the reentrant nature of the
C16.3) in a patient with poor atrioventricular nodal con- arrhythmia and document that the critical isthmus for this
duction, activation occurred in a clockwise pattern (Figure tachycardia was the cavotricuspid isthmus, entrainment
C16.5), with activation propagation from AB 1,2 to AB 19,20 mapping was performed.
(placed on the cavotricuspid isthmus) and then up the lateral
Case 16 493
Figure C16.6
Pacing is being performed from the lateral cavotricuspid Entrainment of reentrant atrial flutters may be associated
isthmus (Figure C16.6). Which observation is accurate? with difficulty analyzing the P waves. Even though the slow
A. Concealed entrainment is present ventricular rates in Figure C16.6 show the P waves clearly, the
B. Manifest entrainment is present pacing artifact and the fact that the P-wave amplitudes are
C. The pacing site is at the exit of a reentrant tachycardia so much smaller than the QRS complexes make concealment
D. The pacing site is at the focus of an automatic and other aspects difficult to define accurately. Similar argu-
tachycardia ments can also be extended to the difficulty in performing
E. None of the above pace mapping (see Case 13) when mapping or ablating auto-
Answer: E—None of the above. matic atrial tachycardia.
Lateral isthmus Septal isthmus
Figure C16.7
A surrogate for P-wave morphology is the atrial acti- Figure C16.7 that pacing both in the lateral and the septal
vation sequence seen when using multielectrode cath- portions of the cavotricuspid isthmus produces activation
eters. In patients with reentrant ventricular tachycardia patterns identical to the clinical flutter as assessed by the
(see Case 14), the QRS is a good index for pace mapping multielectrode catheters. Further, the postpacing interval
and for assessment of concealment during entrainment approximates the tachycardia cycle length. Having the sep-
maneuvers, but for patients with atrial flutters, multielec- tal and lateral portions of the isthmus in the tachycardia
trode catheters are required to assess whether the pacing circuit is strongly suggestive of a cavotricuspid isthmus–
site is associated with concealed entrainment. Note in dependent atrial flutter.
Case 16 495
RAA
RV
TA
HB
IVC-CS ABL
ABL
ABL
Figure C16.8 (Adapted from Nakagawa H, Lazzara R, Khastgir T, Beckman KJ, McClelland JH, Imai S, et al. Role of the tricuspid
annulus and the eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of the septal isthmus and a new technique for rapid
identification of ablation success. Circulation. 1996 Aug 1;94[3]:407–24. Used with permission.)
Because cavotricuspid isthmus–dependent flutter was the catheter then was dragged back to the inferior vena cava
diagnosed, radiofrequency ablation was performed using (IVC), where atrial potentials were no longer observed. Figure
a pullback technique, with the ablation catheter first posi- C16.8 shows RAO fluoroscopic images of sequential ablation
tioned on the ventricular aspect of the tricuspid annulus and catheter position during the cavotricuspid isthmus line cre-
then continuing ablation at each point until either the local ation. After completion of the procedure, widely spaced dou-
potential was abolished or double poten noted throughout the ablation line.
Before ablation After ablation

I
II
V1
HIS dist
AA 19,20
AA 15,16
AA 11,12
AA 7,8
AA 3,4
AA 1,2
AB 19,20
AB 15,16
AB 11,12
AB 7,8
AB 3,4
AB 1,2
Figure C16.9
Coincident with completion of the ablation line, a change only in a counterclockwise direction. This pattern of reversed
in activation suggesting lateral-to-medial isthmus block was conduction across the isthmus, observed when using closely
noted on the multielectrode catheters. Note that during coro- spaced isthmus-spanning electrodes, is virtually diagnostic
nary sinus pacing before block across the ablation line (Figure of cavotricuspid isthmus block in a medial-to-lateral direc-
C16.9), initial activation of the lateral wall of the tricuspid tion. Further pacing was performed from the lateral tricus-
annulus occurs in a fused pattern, with activation occur- pid annulus, and lateral-to-medial isthmus block also was
ring in both a clockwise direction across the isthmus and a documented. Widely spaced, double potentials were recorded
counterclockwise direction around the anterior and ante- all along the ablation line, and bidirectional block across
rolateral tricuspid annulus. After block across the ablation the ablation line persisted after administering isoproterenol
line, an abrupt change in activation sequence was observed, (2 mcg/min) and waiting for 30 minutes. These characteristics
with a loss of potentials on AB 11,12 and the lateral wall and are associated with a high likelihood (≥98%) of permanent
lateral portion of the cavotricuspid isthmus being activated elimination of the cavotricuspid isthmus–dependent flutter.
Case 16 497
(A)
(B)
TI 19,20
Fossa
ovalis
Crista
TI 19,20 terminalis
TI 1,2 A
IS 1,2
B
TI 1,2 IS 19,20
IS 19,20 IS 1,2 Coronary
Gap in Isthmus sinus
Isthmus catheter ablation line catheter
Figure C16.11
Figure C16.10
The electrogram shown in Figure C16.10A was obtained Figure C16.11A shows electrograms recorded with the
during proximal coronary sinus pacing. The arrow indicates multielectrode catheter placed on the isthmus, straddling the
the line of activation. The fluoroscopic image shows corre- ablation line. (The arrows show activation wave fronts.) Note
sponding catheter position (Figure C16.10B). that the isthmus catheter shows conduction clearly is pro-
ceeding, albeit slowly, across the ablation line. For activation
What can be concluded from this tracing? of the lateral wall, the wave fronts are competing across the
A. Medial-to-lateral block across the cavotricuspid isth- ablation line. In Figure C16.11B, wave front “A” is occurring
mus is present in a counterclockwise direction across the anterior-superior
B. Lateral-to-medial block across the cavotricuspid isth- wall. As conduction slows across the ablation line, the wave
mus is present front will appear reversed on the lateral wall. This shows the
C. Conduction delay but not block is present importance of using closely spaced electrodes that cross the
D. Conduction block cannot be determined ablation line on the annulus if, during coronary sinus pac-
Answer: D—Conduction block cannot be determined. ing, reversal in the activation sequence (lateral to the ablation
line) is used as the end point for ablation. This case illustrates
The important finding in Figure C16.10A is that the TI
pseudoblock (appearance of block despite continued conduc-
catheter is located on the lateral wall of the right atrium, close
tion) that is caused by inappropriate lateral placement of a
to the tricuspid annulus. Because the site of ablation is con-
multielectrode catheter during coronary sinus pacing.
siderably septal to the location of this catheter, the electro-
grams do not differentiate between slow conduction across
the ablation line vs block. Thus, proximal coronary sinus
pacing shows a counterclockwise pattern of activation on
the lateral wall, with complete block across the cavotricuspid
annulus and markedly slowed conduction.
Fossa
Crista ovalis
terminalis
MEA
IS 19,20 IS 1,2
Coronary
sinus
Gap in Isthmus
ablation line catheter
Figure C16.12
When conduction is slow across a partial ablation line, potentials may also be seen in areas of scar, across areas of
fragmented potentials are sometimes seen (Figure C16.12; normally occurring slow conduction, and in areas such as
the arrow indicates the wave front). These potentials should a subeustachian pouch, where patchy myocardial tissue is
be distinguished from widely spaced double potentials, which found.
typically occur over areas of conduction block. Fragmented
Case 16 499
(A)
Figure C16.13 (continued)

(B)
Figure C16.13 (continued from previous page)
During the start of a cavotricuspid isthmus ablation, with the Although a definitive conclusion cannot be made
line being created close to the coronary sinus, the electrograms on the basis of these tracings and fluoroscopic images,
in Figure C16.13 were seen during spontaneous respiration. In medial-to-lateral conduction is highly likely. As with various
Figure C16.13A, the arrow points to fragmented potentials seen other anatomic and electrophysiologic situations, the key to
on the isthmus multielectrode catheter, close to where the abla- complex electrophysiology tracings is the correct diagnosis of
tion is being performed. In Figure C16.13B, the arrow points to a given potential (see Case 1 and Chapter 4). For example,
intermittent potentials lateral to the ablation line during coro- in Figure C16.13B, the arrow is pointing to a coronary sinus
nary sinus pacing, which is being consistently performed. paced beat without atrioventricular conduction, clearly not a
ventricular far-field signal. The finding of fragmented signals
Which condition is most likely?
(Figure C16.13A, [arrow]), rather than widely spaced double
A. Medial-to-lateral block is present
potentials with a fi xed interpotential interval, strongly sug-
B. Medial-to-lateral conduction is present
gests conduction. What then is the cause of these intermittent
C. Lateral-to-medial block is present
fragmented signals and the appearance of signals that suggest
D. Lateral-to-medial conduction is present
medial-to-lateral block?
Answer: B—Medial-to-lateral conduction
Case 16 501
RAO
Figure C16.14
When a multielectrode catheter is located on the isthmus Sometimes, activation posterior to the eustachian ridge occurs
during ablation, an important confounding factor is the in an opposite direction compared with conduction anterior to
movement of the catheter to positions on or behind the eusta- the eustachian ridge during coronary sinus pacing. When the
chian ridge. In the right anterior oblique (RAO) projection above phenomenon occurs, apparent medial-to-lateral block
shown in Figure C16.14, the tip of the multielectrode catheter will be present when the catheter drifts behind the eustachian
points posterior to the plane of the coronary sinus catheter. ridge. Such a phenomenon is shown in Figure C16.14, with
Different amounts of physiologic delay and block may occur continuation of typical isthmus-dependent flutter but also
across the eustachian ridge, with double potentials being the appearance of conduction block when the multielectrode
found in many patients and fragmented potentials on others. catheter is located on the eustachian ridge.
electrode is placed on myocardial tissue, a single potential is

obtained that times with the passage of the activation wave
front at the electrode-myocardial interface. The presence of
double potentials signifies either conduction delay or block.
If a partially completed ablation line is present, an electrode
placed on an ablation site will register a potential when the
activation wave front reaches one side of the ablation line.
Then, if a gap in the ablation line is present, conduction will
proceed through the gap and propagate to the other side of
the ablation line, close to the electrode, producing a second
potential. The further away the electrode is from the gap in
the ablation line, the wider the split potential will be.
As the catheter moves toward the actual gap site (Figure
C16.15), a single potential or, at times, a fragmented potential
with continuous electrical activity (slow conduction) is seen.
If complete block across an ablation line connects electrically
Figure C16.15 nonconducting structures, then equal, widely split potentials
will be observed all along the line. When double potentials are
seen, mapping along the ablation line to find narrower intervals
A systematic approach to analyzing split potentials and between the double potentials literally will point toward the con-
double potentials during linear ablation can greatly enhance duction gap. When the area of a fragmented or single potential
the understanding of reentrant circuits and determining is found, complete conduction block across the ablation line is
whether conduction block is present. Generally, when an often established (an ablation procedure termed spot welding).
Figure C16.16
Figure C16.16 is an intracardiac tracing obtained from a B. Ablation at AB 19,20 will likely terminate the flutter
patient with congenital heart disease and an atypical flut- C. No comment can be made because the second of double
ter. The AB catheter is a closely spaced multielectrode cath- potentials in the middle beat is a far-field ventricular
eter, placed on the lateral right atrial wall. The catheter was potential
“swept” from an anterior to a posterior location. D. The flutter must have changed to another morphology
Which statement is likely to be true?
A. A gap in a right atrial lateral scar is likely present near Answer: A—A gap in the right atrial lateral scar is likely
AB 19,20 present near AB 19,20.
Case 16 503
If a second potential is found only when atrioventricular Note that it still cannot be predicted whether the flutter
conduction occurs, consider whether the second potential will terminate when ablating near AB 19,20. Th is is because
represents a far-field ventricular signal. If it does, no defini- conduction around a scar on the right atrial free wall may
tive interpretation of the tracings shown in Figure C16.16 can be occurring passively (bystander conduction), with the pri-
be made. However, in this case, the catheter was swept from mary circuit and slow zone occurring elsewhere. However,
an anterior to posterior location. Thus, finding such large ven- in the case shown in Figure C16.16, entrainment maneu-
tricular signals while moving away from the tricuspid annu- vers were used to determine that the slow zone was pres-
lus is highly unlikely. Further, the third beat of the tracing ent at the gap (between a right atriotomy scar and a right
shows an activation sequence that is clearly from atrial acti- atrial cannulation scar cranial to AB 19,20). Ablation at
vation (no ventricular potentials), similar to the second set of this site terminated the flutter, and widely spaced potentials
potentials in the middle beat. After we have determined that now occurred throughout the scar at this site. In addition
the middle beat shows all atrial potentials, the double poten- to using a closely spaced multielectrode catheter across the
tials can be further interpreted. As stated previously, widely ablation line and analyzing double potentials along scars or
split double potentials are seen on AB 7,8. The interelectro- ablation lines, high-density electroanatomic mapping can
gram interval progressively decreases in the proximal direc- be very useful for identifying sites of slow conduction and
tion (approaching AB 19,20). This finding strongly suggests a block.
conduction gap in a scar or ablation line near AB 19,20.
Figure C16.17 (Adapted from Shah D, Haissaguerre M, Jais P, Takahashi A, Hocini M, Clementy J. High-density mapping of activation
through an incomplete isthmus ablation line. Circulation. 1999 Jan 19;99[2]:211–5. Used with permission.)
In Figure C16.17, conduction through a gap was identified of the cavotricuspid isthmus. If mapping points are inadver-
by examining the activation pattern and multiple potentials tently taken septal to the ablation line during coronary sinus
recorded along the cavotricuspid isthmus. Note that an analy- pacing, interpretation of the map becomes exceedingly dif-
sis of the double potentials shown in the inset corresponds to ficult. Electroanatomic mapping is particularly useful for
the expected location of the gap. When using electroanatomic patients who have undergone previous ablations because the
mapping for cavotricuspid isthmus ablation, particularly for presence of fragmented potentials at multiple locations and
assessing block, it is important that all the mapping points be longitudinal dissociation along the cavotricuspid isthmus may
taken on the side opposite of the ablation line, up to where pac- be attributable to previous ablations. When longitudinal dis-
ing is being performed. Thus, during coronary sinus pacing, sociation across the isthmus is present, multielectrode catheter
mapping points should be taken lateral to the ablation line to mapping is challenging because portions of the isthmus may
look for complete reversal of activation throughout the width appear blocked while others show slow or normal conduction.
Figure C16.18
Noncontact mapping can also be used to assess conduction C. Lateral-to-medial conduction is present
block (Figure C16.18). During coronary sinus pacing, a coun- D. Medial-to-lateral conduction block may be present
terclockwise activation occurred along the tricuspid annular Answer: D—Medial-to-lateral conduction block may be
myocardium. This is consistent with medial-to-lateral block present.
across the ablation line (yellow dots). As before, a multielec-
trode catheter placed along the lateral wall may show a coun- The atrial myocardium that surrounds the IVC ostium (ie,
terclockwise pattern of activation that suggests conduction the “lower loop”) is important to remember when interpret-
block during coronary sinus pacing, even though (slow) con- ing relatively complex sequences during cavotricuspid isth-
duction is present. mus ablation. This myocardium may itself be the circuit for
a macroreentrant atrial flutter (lower-loop reentry), but more
If a multielectrode catheter placed on the lateral wall of the commonly, it is a source of confusion when trying to decide
right atrium shows clockwise (low-to-high) activation dur- whether conduction block or slow but continued conduction
ing coronary sinus pacing, which of the following is true? is present.
A. Conduction is present
B. Lateral-to-medial block is present
Case 16 505
Crista terminalis
Lower-loop reentry
TV
IVC Typical
flutter
CS CS
Pacing Pacing
site site
IVC IVC
Figure C16.19
In the scenario described in the preceding question, ablation line on the isthmus. During coronary sinus pac-
low-to-high activation of the lateral wall (clockwise acti- ing, if extremely slow conduction across an ablation line
vation) occurred during proximal coronary sinus pacing. (nearly complete block) is present, reversed (counterclock-
Persistence of this pattern after ablation is suggestive of con- wise) activation will occur along the cavotricuspid isthmus,
tinued conduction across the ablation line. However, in some with a lateral-to-septal pattern for locations on the isthmus,
instances, particularly in patients with relatively rapid atrial lateral to the ablation line. High-density mapping close to
myocardial conduction or those treated with isoproterenol, the ablation line will usually clarify the situation and point
complete block between the tricuspid annulus and IVC may to the gap in the ablation line. As described above, pseudo-
be present. However, because a multielectrode mapping block occurs when a multielectrode catheter placed in the
catheter was placed on the lateral wall, conduction could cavotricuspid isthmus gives the appearance of block because
proceed behind the IVC (lower loop) and then activate the conduction occurs more posterior and lateral to the IVC and
multielectrode catheter on the lateral wall in a low-to-high then the lateral-to-medial activation is anterior to the IVC
fashion, termed pseudoconduction. No further ablation is (Figure C16.19).
required. The situation can be remedied by placing the cath- Differential site pacing can also help distinguish between
eter across the cavotricuspid isthmus, straddling the abla- slow conduction and true block. Generally, if the interelectro-
tion line. Mapping with a circumferential catheter or pacing gram interval across an ablation line changes with the pacing
at sites posterior to the IVC can also clarify this situation site (eg, proximal vs mid coronary sinus), then conduction
(Figure C16.19). block is likely present. However, if slow conduction occurs
Another situation in which the lower loop can cause across the ablation line, the interelectrogram interval is a
considerable confusion when interpreting electrograms reflection of true conduction and will be unaffected by pacing
is when the multielectrode catheter is placed across the sites of varying distance on one side of the ablation line.
Block Across the Isthmus
Reversal of activation lateral wall

Reversal across isthmus
Wide split potentials
Absent potentials
Carto reversal
Appearance of block but Inability to get block

continued typical flutter but no potentials
Pseudoblock Pseudoconduction
Behind eustachian ridge RAO Behind eustachian ridge
Closely spaced electrodes

Local potential Small heart;
Slow conduction fast conduction
Carto
Pace 2 sites
Lower-loop conduction Lower-loop conduction
Map IVC ostium
Figure C16.20
The findings with regard to determining block across the

cavotricuspid isthmus are summarized in Figure C16.20.
Case 16 507
Figure C16.21
The index patient for this case discussion had clear evi- before ablation; usually, the tachycardia cycle length is lon-
dence of bidirectional block across the cavotricuspid isthmus; ger. Flutter may also become incessant when partial ablation
this block had persisted after the use of isoproterenol and a across the isthmus is performed.
relatively prolonged waiting period of 45 minutes (Figure The presence of positive (clockwise) or negative (coun-
C16.9). The chance of recurrent atrial flutter with such a terclockwise) flutter waves is used to distinguish between
good end point, as obtained in this patient, is likely less than counterclockwise and clockwise activation along the tri-
2%. The patient did well for about a week, but palpitations cuspid annulus. However, in many electrocardiograms with
recurred with symptoms identical to what she had experi- continuous atrial activity (sinusoidal P waves), it can be dif-
enced before (fatigue, shortness of breath). An electrocardio- ficult to know whether the waves are positive or negative.
gram was obtained at a local emergency department during Finally, when an “all positive” flutter wave is seen in V1,
these typical symptoms (Figure C16.21). the likelihood of an atypical flutter increases. Although it
is important to recognize these general rules, which in this
Which arrhythmia can be excluded on the basis of this case point to an atypical flutter, remember that all the men-
electrocardiogram? tioned possibilities (eg, typical flutter, fibrillation, automatic
A. Counterclockwise, isthmus-dependent atrial flutter atrial tachycardia, etc) remain in the differential diagnosis,
B. Clockwise, isthmus-dependent atrial flutter particularly when planning an approach in the electrophysi-
C. Atrial fibrillation ology laboratory.
D. Atypical atrial flutter Why did this patient’s arrhythmia recur, despite the
E. None of the above appearance of an excellent ablation result? Several issues must
be considered to answer this question. First, was the diagno-
sis wrong, ie, the patient did not have isthmus-dependent
Although apparent organized atrial activity is seen in this flutter? Could there be multiple diagnoses? In this instance,
electrocardiogram, atrial fibrillation cannot be completely the classic entrainment findings mentioned above firmly
excluded because some patients will have relatively organized diagnose isthmus-dependent flutter. Second, did this patient
atrial activity in certain portions of the atrium (eg, lead V1, have anatomic irregularities that increased the likelihood of
which is close to the right atrial appendage). This possibility recurrence of atrial flutter after an apparently successful abla-
is unlikely because of the apparent organized atrial activity in tion? Anatomic variations that need to be considered include
several leads, but it cannot be excluded. After partial ablation hypertrophied pectinate muscles, subeustachian pouches, or
on the cavotricuspid isthmus, the atrial flutter wave morphol- surgical exclusion of part of the isthmus (from surgery for
ogy may be slightly different compared with the morphology congenital heart disease).
Figure C16.22 (Adapted from Asirvatham SJ, Narayan O. Advanced catheter mapping and navigation systems. In: Huang SKS, Wood MA,
editors. Catheter ablation of cardiac arrhythmias. Philadelphia [PA]: Saunders/Elsevier; c2006. p. 135–61. Used with permission. Courtesy
of T. M. Munger, MD, Mayo Clinic, Rochester, Minnesota. Used with permission.)
Sometimes, mapping systems are used to better establish the coronary sinus ostium in a patient with considerable con-
the diagnosis of macroreentrant atrial tachycardia, includ- duction delay along the cavotricuspid isthmus would produce
ing typical atrial flutter. Figure C16.22 shows an electroana- an identical pattern of activation. Further, a primary arrhyth-
tomic map (left anterior oblique [LAO] view) of the tricuspid mia or primary circuit elsewhere may present with passive
valve annular region, obtained during counterclockwise activation of the annulus that mimics counterclockwise
atrial flutter. Specific findings include nearly complete map- activation. Thus, while mapping systems may aid in visual-
ping of the entire tachycardia circuit (180 milliseconds) and izing the activation pattern, electrophysiologic maneuvers
an appearance of propagation (from red to yellow to green to (entrainment) are the only way to definitively diagnose the
blue to purple and back to red again), ie, “head meeting tail.” reentrant nature of the arrhythmia and identify the culprit
Remember, however, that a focal atrial tachycardia rising near circuit.
Case 16 509
editors. Catheter ablation of cardiac arrhythmias. Philadelphia [PA]: Saunders/Elsevier; c2006. p. 135–61. Used with permission. Courtesy
of T. M. Munger, MD, Mayo Clinic, Rochester, Minnesota. Used with permission.)
Similarly, noncontact mapping (Figure C16.23) in a patient may suggest a diagnosis of isthmus-dependent flutter, but
with counterclockwise atrial flutter identifies only the acti- entrainment maneuvers still are required to firmly establish
vation sequence in the examined region of the heart (coun- the diagnosis.
terclockwise activation around the tricuspid annulus). This
editors. Catheter ablation of cardiac arrhythmias. Philadelphia [PA]: Saunders/Elsevier; c2006. p. 135–61. Used with permission.)
In Figure C16.24, a patient whose primary arrhythmia was The atrial anatomy shown in Figure C16.25 is more rep-
eventually determined to arise in the left atrium was initially resentative of what is encountered in the ablation laboratory.
thought to have cavotricuspid isthmus–dependent flutter. Note the prominent eustachian ridge and valve, the pectinate
Passive activation and occasional induction of right atrial flut- muscles, and the marked variation in the extent of muscula-
ter would occur from the primary arrhythmia located in the ture along the cavotricuspid isthmus.
posterior left atrium. Three-dimensional maps of reentrant
A linear drag approach across the cavotricuspid isthmus is
arrhythmias can be particularly misleading when only 1 cham-
used during radiofrequency ablation. Which finding sug-
ber is mapped. Important clues that suggest that an incorrect
gests the presence of a large eustachian ridge?
diagnosis include comparison of the arrhythmia cycle length
A. Large-amplitude potentials are obtained just atrial to
mapped in that chamber vs the cycle length of the tachycardia
the tricuspid annulus
(if the complete circuit is mapped, these cycle lengths should
B. Application of clockwise torque to the ablation cath-
be equal) and, of course, entrainment mapping.
eter causes the catheter tip to point laterally in the LAO
What about anatomic variation of the tricuspid isthmus?
projection
Might it increase the likelihood of atrial flutter recurrence after
C. Repeated impedance rise and high temperature occur
an apparently successful ablation? An idealized situation for
with relatively low power use
catheter contact and ablation line creation across the cavotricus-
D. The presence of a large atrial potential, even when the
pid isthmus is when the catheter lies parallel to the isthmus at
catheter is advanced beyond the plane of the coronary
all points and the isthmus itself is relatively flat. Either point-to-
sinus in the RAO projection
point ablation or ablating while dragging the catheter back (with
or without a stabilizing sheath) is highly likely to be successful Answer: B—Application of clockwise torque to the abla-
in producing bidirectional block across the cavotricuspid isth- tion catheter causes the catheter tip to point laterally in the
mus and curing the patient of this form of atrial flutter. LAO projection.
Generally, when using a femoral approach to place cath-
eters in the right atrium or right ventricle, if the catheter is
placed in the ventricle and clockwise torque is applied, the
catheter tip will point to the septum. Counterclockwise
torque will make the catheter tip point to the free wall. This
is important for novice electrophysiologists to understand
because once the ventricle is reached, clockwise torque is
applied to avoid advancing the catheter on the thin right ven-
tricular free wall and possibly perforating it. However, when
a large eustachian ridge is present and the catheter must be
advanced from the IVC over the eustachian ridge, this ridge
now acts as a fulcrum. Application of clockwise torque will
cause paradoxic lateral movement of the catheter tip in the
LAO projection.
Figure C16.25
Case 16 511
Crista SVC
terminalis
Prominent IVC LA
Prominent eustachian
pectinates LA
ridge
RA
CS Eustachian valve
Right
atrial CS
Primary
Pouch
focus circuit pouch
IVC elsewhere
Lower-loop
conduction Thebesian valve
Figure C16.27
Figure C16.26
The finding of high impedance, low power, and high

temperature during ablation may indicate that the catheter
has fallen either between 2 large pectinate muscles or into
Eustachian
a subeustachian pouch. Finally, if large atrial potentials are valve
observed along the cavotricuspid annulus, particularly in a
lateral location, a large pectinate muscle traversing the isth-
mus must be considered. Figure C16.26 illustrates the various
causes of difficulty with atrial flutter ablation. These include
prominent pectinate muscles, confusion caused by lower-loop
conduction, a prominent eustachian ridge, subeustachian
pouches, and primary foci or circuits that mimic typical Right atrial
atrial flutter but are located elsewhere. pouch Coronary sinus
If atrial potentials breaking the plane of the coronary sinus
in the RAO projection are found, ie, atrial potentials at sites
where ventricular potentials are expected, apical displacement Thebesian valve
of the tricuspid valve (a type of Ebstein anomaly) is suggested.
In such cases, a relatively long ablation line is required, and
the electrophysiologist should ensure that a large ventricu- Figure C16.28
lar potential is observed at the initial ablation site (tricuspid
annulus) when performing a cavotricuspid isthmus ablation
by dragging the catheter back toward the IVC. The autopsied heart in Figure C16.27 illustrates another
anatomic cause of difficulty with atrial flutter ablation. A sub-
eustachian pouch is located on the cavotricuspid isthmus and
represents a valley formed between a prominent eustachian
ridge and the tricuspid annulus (Figure C16.28). Note that
these pouches are bounded by 3 valvular structures: the the-
besian valve guarding the coronary sinus ostium, the valve of
the eustachian ridge, and the tricuspid valve. Prevalence of a
right atrial pouch is estimated to be 8%.
Pectinates
CS
Even when large pectinates are seen (Figure C16.31), they

tend to be larger more laterally. Thus, when ablation charac-
teristics, ultrasound images, or catheter movement suggest
SVC the presence of prominent pectinate muscles, the ablation
line across the cavotricuspid isthmus should be performed
more septally, where this difficulty is likely to be less evident.
In contrast, because subeustachian pouches tend to occur in
the vicinity of thebesian valve, lateral ablation may circum-
RA vent the problem caused by such pouches.
Pectinates in
isthmus
Pectinates
IVC
Figure C16.30
Figures C16.29 and C16.30 illustrate another anatomic

cause for difficulty during isthmus ablation, encroachment of
large pectinate muscles across the cavotricuspid isthmus that
reach the coronary sinus ostium. In classic anatomy teach-
ing, the crista terminals is described as the septal limit for the
pectinate muscles, but the examples included in this chapter
show that it is not uncommon for pectinates to cross the isth- Figure C16.32
mus and sometimes even extend considerably into the coro-
nary sinus.
Pectinates that extend across the tricuspid valve and IVC Figure C16.32 illustrates an unusual abnormality, the
isthmus are fairly common in structurally normal hearts pectinates are haphazardly oriented within a subeustachian
(estimated 74%) but are usually small when nearing the coro- pouch. If this difficult situation is recognized, best placement
nary sinus ostium. of the ablation line is lateral to the pouch.
Case 16 513
Box C16.2
Applications of Intracardiac Ultrasonography in
Cavotricuspid Isthmus Ablation
1. Verifying catheter contact
2. Verifying adequacy of lesion formation
3. Documenting that the start of the ablation line is ventricular
to the tricuspid valve
4. Identifying subeustachian pouches
5. Identifying a prominent eustachian ridge (Figure C16.33)
6. Finding prominent pectinate muscles
Figure C16.34
Electroanatomic mapping using unipolar (Figure C16.34)

or bipolar voltage maps can also be used to identify promi-
nent pectinate muscles and to design an ablation line. Note
that some portions of the isthmus have relatively high volt-
age (purple and dark blue), whereas other sites have low volt-
age (red). Generally, ablation through areas of low voltage is
easier because transmural lesion creation likely occurs more
quickly and definitely. If multiple areas or large-amplitude
local potentials are seen, a line can be designed to avoid these
areas and successfully ablate the cavotricuspid isthmus.
Various strategies are available to negotiate the difficulties
in ablating atrial flutter due to unusual anatomy. These include
using an electroanatomic mapping system to custom design a
line around the pectinate muscles, as well as catheters capable of
creating deeper or larger lesions and various guiding sheaths.
Figure C16.33
Intracardiac ultrasonography (Figure C16.33) using a lin-

ear phased-array imaging probe in the right atrium (often Figure C16.35
placed via the right femoral vein) can be useful with atrial Sheaths of varying curvature are available to help with
flutter ablation, particularly in difficult cases (Box C16.2). flutter ablation (Figure C16.35); these facilitate catheter con-
tact and direct the electrode tip catheter away from areas of
anatomic difficulty. Sharply curved sheaths are primarily
designed to improve reach and contact with the ventricular
aspect of the tricuspid annulus and provide stable support
when pulling the catheter back toward the atrial portions of the catheter tip, particularly for cases in which the eustachian
the isthmus line. Less curved sheaths primarily help direct ridge is serving as an unwanted fulcrum.
Figure C16.36
Note in Figure C16.36 that the catheter placed on the of the catheter tip and pull the electrode tip back to a rela-
isthmus via the IVC has difficulty maintaining contact with tively atrial location. Th is is because of the alteration in the
relatively ventricular portions of the isthmus, even with the mechanics of catheter support created by the eustachian
catheter maximally bent. Further, inferior deflection of the ridge and the right angle between the cavotricuspid isthmus
catheter will necessarily create a more septal orientation and the IVC.
Figure C16.37
A sheath with a fairly strong curve (Figure C16.37) can be location. Note that the strong curve of the sheath is not being
used to direct the catheter down and toward the isthmus tissue used to direct the catheter more laterally; rather, it facilitates
for better contact. If a less septal orientation is needed, further better contact at multiple locations in a septal-to-lateral ori-
lateral deflection of the sheath or counterclockwise rotation entation. A sheath with less curvature can be used to avoid a
of the sheath will cause the electrode to drag to a more lateral medially located isthmus and to ablate more laterally.
Case 16 515
Confirm diagnosis
Entrain lateral and

septal isthmus
Difficult anatomy Difficult EGMs
Large Prior ablation

Pouch Pectinates
eustachian ridge contact pouch
Irrigation 8-mm Lateral Medial

tip
Internal jugular
“Knuckle” vein or Irrigation Carto/lateral
flutter sheath bidirectional curved 8-mm tip
ablation catheter
Internal jugular Irrigation 8-mm tip

vein or lateral
Excluded isthmus Confirm diagnosis
Figure C16.38
Again, large pectinates tend to be less of a problem closer of the cavotricuspid isthmus is excluded from access via the
to the coronary sinus ostium. However, when a large sub- right atrium, because of either previous surgery or congenital
eustachian pouch is found, more lateral ablation is preferred. heart disease.
These approaches to ablating a difficult isthmus-dependent For the patient being described here, the recurrence of her
flutter are summarized in Figure C16.38. The internal jugular symptoms and the electrocardiogram findings suggested a
vein approach gives a different orientation for contact. The likely diagnosis of atypical atrial flutter. She returned to the
“knuckle” maneuver is to overly curve an electrode so that electrophysiology laboratory, and a new attempt at ablation
the bent catheter is extended onto the isthmus to obtain con- was made using multiple mapping systems and intracardiac
tact. Excluded isthmus refers to situations in which a portion ultrasonography.
Figure C16.39
She was monitored before her arrival in the electrophysi- showed multiple arrhythmias with different cycle lengths and
ology laboratory. A 12-lead electrocardiogram and monitor varying P-wave and flutter morphologies (Figure C16.39).
Figure C16.40
Case 16 517
In the electrophysiology laboratory, the patient had con- If tachycardia continues after the flutter is induced, and
tinuation of atrial arrhythmia and cavotricuspid isthmus if the tachycardia cycle length is less than the cycle length
block was documented (Figure C16.40; arrows indicate wave of the induced flutter, the automatic tachycardia may con-
fronts). The block was present both during the arrhythmia tinuously reset (entrain) the flutter. An interesting phe-
and after cardioversion and performance of pacing maneu- nomenon may be recognized during entrainment mapping
vers on either side of the cavotricuspid isthmus. A closely attempts. When entrainment mapping is attempted from the
spaced multielectrode catheter was placed along the isthmus, cavotricuspid isthmus, entrainment of the flutter circuit and
straddling the prior ablation line as described earlier. overdrive suppression of the automatic tachycardia occur
simultaneously. Thus, on cessation of pacing, the flutter cycle
Which diagnosis should be considered when multiple atrial
length observed during pacing is the cycle length of pacing,
flutters are present?
then the slower natural cycle length of the flutter, and then as
A. Scars from previous surgery acting as a substrate for
the atrial tachycardia warms back up (cycle length shortness)
flutters
and entrains and continuously resets the flutter, the flut-
B. One culprit flutter possibly inducing other flutters
ter will now be at the cycle length of the atrial tachycardia.
C. An automatic atrial tachycardia possibly inducing other
An astute observer will also notice, particularly if multiple
flutters
electrodes are present, that fusion in portions of the atrium
D. Nonsurgical, connective tissue disease–related scarring
occur after a few beats of atrial flutter upon cessation of pac-
E. All of the above
ing when the atrial tachycardia that is more rapid than the
Answer: E—All of the above. flutter has warmed up.
Although scars in the atrium are usually from prior atri-

otomy, the greater use of electroanatomic mapping and intra-
cardiac echocardiography has increasingly identified scarring
(as shown by absence of potentials or distinct wall-motion
abnormality) in patients who present with multiple atrial flut- Induces
ters but no history of atriotomy. An analysis of 13 consecu-
tive patients with macroreentrant atrial tachycardia (flutter)
and no prior atriotomy at the site of the culprit circuit showed Resets
6 patients had known connective tissue disease (eg, Sjögren Entrains
syndrome, mixed connective tissue disease, systemic lupus
Passive
erythematosus), 1 had a history of radiotherapy for lym-
phoma, and 3 had a history of coronary disease and bypass
surgery but the “scar” associated with the flutter was not in
the atriotomy region. In other patients, no obvious cause was
found.
Another important but easily overlooked scenario is
when atrial flutter is diagnosed correctly but is not the pri-
mary cause of the patient’s arrhythmia. For example, in the
electrophysiology laboratory, atrial flutter can be relatively
easily induced in most patients with structurally normal
hearts. Frequently, rapid pacing from the coronary sinus or Figure C16.41
left atrium will cause counterclockwise cavotricuspid isth-
mus–dependent flutter, whereas rapid pacing on the right
atrial free wall will cause induction of clockwise cavotri- As illustrated in Figure C16.41, the primary flutter may
cuspid isthmus–dependent atrial flutter. Once induced, induce or entrain other flutters or passively conduct in a
the atrial flutter can be entrained and the circuit mapped circuit-like manner around scars or areas of slow conduc-
with no way to ascertain exactly where the initial pacing tion. The clinical presentation in such a case may be that
site that induced the flutter was located. In an analogous of varying flutter morphologies during different periods of
situation, a pulmonary vein tachycardia, left atrial tachy- observation.
cardia, or crista terminalis tachycardia, if rapid enough, Because the patient had multiple arrhythmias, further abla-
may induce cavotricuspid isthmus flutter. If the tachycardia tion was not performed. The patient began serial trials of anti-
itself stopped, all that remains is isthmus-dependent flut- arrhythmic medications: flecainide, sotalol, and dofetilide were
ter. In the electrophysiology laboratory, it would be impos- tried, but all were equally ineffective. The patient returned to
sible to know where the original flutter-inducing focus was the electrophysiology laboratory with the plan to either iden-
located. tify atrial scars or the primary focal source.
Figure C16.42
During the ablation procedure, the patient was in a Early sites of activation relative to the P wave were found in
supraventricular tachycardia that was thought to be an the left atrium, near the roof (Figure C16.42). Spontaneous
atypical flutter. However, when entrainment mapping was initiations of tachycardia were noted, particularly with
attempted, clear evidence of overdrive suppression was noted. low-dose isoproterenol.
Case 16 519
Figure C16.43
The tracings shown in Figure C16.43 are most consistent PACs may initiate either a reentrant tachycardia or cer-
with what diagnosis? tain automatic tachycardias. However, if the initial beat of
A. An automatic tachycardia because it was initiated by a tachycardia is identical to the subsequent beats, an auto-
spontaneous premature atrial contraction (PAC) matic focus is highly likely. Th is is because when a PAC ini-
B. A reentrant tachycardia because the PAC that initiated tiates a reentrant tachycardia, a randomly located PAC focus
tachycardia had a short coupling interval is unlikely to have the same activation sequence as the exit
C. An automatic tachycardia because the P wave and inter- of a reentrant circuit. Similarly, with ventricular tachycar-
cardiac sequence of the initiating beat were similar to dias, if the QRS of the initial beat is identical to subsequent
subsequent beats of tachycardia beats, an automatic focus must be considered. The sponta-
D. None of the above neous nature of initiation and considerable variation in the
cycle length of the initial beats of tachycardia all favor an
Answer: C—An automatic tachycardia because the P wave automatic focus.
and intracardiac sequence of the initiating beat were simi-
lar to subsequent beats of tachycardia.
Figure C16.44
With continued mapping, a catheter placed in the right

superior pulmonary vein (RSPV) identified sites where the
tachycardia cycle length (interelectrogram interval) was con-
siderably less than the tachycardia cycle length in the coro-
nary sinus, neighboring left atrial roof, or right atrium (Figure
C16.44). With prolonged observation, an integral multiple of
the fundamental RSPV cycle length was noted in the coro-
nary sinus. This strongly suggests an origin of the tachycardia
in the RSPV, with varying exit block to the remainder of the
atrium and coronary sinus.
Figure C16.45
Case 16 521
In the electroanatomic map shown in Figure C16.45, sites lengths were found relatively deep within the RSPV (red
of earliest activation and, more importantly, shorter cycle area).
Figure C16.46
Within a third-order branch of the RSPV, an even more presented to the electrophysiology laboratory before the era of
rapidly firing tachycardia (also a potential microreentrant pulmonary vein isolation for atrial fibrillation. Thus, a single
tachycardia) was identified (Figure C16.46). Either this focus application of radiofrequency energy was applied at the site of
could be ablated or the ostium of the pulmonary vein encir- the earliest and most rapid tachycardia.
cled to successfully cure these arrhythmias. This patient had
Figure C16.47
Abbreviations
Box C16.3
Points to Remember: Atrial Flutter That Is Difficult
to Ablate ABL, ablation catheter [f]
CL, cycle length [f]
1. Understand and develop an approach to deal with anatomic
coronary sinus-A, proximal coronary sinus atrial electrogram
obstacles
2. Be wary of automatic tachycardias or primary flutters CS, coronary sinus [f]
that may have induced a secondary flutter, if the primary CSO, coronary sinus ostium [f]
arrhythmia terminates as an electrocardiogram is obtained EGM, electrogram [f]
or during electrophysiologic study and ablation HB or His, His bundle [f]
3. Just as the substrate and originating focus both are con-
His-A, His bundle atrial electrogram
sidered for atrial fibrillation, analogous reasoning must be
applied to macroreentrant flutters, particularly in patients IVC, inferior vena cava
with relatively structurally normal hearts LA, left atrium [f]
LAO, left anterior oblique
MEA, multielectrode array [f]
PAC, premature atrial contraction
The tachycardia terminated during ablation (Figure
RA, right atrium [f]
C16.47), and the patient has done well for more than 7 years,
RA-A, right atrial electrogram
with no recurrence of any flutter or tachycardia. The patient
RAA, right atrial appendage [f]
also has not used antiarrhythmic drugs, nor did pulmonary
RAO, right anterior oblique
vein stenosis develop (Box C16.3).
RF, radiofrequency [f]
RSPV, right superior pulmonary vein
RV, right ventricle [f]
SVC, superior vena cava [f]
TA, tricuspid annulus [f]
TV, tricuspid valve [f]
TVA, tricuspid valve annulus [f]
Case 17
An active 30-year-old woman sought advice for intracta- ablation around the pulmonary vein and 3 subsequent pro-
ble atrial fibrillation and multiple atrial flutters. Prior therapy cedures that included extensive linear ablation for flutter cir-
included a trial of flecainide, sotalol, and dofetilide. Because cuits and recurrent fibrillation in the left and right atria. The
of continuous symptoms, she has had a radiofrequency abla- cavotricuspid isthmus was ablated with bidirectional conduc-
tion procedure that included wide-area circumferential tion block.
Figure C17.1
Because of continued symptoms, she was brought to the pacing, the arrhythmia in Figure C17.1 was noted.
electrophysiology laboratory. During decremental atrial

Terms with “[f]” denote abbreviations that appear in the figures only.
523
Which statement about the tracings in Figure C17.1 is Junctional tachycardia is a much less common but still
false? important entity that may present as atrial fibrillation (Box
A. Junctional tachycardia may be present C17.2). Rapid junctional tachycardia may have multiple
B. Atrioventricular nodal reentrant tachycardia (AVNRT) potential clinical manifestations. These include 1) atrial
may be present fibrillation when rapid retrograde conduction occurs; 2)
C. Atypical AVNRT may be present junctional tachycardia or ventricular fibrillation when rapid
D. Retrograde accessory pathway conduction may be ventricular conduction occurs; 3) supraventricular tachycar-
present dia mimicking AV node reentry when 1:1 junction-to-atrium
E. The findings may explain the patient’s intractable atrial and ventricle conduction occurs; and 4) AV block when per-
fibrillation sistent junctional tachycardia has exit block to the ventricle
Answer: D—Retrograde accessory pathway conduction and atrium but keeps the AV node refractory such that the
may be present. sinus impulse can no longer penetrate the AV node and reach
the ventricle.
The tracing in Figure C17.1 shows 2 beats of tachycar-
dia during decremental atrial pacing for which the earliest
Box C17.1
electrical potential is seen in the His bundle electrogram.
Arrhythmias Associated With Atrial Fibrillation
Consider the possibility that the first beat of junctional tachy-
Accessory pathway–mediated tachycardia cardia shows retrograde activation to the atrium and the sec-
Atrial flutter
ond shows conduction to the ventricle only (no conduction to
Monomorphic atrial tachycardia
Junctional tachycardia the atrium). Junctional tachycardia characteristically is asso-
Atypical atrial flutter ciated with spontaneous onset of arrhythmia that often can
be exacerbated with catecholamine. Junctional tachycardia
may, however, occur during decremental atrial or ventricular
Radiofrequency ablation for atrial fibrillation currently pacing.
involves procedures that target the pulmonary veins, other Can the true beats of tachycardia be attributable to AV
venous structures, ganglionated retroatrial plexuses, or frag- node reentry? Rarely, AV node reentry may be induced with-
mented electrograms in the atrium. However, other arrhyth- out an apparent “jump” in the atrial-His (A-H) interval. The
mias may coexist with atrial fibrillation (Box C17.1). so-called 2-for-1 phenomenon involves double activation of
Atrioventricular (AV) reentrant tachycardia classi- the ventricle and His bundle from a single atrial extrastimu-
cally is associated with atrial fibrillation. Numerous studies lus or atrial-paced lead or sinus beats. The first His bundle
have shown that ablation of the culprit accessory pathway and ventricular potential occur via conduction down the fast
will nearly always eliminate recurrent episodes of atrial pathway and AV node and the second through conduction
fibrillation. via the slow pathway and AV node. Usually, when antegrade
The relationship between atrial fibrillation and atrial flutter fast-pathway conduction occurs, antegrade slow-pathway
is complex (see Case 16). Although atrial flutter may degener- conduction cannot occur because of retrograde penetration
ate into atrial fibrillation, this rarely occurs. More commonly, of the slow pathway via the fast pathway.
atrial fibrillation is organized into a stable reentrant flutter Distinguishing single 2-for-1 episodes from junctional
circuit, particularly when membrane-active antiarrhythmic extrasystoles can be difficult. If the phenomenon is seen dur-
drugs are used. A less-recognized but also common source of ing atrial extrastimulus testing, when atrial capture or AV
flutter and atrial fibrillation is a monomorphic atrial tachy- nodal conduction is lost, the second beat is no longer seen;
cardia, which often arises from the pulmonary veins. in contrast, a junctional escape generally is unaffected by the
presence or absence of atrial capture or initial AV nodal con-
duction. Another useful and simple maneuver involves plac-
ing a second extrastimulus before the beat being analyzed. If
Box C17.2
this second extrastimulus advances the beat in question with
Clinical Presentation of Junctional Tachycardia
a normal A-H interval, then a junctional escape mechanism
Regular narrow complex tachycardia, similar to atrioventricular for the beat in question can be ascertained. However, if there
node reentry
is no effect or delay of this second beat, then the underlying
Atrial fibrillation
Ventricular arrhythmia, including premature ventricular mechanism is probably a 2-for-1 phenomenon. This maneu-
contractions and ventricular fibrillation ver is similar to placing premature atrial contractions (PACs)
In young patients, paroxysmal complete heart block during a narrow complex tachycardia to distinguish between
Postoperative regular or irregular narrow complex tachycardia junctional tachycardia and AV node reentry. Because of the
(eg, after valve surgery, coronary artery bypass surgery)
narrow excitable gap in AV node reentry, late-coupled PACs
Fetal tachycardia
In children, irregular narrow complex tachycardia associated do not reset the tachycardia and early coupled PACs generally
with exercise will reset the tachycardia with a long A-H interval (antegrade
conduction through a partially refractory slow pathway).
Case 17 525
PACs or even competing sinus rhythm generally advances occur in compartmentalized hearts, after transplant, after a
a junctional rhythm or junctional tachycardia fairly eas- maze procedure, and in other rare conditions).
ily, with a normal A-H interval. Even when a tachycardia is The phenomenon of nonsustained beats (Figure C17.1) was
nonsustained, if AV dissociation is seen, one can generally seen repeatedly. In Figure C17.2, a sustained tachycardia was
exclude an AV reentrant tachycardia mechanism (exceptions induced with a very similar initiating pattern.
Figure C17.2
Which of the following is true? These findings should strongly suggest junctional tachy-
A. Junctional tachycardia is present cardia as the underlying mechanism for the arrhythmia.
B. AV node reentry is present However, AV node reentry may be completely disassociated
C. The cause of atrial fibrillation is established from the atrium or the ventricle. Although junctional tachy-
D. AV nodal ablation should be performed cardia may be the cause of this patient’s atrial fibrillation,
E. Insufficient data to determine whether A-D are true other causes such as remaining pulmonary venous conduc-
Answer: E—Insufficient data to determine whether A-D are tion must still be excluded. It would be premature to perform
true. AV nodal ablation at this point because the diagnosis may
yet be AV nodal reentry. Further, certain types of junctional
A narrow complex tachycardia was induced (Figure tachycardia can be ablated without necessarily obliterating
C17.2) and several characteristics are noteworthy. First, the the compact AV node (thus necessitating permanent implan-
His-to-His (H-H) activation intervals are constant. Second, tation of a pacemaker). The variation in the AV interval is best
the ventricular activation sequence is constant. Th ird, the noted by examining the electrogram from the mid coronary
AV and His-to-atrium (H-A) activation intervals are chang- sinus, between the first and second beats of tachycardia, and
ing. Fourth, the atrial activation sequence for each beat by examining the differences in the H-A interval between the
is identical. Therefore, there is evidence of AV and H-A second and subsequent beats of tachycardia.
dissociation.
Figure C17.3
Measurement of the H-A interval from the His bun- finding suggests junctional tachycardia and AV node reentry.
dle potentials to the onset of the atrial potentials on the If the H-A interval increases, tachycardia should slow by a
distal hRA catheter shows this variation (Figure C17.3). similar amount (decrease in atrial-to-atrial interval). In rare
Importantly, however, this variation in the H-A interval (69 instances, H-A changes may not predict changes in the cycle
and 88 milliseconds) is occurring in the context of a con- length of tachycardia; this occurs in an unusual form of AV
stant His-His interval and atrial activation sequence; this nodal reentry.
Figure C17.4
Case 17 527
In Figure C17.4, the tachycardia terminates. The first 3 An important dictum in electrophysiology states that
beats show a regular narrow tachycardia with a very short AV node reentry is favored over junctional tachycardia if
ventriculoatrial (VA) interval and consistent atrial activa- repeated termination of the arrhythmia is associated with
tion sequence. The fourth beat shows a decreasing H-H cycle H-A block. This is because such termination would involve a
length with termination of the tachycardia. chance occurrence of junctional rhythm ceasing simultane-
ously with retrograde block to the atrium (analogues to atrial
Which statement best summarizes the inference that can
tachycardia are unlikely when termination occurs with failure
be made with this observation?
to conduct to the ventricle). However, important exceptions
A. AVNRT is the probable diagnosis because a junctional
exist, including variations in the junctional tachycardia rate
tachycardia is unlikely to terminate after block from
that often are seen at initiation and just before termination of
the junctional focus to the atrium
tachycardia. If this change in rate is significant enough, ret-
B. AVNRT is present because spontaneous changes in the
rograde block to the atrium via the compact AV node may
His bundle interval are common
occur simply because of the premature nature of early beats
C. Junctional tachycardia is present because spontaneous
just before tachycardia cessation. Thus, on the basis of this 1
changes in the His bundle interval are common
tracing, neither AV node reentry nor junctional tachycardia
D. None of the above
can be excluded.
Answer: D—None of the above.
HA block terminates tachycardia
Figure C17.5
Figure C17.5 shows an example (from another patient) in H-A block occurred, tachycardia was terminated. This is
which the H-H interval is relatively constant. (The arrows highly suggestive of AV node reentry because part of the cir-
and “x” point to His bundle to atrial activation followed by cuit involved tissue that also was responsible for conduction
His bundle activation without block to the atrium.) When between the His bundle and the atrium.
Figure C17.6
Even more compelling is the finding shown in Figure C17.6. the next A-H interval. Such findings strongly suggest a reen-
Here, the changes in the H-A interval result in subsequent trant circuit (AVNRT).
predictable changes in the cycle length of the tachycardia and
Figure C17.7
Case 17 529
The index patient had repeated episodes of tachycar- relative H-A interval. Although these findings are consistent
dia that occurred during atrial pacing, catheter manipula- with AV node reentry, they are seen more frequently with
tion, and isoproterenol administration (Figure C17.7). Note automatic junctional tachycardia.
the marked changes in the tachycardia cycle length and the
Figure C17.8
With isoproterenol administration, the findings illustrated initiation, possibly from an atrial tachycardia. Because this
in Figure C17.8 were noted multiple times. Degeneration to a phenomenon occurred repeatedly, the narrow, complex,
regular tachycardia, which in some instances was relatively relatively regular tachycardia (likely junctional tachycardia)
sustained atrial fibrillation, occurred during episodes of was attributed to atrial fibrillation; thus, it became the focus
the supraventricular tachycardia that were initially irregu- of attention for further electrophysiology maneuvers and
lar. In fact, if the His bundle catheter had not been in place, attempts at ablation.
the diagnosis could have been spontaneous atrial fibrillation
Figure C17.9
In Figure C17.9, initiation of tachycardia is seen during The ventricle is not an integral part of the circuit for AV
ventricular pacing from close to the right ventricular apex, node reentry, atrial tachycardia, or junctional tachycardia.
at a constant pacing cycle length. Note the change in the Thus, the findings shown in Figure C17.9 do not necessarily
VA interval and then clear initiation and dissociation of the exclude AV node reentry or even make it more likely than
arrhythmia from ventricular pacing. junctional tachycardia. Onset of certain ventricular tachy-
cardias (eg, those associated with triggered automaticity)
The finding of dissociation of the ventricle from the
may occur during ventricular pacing, specifically decremen-
arrhythmia is consistent with all of the following except:
tal ventricular pacing (rather than ventricular extrastimulus
A. Junctional tachycardia
testing). With reentrant ventricular tachycardia (eg, those
B. AV node reentry
associated with ischemic cardiomyopathy), such an initiation
C. Atrial tachycardia
would be distinctly unusual.
D. Ventricular tachycardia
E. May be seen in any of the arrhythmias listed above
Answer: E—May be seen in any of the arrhythmias listed
above.
Case 17 531
Figure C17.10
The measurement of several intracardiac intervals and tachycardia, AV node reentry, and other supraventricular
the correct interpretation for the reason and variation of tachycardias, if a multielectrode catheter is placed over the
these intervals can be very helpful in distinguishing between His bundle region, then the His bundle activation sequence
AVNRT and junctional tachycardia; these measurements (proximal to mid to distal) is similar in sinus rhythm to any
can also help further define the precise variant of junctional arrhythmia that actively activates the His bundle in the ante-
tachycardia that is present. In Figure C17.10, the interval grade direction. If automaticity (or microreentry) arises from
between the most proximal His bundle deflection to the most somewhere in the His bundle itself, then the intrahisian acti-
distal His bundle deflection is being measured. vation sequence changes. A manifestation of this change is
If the interval from proximal His to distal His signals in marked variation in the intrahisian interval when measured
sinus rhythm differs by more than 10 milliseconds com- in tachycardia vs sinus rhythm; that is, a local His bundle
pared with the interval from the proximal His to distal deflection will be “bracketed” somewhere along the His
His during tachycardia, which of the following diagnoses bundle–right bundle region, and if the focus is between the
is most likely? proximal His recording electrode and the distal His record-
A. Atrial tachycardia ing electrode, then both of these sites (proximal and distal)
B. AVNRT will be activated nearly simultaneously.
C. Tachycardia arising from the His bundle Several important caveats to the interpretation of this rule
D. Tachycardia arising from the compact AV node should be remembered. First, if a multielectrode catheter in
E. Tachycardia arising from a protected zone in the the His bundle region is placed too distally, rate-dependent
slow-pathway region right bundle branch block may cause marked variation in the
interval from the His bundle to the right bundle. However,
Answer: C—Tachycardia arising from the His bundle.
true intrahisian delay or block is very rare. Second, if a His
This rather simple interval can be highly informative, par- bundle tachycardia arises very close to the junction between
ticularly if a multielectrode catheter has been used to mea- the His bundle and compact AV node, the activation sequence
sure multiple His bundle deflections. The underlying premise in the remainder of the His bundle electrogram (mid and
for this maneuver is as follows. In most variants of junctional distal) will be similar to that seen in sinus rhythm.
Figure C17.11
Table C17.1
Variants of Junctional Tachycardia
Type of Junctional Tachycardia Description Ablation Technique
His bundle tachycardia Automaticity or microreentry arising within the His Cryoablation or specific mapping of the earliest
bundle His site can be done; this site should be
The His bundle activation sequence is bracketed, targeted for ablation
and the intrahisian interval during tachycardia is
markedly different compared with that seen in sinus
rhythm
Tachycardia arising in the Tachycardia arising from this site may present as For a distinct atrial type of potential, the site of
atrial musculature, between junctional tachycardia if there is retrograde block to earliest activation in the slow-pathway region
the coronary sinus and the atrium from the site of origin of the tachycardia can be targeted for ablation
the compact AV node The musculature between the coronary sinus and Tachycardia often resolves with empiric
(slow-pathway tachycardia) compact AV node houses the tachycardia focus, but slow-pathway ablation
the only way to activate the rest of the atrium from
this site is to have the wave front proceed first to
the compact AV node and then to the retrograde
fast pathway and atrium, with near-simultaneous
activation of the His bundle and ventricle in an
antegrade fashion
Tachycardia arising from the In compact junctional tachycardia, when the H-A ...
compact AV node intervals during tachycardia and ventricular pacing
are compared, the interval will be shorter during
tachycardia because of the near-simultaneous
activation from the focus to the His bundle and
atrium
In His bundle tachycardia, the H-A intervals in
tachycardia and ventricular pacing are similar
(continued)
Case 17 533
Table C17.1
(Continued)
Type of Junctional Tachycardia Description Ablation Technique
Tachycardia arising from the Similar to atrial tachycardia, except that it arises The A-H interval and intrahisian activation
fast-pathway region, close to anterior to the tendon of Todaro, with possible sequence is similar to sinus rhythm (depends
the compact AV node retrograde block and conduction to the atrium only on rate)
via the AV node The A-H interval will be the same as that
in tachycardia if paced from near the
fast-pathway region; it will be markedly
different if paced from the coronary sinus
(pacing at the same rate)
The H-A interval during pacing has no constant
relationship with the H-A interval during
tachycardia: the H precedes the A in pacing
and the A precedes the H in tachycardia
Abbreviations: A, atrium; AV, atrioventricular; H, His.
Note that during tachycardia and right bundle branch with no lengthening of the A-H interval), then the findings
block, the intrahisian conduction interval is very similar shown in Figures C17.10 and C17.11 would suggest an ori-
to that seen in sinus rhythm. If AVNRT has been excluded, gin of the tachycardia either in the compact AV node or in
or if junctional tachycardia could be diagnosed confidently a protected zone in the slow pathway leading to the AV node
(eg, late-coupled PACs easily resetting the tachycardia, (Table C17.1).
Figure C17.12
In Figure C17.12, tachycardia was initiated during ventricu- the atrial activation sequences during ventricular pacing and
lar pacing. Note that in the third paced beat, a retrograde His tachycardia are identical. The remaining possibilities are AV
bundle deflection is seen (yellow arrow). Observe the H-A inter- node reentry and junctional tachycardia, although a marked
val and the atrial activation sequence during ventricular pacing change occurs in the VA interval and the His-ventricular inter-
and during tachycardia. Atrial tachycardia is unlikely because val (H-V) between the third and fifth beats (arrows).
Figure C17.13
Figure C17.13 shows that there is no difference in the H-A activation sequence is completely unchanged. This must be
activation time or in the activation sequence of the tachycar- definitely determined by careful measurement of each atrial
dia. What is the significance of having similar H-A intervals potential during tachycardia and comparing them with the
(69 milliseconds) during ventricular pacing and tachycardia? corresponding potentials recorded during ventricular pacing.
If the His bundle recording catheter has been appropriately If the sequence is unchanged, then any atrial potential can
positioned, this would be strong evidence for the site of origin be used. In Figure C17.13, the atrial potential from the hRA
being somewhere in the distal His bundle region. This infor- catheter was used.
mation may help the ablationist select the right catheter and Th ird, note the marked variation in the VA interval
perform appropriate mapping in the His bundle region. between the paced beat and the tachycardia beat, yet the
Figure C17.13 illustrates some of the difficulties in appro- H-A interval is unchanged. How is this possible? The VA
priately measuring and interpreting intervals with regard interval may be a pseudointerval during tachycardia. Th is
to junctional tachycardia and AV node reentry. First, when means that during pacing from a particular site in the ven-
measuring the H-A interval, should the initial or terminal tricle, there is a certain time to get up the AV node to the
part of the His deflection be considered? In Figure C17.13, the atrium, but during tachycardia, there is no real VA conduc-
initial portion is used. The disadvantage of this approach is tion and some common point is responsible for the tachy-
that if prominent intrahisian delay is present during tachycardia (exit or focus) that activates the ventricle and atrium.
cardia but absent during ventricular pacing, then an inap- Th is can be seen in various arrhythmias, including AV node
propriately longer H-A interval will be measured during reentry and all forms of junctional tachycardia; but in this
tachycardia compared with pacing. Thus, when H-A intervals case, the VA interval is associated with lack of change in the
are measured to diagnose variants of AVNRT and to distin- H-A interval. Further, the intrahisian sequence does not
guish them from variants of junctional tachycardia, the H-A change, which strongly suggests that the common focus (or
interval should be measured from the end of the His potential exit) responsible for VA activation is the His bundle. Thus, a
to an atrial potential. However, the difficulty with this tech- leading diagnosis here is His bundle tachycardia. Note that
nique is that the terminal portion of the His bundle potential with AV node reentry, the VA interval is also a pseudoin-
may be obscured by the ventricular potential (Figure C17.13, terval, but changes are expected in the H-A interval as well.
the first paced beat). A common practice, however, is to use Further, the intrahisian sequence between ventricular pac-
the onset of the His bundle potential if it is obvious that there ing and tachycardia should be different; as in tachycardia
is no significant intrahisian delay. with AV node reentry, the His bundle shows antegrade acti-
Second, which atrial potential should be used to mea- vation, whereas during ventricular pacing, it shows retro-
sure the H-A interval? Here, the key finding is that the atrial grade activation.
Case 17 535
Fourth, why does the proximal His bundle potential occurring in an antegrade manner, or there may be fusion
appear to precede the distal His bundle potential, even between antegrade and retrograde conduction. Similarly,
during ventricular pacing? This is an important confound- one could cautiously argue that an intrahisian sequence
ing variable when interpreting complex electrograms. The during tachycardia that is similar to pacing suggests a
His bundle catheter often straddles the junction between tachycardia origin in the His bundle. Thus, even with a
the His bundle and the right bundle branch of the con- suprahisian exit, the intrahisian sequence may be similar
duction system. During ventricular pacing, there may be in tachycardia and during ventricular pacing if there is
retrograde right bundle branch block or delay. Thus, even proximal right bundle delay and the His bundle catheter
with ventricular pacing, the His bundle itself may be acti- straddles the junction between the His bundle and right
vated via the left bundle, right bundle activation may be bundle.
Figure C17.14
An analogous situation arises when trying to determine C. Orthodromic AV reciprocating tachycardia

whether His bundle activation is antegrade or retrograde in D. Junctional tachycardia
the context of a wide complex tachycardia. Retrograde activa- E. His bundle tachycardia
tion is expected in ventricular tachycardia and in antidromic Answer: C—Orthodromic AV reciprocating tachycardia.
tachycardia. However, with other supraventricular tachycar-
dia giving rise to a wide complex tachycardia with bundle Of the listed tachycardias, the only one that involves infra-
branch block, the His bundle activation should be antegrade. hisian tissue (bundle branches, ventricular myocardium) is
Here again, careful analysis of the location of the His bundle AV reentrant tachycardia. Thus, if the H-V interval increases,
and identification of proximal right bundle delay is necessary the ventricle takes longer to activate; this in turn likely delays
before concluding whether His activation is antegrade or ret- activation of the accessory pathway musculature and subse-
rograde (Figure C17.14) (see Chapter 4). quently lengthens the circuit time (ie, return to the atrium)
The H-V interval, measured in tachycardia, also requires and slows the tachycardia. With antidromic tachycardia,
careful interpretation. the H-V interval is negative, that is, the ventricle is activated
before the His. In this situation, if a change in the V-H inter-
A change in the H-V interval is predictive of subsequent val predicts the change in the tachycardia cycle length, an AV
changes in the cycle length (eg, atrial-to-atrial interval) in tachycardia (an antidromic circuit) can be diagnosed. This
which tachycardia mechanism? phenomenon is seen when retrograde bundle branch block
A. Typical AV node reentry occurs, eg, with a Mahaim-mediated tachycardia.
B. Atypical AV node reentry
Figure C17.15
The ease with which a tachycardia is reset from various penetrated. With junctional tachycardia, very late coupled
sites in the atrium also provides important information. In PACs (Figure C17.15, placed from the coronary sinus or
general, it is difficult to reset AV node reentry from any- other sites in the atrium) can reset the tachycardia without
where in the atrium without increasing the A-H interval. a major change in the A-H interval. The maneuver is dif-
The excitable gap in AV node reentry is relatively small; thus, ficult to interpret, however, because significant spontaneous
closely coupled PACs or rapid atrial pacing is required, and variation in cycle length may occur with junctional tachy-
because of decremental tissue in the AV node, the A-H inter- cardia (that variation in itself can help distinguish it from
val almost always will be lengthened whenever the circuit is AV node reentry).
Figure C17.16
Case 17 537
Figure C17.16 shows little or no variation in the H-A inter-

val, yet in the last beat of tachycardia, the His bundle deflec-
tion occurs very early, with subsequent termination of the
tachycardia. (Arrows in the figure indicate atrial activation.) A>V, no His
If changes in the H-A interval precede subsequent changes AV node
Coronary
in the H-H interval, AV node reentry should be strongly sus- sinus
pected. In contrast, if marked changes in the H-H interval FP
are associated with little or no change in the H-A interval, Upper
junctional tachycardia is a leading diagnostic possibility. common Infrahisian
It is possible that the shortened A-H interval between the pathway
A>V, His+
second and third beats in Figure C17.16 is the reason why V>A
the His bundle potential is earlier. This suggests that the AV Lower
node is part of the circuit (eg, AV node reentry). Such a sce- common pathway
nario may occur when the antegrade limb for AV node reen- A>V, no His
try involves more than 1 antegrade slow pathway. However,
it would be unusual for a tachycardia to transition from a
circuit using a longer conducting slow pathway to one that
conducts faster during tachycardia. The various maneuvers
described to distinguish between AV node reentry and junc- Figure C17.17 (Adapted from Macedo PG, Patel SM, Bisco SE,
tional tachycardia should be used, and junctional tachycardia Asirvatham SJ. Septal accessory pathway: anatomy, causes
or one of its variants should be suspected if there is marked for difficulty, and an approach to ablation. Indian Pacing
Electrophysiol J. 2010 Jul 20;10[7]:292–309. Used with permission
spontaneous variation in the cycle length of the H-H interval
without significant changes in the H-A interval.
The rule is that with AVNRT, association of atrial, ventric-
ular, and His bundle potentials is expected, as is an associa- As seen in Figure C17.17, the AV node reentrant circuit
tion of A-H and H-A intervals with the tachycardia. In other may involve common pathways, both where the retrograde
words, when the H-A interval changes or the A-H interval fast pathway turns around to the antegrade slow pathway or a
changes, the tachycardia cycle length changes; conversely, if common pathway between 2 slow pathways before approach-
these intervals are markedly dissociated from the His bundle ing the AV node. Of course, if the intrahisian and infrahisian
cycle length, AV node reentry is unlikely. However, because tissues are separate from the AVNRT circuit block at any of
there are many situations in which dissociation between the these sites, potentials may be dissociated in AV node reentry.
AV and His can occur, distinguishing between AVNRT and
junctional tachycardia remains challenging.
Figure C17.18
Figure C17.19
Figure C17.18 shows that the H-A intervals were very potentials at an anatomic location close to the junction of
similar in tachycardia and during pacing. Further, the intra- the right bundle and His bundle electrograms. With further
hisian activation sequence was very dissimilar during tachy- mapping at this site, multiple His bundle deflections were
cardia and sinus rhythm, which suggested a focal origin in seen repeatedly, without conduction to the atrium or ven-
the His bundle system. Careful point-to-point mapping on tricle. Thus, a focal His bundle tachycardia was diagnosed
the His bundle itself revealed bracketing of the His bundle (Figure C17.19).
Case 17 539
Figure C17.20
The ABL d catheter was then used for mapping to maxi- deflection (Figure C17.20). Cryoablation was performed at
mize the potential at the site of the earliest His bundle this site.
Figure C17.21
During cryoablation, rapid His bundle tachycardia gave The ablation had no significant effect on the AV interval,
rise to brief flurries of atrial fibrillation and rapid ventricular and the tachycardia was no longer inducible or seen sponta-
tachycardia. His bundle tachycardia with rapid conduction neously with high doses of isoproterenol.
to the ventricle was noted. The tachycardia then terminated
(Figure C17.21).
Figure C17.22
This tracing in Figure C17.22 was obtained from interro- same rate. At the end of the bottom panel, the tachycardia
gation of an automatic external defibrillator. The patient was degenerates to a more rapid irregular rhythm consistent
an otherwise healthy woman who previously had palpita- with ventricular fibrillation. T waves can be seen just before
tions followed by syncope but this time had palpitations and the trough of the T wave, and a consistent 1:1 relationship
collapsed. between the QRS complexes and the P wave is seen. The P
waves are closer to the preceding QRS complex than to the
What features are evident in this tracing?
succeeding QRS complex (short RP tachycardia). The differ-
A. A short RP tachycardia
ential diagnosis for this arrhythmia would include AVNRT,
B. Ventricular tachycardia
orthodromic AV reciprocating tachycardia, and junctional
C. Possible AVNRT
tachycardia. The variation in the QRS amplitude is sugges-
D. Atrial fibrillation
tive of electrical alternans. Alternans is somewhat better
E. A and C
associated with AV reciprocating tachycardia but may be
F. B and D
seen in any very rapid arrhythmia. The distinctly unusual
Answer: E—Short RP tachycardia and possible AVNRT. part of this tracing is the degeneration of tachycardia into
A regular narrow complex tachycardia is seen in the another arrhythmia.
top panel and continues in the bottom panel at about the
Case 17 541
Figure C17.23
Figure C17.23 is a continuous strip showing clear change ventricular tachycardia or ventricular fibrillation.
from a regular narrow complex tachycardia to polymorphic
Figure C17.24
Figure C17.24 shows the device appropriately detected the tachycardia with rapid atrial conduction can degenerate into
arrhythmia and delivered a shock to terminate it. This case atrial fibrillation. In some patients, rapid junctional tachycar-
illustrates another manifestation of junctional tachycardia, dias may give rise to ventricular fibrillation.
as described earlier in this case series, in which junctional
Figure C17.25
Although rare, AV tachycardia may give rise to malignant isoproterenol. At various times, this tachycardia was dissoci-
ventricular arrhythmia when the following sequence of events ated from the atrium and from the ventricle. Marked changes
occurs: 1) a bidirectionally conducting accessory pathway is pres- in the H-A and H-V intervals occurred with no significant
ent; 2) orthodromic reciprocating tachycardia occurs; 3) atrial effect on the H-H interval. Further, late coupled PACs could
fibrillation is precipitated; 4) rapid ventricular conduction of reset the tachycardia (bring in the next His deflection) with
the atrial fibrillation to the ventricle via the antegrade accessory a normal A-H interval. All of these features are strongly sug-
pathway and AV node occurs; and 5) with spontaneous AV node gestive of junctional tachycardia.
blockade, ventricular fibrillation may result (Figure C17.25). A young woman was brought to the electrophysiology
In the electrophysiology laboratory, multiple episodes laboratory because of palpitations and a Holter monitor diag-
of a narrow complex tachycardia with a short RP interval nosis of frequent premature ventricular contractions (PVCs).
were seen; these occurred spontaneously and with the use of She was otherwise healthy.
Figure C17.26
Case 17 543
On the basis of the 12-lead electrocardiogram (Figure outflow tract PVC. The right ventricular outflow tract is the
C17.26), which site will most likely successfully ablate these most frequent site for symptomatic monomorphic PVCs in
wide complex beats? otherwise healthy patients. The electrophysiologist, however,
A. Right ventricular outflow tract should be alert to the possibility of an unusual site of origin
B. Left ventricular outflow tract for these PVCs. This is because the R wave in lead III is not
C. His bundle particularly tall and because lead aVL is isoelectric. Usually,
D. Right ventricular free wall from a site of right ventricu- very tall R waves are seen in all the inferior leads when the ori-
lar dysplasia gin is in a classical site in the right ventricular outflow tract.
E. Anterior trigone region of the heart As discussed in Case 16, with most outflow tract origins for
PVCs, both aVR and aVL are strongly negative, keeping with
Answer: A—Right ventricular outflow tract.
their origin in the superior quadrant of the heart. The portion
The PVCs show a left bundle branch block morphology of the outflow tract furthest from the positive electrode for
consistent with an origin in the right ventricle. The R waves aVL is the myocardial region between the inflow and outflow
are strongly positive in the inferior leads (leads II, III, and portions of the right ventricle. This includes the region where
aVF). These features are consistent with right ventricular the His bundle transitions to the right bundle branch.
Figure C17.27
Figure C17.27 was obtained during the invasive electro- conduction time from the His bundle to the right bundle
physiologic study. Note that with the PVCs, the earliest ven- branch exit closer to the apex of the heart plus the time for
tricular potential is a far-field deflection on the RVp catheter. the ventricular activation wave front to travel from that exit
However, the near-field His bundle potential clearly precedes site back to the His bundle region (location of the recording
any discernible ventricular potential, and it precedes the catheter). If the His bundle itself is the origin for these PVCs,
onset of the QRS complex in the 4-lead electrocardiogram. the H-V interval with the premature beat is expected to be
Although this suggests a His bundle origin for these PVCs, at least as long as the H-V interval during sinus rhythm.
the electrophysiologist should question the relatively short With a shorter interval, the possibility of a pseudointerval
local H-V interval during the PVC, which is even shorter than should be considered. Another possibility is a myocardial
that observed during sinus rhythm. origin for the PVCs, close to but possibly proximal to the
What is the significance of this shorter H-V interval? right bundle exit or left bundle exit. Thus, the PVC enters
The local H-V interval during sinus rhythm reflects the the conduction system and travels retrograde through the
His bundle catheter, producing an early His bundle activa- one component occurs because of right ventricular septum
tion, and the ventricular excitation wave front reaches this activation and the other because of left ventricular septum
same location a little later. A second interesting feature is activation). What can be surmised from these subtle but
that the complex ventricular potential in sinus rhythm has significant fi ndings? From this tracing alone, the impor-
2 distinct components. With the PVC, however, the ventric- tance of these fi ndings is unclear, but the ablationist should
ular potential has essentially only 1 component. Complex be aware of the possibilities mentioned above and should
ventricular potentials may be seen in a patient with a pre- be prepared for more extensive mapping and diagnostic
vious ablation or with bundle branch block (presumably, maneuvers.
Figure C17.28
The interval from the earliest His bundle deflection to activation. Mahaim fibers and other antegrade-conducting
the onset of the QRS complex consistently was from 35 to 40 accessory pathways may also produce a second His bundle
milliseconds (Figure C17.28). The consistency of this interval deflection after the ventricular potential on the His bundle
does not prove an origin in the His bundle, but it suggests that catheter because of retrograde conduction of the right bundle.
a fascicular origin, His bundle origin, or ventricular myocar- Another unusual pathway to consider can occur via connec-
dium origin close to the conduction system is associated con- tions from the right atrial appendage to the right ventricular
sistently with proximal conduction tissue activation. Again, outflow tract. These occur congenitally or may be associ-
the complex ventricular potential on the His bundle catheter ated with ventricular corrective surgery for congenital heart
is seen during sinus rhythm but not the PVC. disease.
Case 1 described one cause of complex signals on the His In general, a His bundle potential cannot be the earliest
bundle catheter in patients with an anteroseptal accessory evidence of activation; if this were from an accessory path-
pathway. For those patients, a complex atrial potential rep- way, some ventricular activation would precede His bundle
resented pathway conduction and an early local ventricular activation. However, this possibility cannot be excluded
potential from ensuing activation. Could these tracings be completely because ectopy from accessory pathways, includ-
consistent with an accessory pathway? Unusual accessory ing Mahaim-type fibers, has been described. A more likely
pathways may cause complex signals on the His bundle possibility is a His bundle origin for the PVCs. However, the
catheter. With Mahaim fibers, activation of the right bundle diagnosis must account for the complex ventricular potential
may produce a second ventricular activation or right bundle and the paradoxic shortening of the H-V interval with PVCs.
Case 17 545
Figure C17.29
In Figure C17.29, the ABL d catheter was manipulated to main ventricular potential. The catheter recorded a very com-
maximize the early potential (possibly a His bundle deflec- plex electrogram. This could be an artifact, but it appeared
tion). Note also in the sinus beat between the 2 PVCs, the consistently when mapping in the region of the His bundle
ABL d catheter shows a late ventricular potential after the and the anterior tricuspid annulus.
Figure C17.30
In Figure C17.30, a 12-lead electrocardiogram is shown. with several potential explanations about its origin, the lead-
The first and third beats show sinus rhythm, with a right bun- ing diagnostic possibilities being a PVC arising from the right
dle block morphology. The second beat is a wide complex beat ventricle or a right-sided accessory pathway. Some patients
can be highly symptomatic, even in the absence of sustained monitors show clear correlation between these phenomena
tachycardias, with intermittent phenomena such as PVCs and troublesome symptoms, electrophysiology study and
or preexcitation. If medical therapy is ineffective and event ablation can be offered, as was done for this patient.
Figure C17.31
Figure C17.31 shows the intracardiac electrograms between the His bundle and right bundle), then His bundle
recorded simultaneously with the 12-lead electrocardiogram activation occurs, giving rise to the His bundle potential in
in Figure C17.30. The arrow points to a signal after the ven- sinus rhythm, and then ventricular activation occurs via the
tricular potential on the His bundle catheter that was consis- left bundle, giving rise to the ventricular potential. Next, ret-
tently seen in sinus rhythm and consistently absent during rograde penetration of the right bundle occurs, and the right
wide complex beats. bundle potential thus may be seen considerably after the His
Which is a possible explanation for this phenomenon? bundle potential or ventricular potentials on the His bundle
A. Intermittent preexcitation catheter.
B. PVCs arising from diseased tissue near the His bundle If ectopy arises from the mid or distal portion of the right
region bundle, then during those ectopic beats, the right bundle
C. Intermittent conduction via a Mahaim fiber potential will occur earlier, possibly intermingling with either
D. Intermittent right bundle ectopy the ventricular or His bundle potential. From what is shown
E. All of the above in Figure C17.31, this remains a possibility if the wide com-
plex beat represents fusion between sinus rhythm and right
Answer: E—All of the above.
bundle ectopy.
Examine the various possible explanations for the phe- Could this phenomenon be explained by some form of
nomenon in Figure C17.31. First, right bundle branch block preexcitation? In patients with Mahaim-type accessory path-
is associated with the sinus beats. In most instances of right ways, the accessory bypass tract is essentially a second AV
bundle branch block, conduction potentially can occur node–His bundle with a fascicle akin to another right bundle.
through the right bundle, although it is considerably delayed This Mahaim tract often inserts into the right bundle in the
compared with left bundle conduction. If penetration up the usual location. If antegrade right bundle branch block occurs
right bundle is concealed, a right bundle branch block pat- at the junction of the His bundle and right bundle, then the
tern could be maintained on the electrocardiogram. If the right bundle tissue itself may be activated by the Mahaim
right bundle is blocked fairly proximally (ie, at the junction fiber. Antegrade block to the ventricle may occur because in
Case 17 547
sinus rhythm, the ventricle and distal right bundle (which with the His bundle or ventricular signal. In any of these
may have been activated retrograde via the left bundle) are potential scenarios, the timing of the extra potential (arrow)
refractory after ventricular activation. If preexcitation occurs is expected to correlate with either the degree of preexcitation
through the Mahaim fiber, near-simultaneous activation of or the amount of fusion (if a PVC or fascicular beat occurs).
the His bundle (antegrade) and the right bundle tissue (distal That is, with more preexcitation or less fusion with the sinus
to the level of right bundle branch block) will occur. Thus, the rhythm, along with the PVC, this potential should occur rela-
right bundle tissue in sinus rhythm will not be activated early, tively earlier; thus, some beats could have a distinct potential
and this potential would then be seen elsewhere, intermingled that occurs even before the antegrade His bundle potential.
Figure C17.32
In Figure C17.32, the third beat on the tracing shows a a relatively later coupled PVC. Again, observe the consistent
more subtle manifestation of the wide QRS complex than absence of the extra potential after the His bundle ventricular
was seen previously. This may represent less preexcitation or potential whenever the QRS changes.
Figure C17.33
With continued monitoring (Figure C17.33), the unex- His bundle potential. When the atrium-to-His activation for
plained potential now occurred distinctly and with different this complex is compared with the timing of the A-H interval
timing relative to the His bundle or other potentials on the His during sinus rhythm, we know that the earlier of the 2 poten-
bundle catheter. On the HBE catheter, during the sinus beat tials (occurring early with the wide complex beat) is likely to
with right bundle branch block, the extra potential occurred be what was seen as the later potential (during sinus rhythm).
after the ventricular potential, as previously noted. When With recurrence of this phenomenon, the potential (late in
the QRS morphology changed to the wide QRS complex as sinus rhythm, early with wide QRS beats) likely is responsible
described above, a second potential clearly was seen near the for the symptomatic, intermittent, wide complex beats.
Figure C17.34
Case 17 549
Figure C17.34 shows atrial pacing. Note the prolongation Nodofascicular bypass tracts are very rare, and some
in the A-H interval with continued right bundle branch block. have questioned their existence. To distinguish between
The key finding on this tracing is that the second potential these tracts and a Mahaim fiber, recall that a Mahaim fiber
(arrow) also occurs later. Does this finding help exclude any has an AV or atriofascicular connection distinct from the
explanations for the phenomenon? Clearly, delay to the tissue normal AV node, whereas with a nodoventricular or nodo-
responsible for the extra potential occurs when there is delay fascicular tract, a portion of the AV node bypasses the dis-
through the compact AV node. Thus, the tissue could reason- tal AV node and His bundle and connects either directly
ably be assumed to be an AV node–dependent structure. The to the ventricle (nodoventricular) or into the right bundle
possibilities then would be retrograde activation of the right system. Because the proximal AV node is common to the
bundle (which would depend on ventricular activation via the nodoventricular or nodofascicular tract and the regular AV
AV node) or an AV node–dependent accessory pathway (nodo- node–His bundle conduction system, similar effects will
fascicular or nodoventricular pathway). It would be difficult be seen with atrial pacing. Thus, the 2 main possibilities
to explain the phenomenon via effects of atrial pacing with to consider in this patient are 1) intermittent right bundle
a Mahaim fiber. For this to occur, very similar decrement ectopy in sinus rhythm, occurring from a portion of the
in conduction down the Mahaim fiber and the AV node is right bundle that is distal to the location of right bundle
needed. Although this is possible, prolonged atrial pacing at branch block or 2) a nodofascicular tract inserting into the
various rates showed consistent correlation between the delay right bundle, distal to the location of antegrade right bun-
in the AV node and delay to the extra potential. dle branch block.
Figure C17.35
Figure C17.35 shows that with even more decrement in is seen, with further delay in activating the tissue responsible
conduction down the AV node, a relatively fi xed relationship for the extra (unexplained) potential (arrow).
Mahaim Nodoventricular or nodofascicular
Sinus
node
AV node
Mahaim
fiber
Fasciculoventricular
Figure C17.36 (Adapted from Macedo PG, Patel SM, Bisco SE, Asirvatham SJ. Septal accessory pathway: anatomy, causes for difficulty, and
an approach to ablation. Indian Pacing Electrophysiol J. 2010 Jul 20;10[7]:292–309. Used with permission of Mayo Foundation for Medical
Education and Research.)
Table C17.2
An Important Pseudointerval in Cardiac Electrophysiology
Pseudointerval Description Interpretation
Ventriculoatrial A shorter ventriculoatrial interval with In atrioventricular node reentry, ventriculoatrial time is shorter
interval in tachycardia than with pacing occurs in during tachycardia than with pacing
tachycardia vs various situations In antidromic tachycardia, pacing from near the site of earliest
pacing Suggests that ventriculoatrial conduction ventricular activation produces a similar ventriculoatrial interval
time is not a true interval and that when pacing at a similar cycle length as tachycardia to the
a common site (from which the ventriculoatrial interval measured from the earliest ventricular
ventricular and atrial musculature potential to the earliest atrial potential during tachycardia
are near-simultaneously activated) is If the ventriculoatrial interval during tachycardia is markedly
responsible for the focus or exit of the shorter than with pacing yet the His-atrial interval is similar with
tachycardia a similar intrahisian activation sequence, suspect a His bundle
tachycardia
Case 17 551
Th ree uncommon but important types of AV con- during sinus rhythm, then right-bundle activation occurs
duction anomalies are often confused with each other. via the nodofascicular tract or as a result of retrograde pen-
Figure C17.36 illustrates the differences between Mahaim, etration via the left bundle and across the intraventricular
nodoventricular or nodofascicular, and fasciculoventric- septum. If the proximal right bundle or the nodofascicu-
ular accessory pathways, as explained above. Note that lar tract itself is responsible for ectopy or early activation,
with a Mahaim fiber, a distinct connection between the the phenomenon shown in the tracings above would occur
atrium and the ventricle occurs through an AV node and (Table C17.2).
fascicle-like structure that often connects into the right
bundle branch. With a fasciculoventricular tract, no true In the context of the discussion above, which of the follow-
AV bypass tract occurs, and reentrant tachycardia is not ing can cause the intermittent wide complex beats?
associated with this anomaly. Here, a simple breach is pres- A. Intermittent preexcitation via a nodofascicular tract
ent in the insulation of the His bundle and proximal right B. Intermittent preexcitation via a Mahaim tract
bundle, and preexcitation of the ventricle thus occurs closer C. Right bundle ectopy
to the base than the usual right bundle exit. Note that with D. Ectopy from a nodofascicular tract or Mahaim fiber
a nodofascicular tract, a portion of the compact AV node E. A and B
bypasses the distal AV node and His bundle and connects F. C and D
into the right bundle. In this scenario, if bundle-branch Answer: F—Right bundle ectopy and ectopy from a nodo-
block is seen between the His bundle and the right bundle fascicular tract or Mahaim fiber are possible causes.
Figure C17.37
We can effectively exclude intermittent preexcitation on right bundle branch block, with fascicular ectopy occurring
the basis of the tracings shown in Figure C17.37. As before, the from the mid or distal portion of the right bundle.
extra potential in sinus rhythm continues to occur well after Invasive electrophysiologists should always be alert to
the ventricular potential on the His catheter and occurs early phenomena on tracings that allow exclusion of possibilities
during the wide complex beats. The new feature seen in this in the differential diagnosis. After a possibility clearly can
tracing is that the potential occurs even before atrial activa- be excluded (eg, preexcitation in the case being discussed),
tion at the His bundle region and very soon after activation in efforts can focus on the remaining possibilities. Note that the
the high right atrium during sinus rhythm. Conduction from information from the tracings shown so far cannot exclude
the atrium to ventricle cannot occur that rapidly, regardless of the possibility of intermittent ectopy from a nodofascicular
the type of bypass tract, so intermittent preexcitation can be or atriofascicular tract; however, this would be a rare mani-
excluded. The most likely remaining possibility is antegrade festation of a rare disease.
Figure C17.38
Because right bundle ectopy was statistically a more likely large ventricular electrograms recorded a very small potential
explanation, we placed an ablation catheter just distal to the His that correlates with a large potential seen on the His bundle
bundle to determine whether the right bundle potential could catheter. Further mapping of the mid and distal right bundle
be visualized more clearly (Figure C17.38). Note that the arrow failed to show a potential that correlated with the potential in
points to the ABL p catheter, where a small His bundle and question that always preceded the ectopic beats.
Figure C17.39
Case 17 553
For further mapping, the ablation catheter was moved to

the anterior tricuspid annulus just lateral to the His bundle. Box C17.3
Here, a large potential is seen on the ABL p catheter that occurs Points to Remember
at the same time as the potential seen on the His bundle cath- When confronted with an unusual phenomenon, a differential
eter late in sinus rhythm and right bundle branch block; it diagnosis should be created
With various pacing maneuvers and spontaneous occurrence
occurs early with the ectopic beats. Note that the arrow points
of arrhythmia or ectopy, association and dissociation from
to the signal in question now seen very early on the ablation potentials of known origin should be determined
catheter and preceding the wide QRS complex. This site was Potential mechanisms should be eliminated from the differential
near the 12:00-o’clock position in the tricuspid annulus in the diagnosis as soon as a phenomenon that precludes the
left anterior oblique view. This spike was about 2 to 3 cm from mechanism is recognized
If ablation can be performed in a reasonably safe manner, it
the mid right bundle branch location. Although the exact
often can be performed successfully after the above steps
cause of this potential is unknown, the most likely explana- are completed, even if the exact origin of an arrhythmia or
tion remaining is ectopy from a nodofascicular connection ectopy is unknown
or atriofascicular connection to the proximal right bundle.
Regardless of the origin, by using the processes of association
and dissociation, it could be determined whether this spike The purpose behind presenting a case such as the one dis-
was pathogenic for the wide complex beats (Figure C17.39). cussed above is not to prepare students for highly unusual
This site was then targeted for radiofrequency ablation. cases; rather, it is to emphasize that adherence to basic elec-
During ablation, the amplitude of this potential decreased, trophysiology principles can be helpful in highly extraordi-
and the wide-complex beats were no longer seen. nary situations, just as it is in the average case (Box C17.3).
Figure C17.40
Various reentrant or automatic tachyarrhythmias may be severe infrahisian conduction delay. In the context of junc-
seen in patients with conduction system disease. Discussed tional tachycardia or His bundle tachycardia, variations of
elsewhere in this textbook are examples of bundle branch which are described in the preceding examples, one relatively
reentrant tachycardia and interfascicular tachycardia, typi- unusual arrhythmia involves reentry within the His bundle
cally seen in patients with left bundle branch block and itself (Figure C17.40).
Split His
Figure C17.41
The patient described above had right bundle branch block be present while AV conduction is intact? In most cases, fibers
that occurred fairly proximally, possibly at the junction of the apparently are “committed” to eventually becoming the right
His bundle and the right bundle branch. The surface electro- bundle or left bundle within the compact His bundle, and
cardiogram sometimes showed right bundle branch block severe intrahisian delay or intrahisian block thus can occur
(Figure C17.41). However, the level of conduction block can with or without AV node conduction. Such prominent delay
be so proximal in the right bundle that it effectively becomes within the His bundle system may occur in patients with a rare
a distal intrahisian level of block. How can intrahisian block variant of junctional tachycardia, termed intrahisian reentry.
Case 17 555
2nd-degree intrahisian block
H H
Figure C17.42
An intracardiac electrogram (Figure C17.41), specifi- appears to be split. The preceding example described a tre-
cally in the region of the His bundle, was obtained from mendous delay between the His bundle and right bundle
the patient whose electrocardiogram was shown in Figure potentials during a right bundle branch block and possibly
C17.40. Note that the HIS dist electrogram shows 4 poten- retrograde activation of the right bundle. The patient here
tials. A fairly large atrial potential is seen at times with a does have right bundle branch block, but 2 distinct His
P wave; thus, the electrode is not in the region of the right bundle potentials are noted at a more proximal location.
bundle itself. A large ventricular potential is also seen, as Th is likely is from marked conduction delay within the His
would be expected in this location. The His bundle potential bundle itself (Figure C17.42).
After procainimide
Figure C17.43
During atrial pacing or with procainamide administration, intrahisian or infrahisian. However, the patient had a split
the phenomenon seen in Figure C17.43 was noted. AV block His potential and only the initial deflection of the His bundle
is clearly documented. Where is the level of block between potential was present in the blocked beat; this is diagnostic
the atrium and ventricle? of intrahisian block. If a “junctional” tachycardia is seen in
A. Compact AV node a patient with intrahisian delay or block, possible intrahisian
B. Slow pathway reentry should be considered.
C. Within the His bundle (intrahisian block) With further monitoring, complete AV block is seen
D. Infrahisian block (Figure C17.43). Again, the initial component of the His
E. Bilateral bundle branch block bundle potential is seen, whereas the second component is
absent.
Answer: C—Within the His bundle (intrahisian block).
A clear His bundle potential is noted after the atrial poten-
tial in the blocked beat. Thus, the level of block is either
Case 17 557
Figure C17.44
Although the level of block may be in the proximal right was straddling the level of block. In such a case, the right bun-
bundle (Figure C17.44), the large atrial potential on the His dle would have to be activated after the left bundle, left side
bundle catheter makes a distal His or right bundle location of the intraventricular septum, and transseptal conduction,
for the catheter unlikely. Further, because surface electro- which would allow activation of the ventricular myocardium
cardiograms show that the patient had right bundle branch on the right side of the septum and then retrograde activation
block, a much longer delay between the His bundle and right of the right bundle.
bundle electrogram would be expected if a mapping catheter
HA block terminates tachycardia
Figure C17.45
Table C17.3
Variants of Junctional Tachycardia
Junctional Tachycardia Potential Ablation Site
Slow-pathway tachycardia (exit through fast pathway via AV node) Slow pathway
AV node reentry with upper common pathway block Slow-pathway region
His bundle tachycardia Possible ablation at earliest His bundle activation site
Compact AV node tachycardia Unlikely that successful ablation can be performed without AV
block
Right bundle branch or left bundle branch (fascicular tachycardia) Ablation at junction of His bundle and right bundle or junction of
His bundle and left bundle; this results in bundle branch block
but AV node conduction is otherwise intact
The patient in Figure C17.45 had clinically significant (such as those presented earlier in this case series), block to
infrahisian conduction disease and rapid tachycardia. The the atria always occurred at termination of tachycardia. This
patient did not have dual AV nodal physiology, and PVCs signifies the reentrant arrhythmia, in which block of 1 limb
placed in the tachycardia did not preexcite the atrium, despite can terminate the tachycardia. This patient likely had intra-
preexciting the His by approximately 20 milliseconds. These hisian reentry, a variant of so-called junctional tachycardia,
findings argue against the diagnosis of AV node reentry. and underwent successful cryoablation at the junction of the
However, unlike the usual cases of junctional tachycardia His bundle and right bundle branch (Table C17.3).
Case 17 559
Abbreviations H-H, His-His

H-V, His-ventricular
A, atrium [f] PAC, premature atrial contraction
A-H, atrial-His PVC, premature ventricular contraction
AV, atrioventricular V, ventricle [f]
AVNRT, atrioventricular nodal reentrant tachycardia VA, ventriculoatrial
FP, fast pathway [f]
H-A, His-atrial
Case 18
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure C18.1
A 56-year-old woman presented with symptoms of recur- D. Reentrant tachycardia with the slow zone in the right
rent tachyarrhythmia. She previously underwent ablation atrium
for atrial fibrillation that involved wide-area circumferential E. All of the above are possible and equally likely
lesions and linear ablation in the right and left atria. An elec- diagnoses
trocardiogram was obtained (Figure C18.1). Answer: E—All of the above are possible and equally likely
Which diagnosis is most likely? diagnoses.
A. Automatic atrial tachycardia arising in the left atrium For patients with atrial tachyarrhythmias that occur after
B. Reentrant atrial tachycardia with the slow zone in the ablation of atrial fibrillation or after cardiac surgery, the
left atrium 12-lead electrocardiogram must be interpreted with caution.
C. Automatic atrial tachycardia arising from the right For a patient with known surgical scars or linear ablative
atrium scars, a macroreentrant tachycardia is likely, although auto-
matic tachycardias may also occur. There is no good way, on
Abbreviations are expanded at the end of this chapter. the basis of a 12-lead electrocardiogram, to know whether an
Terms with “[f]” denote abbreviations that appear in the figures only. arrhythmia is automatic or reentrant. Without knowing this
561
fundamental distinction, the correct interpretation of the The tachycardia may be automatic or reentrant, with the
P-wave axis and morphology is not possible. For example, in arrhythmogenic substrate in the vicinity of the mitral annu-
Figure C18.1, the P wave is all positive in leads V1 and V2. lus. Understand that 3-dimensional mapping by itself cannot
In an automatic tachycardia, this finding suggests that the define the mechanism of a tachycardia. At first glance, Figure
focus is located in the left atrium (posterior origin, with the C18.2 seems to show a point of early activation (blue dot), with
vector going toward the anteriorly placed leads). However, if a later activation site that is fairly symmetric from that loca-
this was a known reentrant arrhythmia, the exit site from the tion, thus suggesting a diagnosis of an automatic tachycar-
slow zone may be in the left atrium. However, in reentrant dia arising anteriorly, near the mitral annulus. However, this
arrhythmia, the exit site from the slow zone may be in the patient had multiple ablations, which cannot exclude reen-
left atrium. In structurally abnormal hearts with myocardial trant tachycardia exiting at or near the mitral annulus, with
scars, the entrance site, predominant portion of the circuit, a slow zone in a gap either in the wide-area ablation circle or
and the slow zone may be located in the intra-atrial septum between the ablation circle and the mitral annulus, particu-
or right atrium. Thus, it is crucial that the electrophysiologist larly given the paucity of mapping points in these locations.
obtain a clinical history to determine whether a macroreen- A pulmonary vein focus can be reasonably excluded
trant tachycardia or an automatic tachycardia is present before because the activation sequence appears to proceed toward
analyzing P waves, interpreting intracardiac electrograms, or each of the pulmonary veins. If a circumferential catheter
determining an ablation strategy. was placed in the pulmonary veins, and even if residual pul-
monary vein potentials were present, they would be expected
to activate after the far-field left atrial signal. If the 12-lead
electrocardiogram or even detailed point-to-point electro-
anatomic mapping cannot define whether a tachycardia is
automatic or reentrant, how should the electrophysiologist
make this distinction (Figure C18.3)? (Note in the figure that
the stars, circles, and arrows indicate ablation sequences and
sites.)
LS
RS
RI LI
Figure C18.3
MVA
Although the P-wave morphology clearly cannot be used
Figure C18.2 to define the mechanism of an atrial arrhythmia, it is use-
ful to know the morphology associated with automatic atrial
Figure C18.2 shows a detailed electroanatomic activation tachycardias arising from the more common locations. The
map in another patient with tachycardia after ablation of primary sites associated with automatic atrial tachycardias,
atrial fibrillation. especially in otherwise structurally normal hearts, include
the crista terminalis, coronary sinus ostium, and superior
Considering the activation sequence in Figure C18.2 vena cava (SVC) in the right atrium. Common left atrial sites
(red circles indicate ablation lesions), what is a possible for ectopic atrial tachycardia include the pulmonary vein, the
diagnosis? mitral annulus, the vein of Marshall, and left atrial append-
A. Automatic atrial tachycardia occurring near the mitral age. Specific characteristics associated with arrhythmias from
annulus these sites are discussed elsewhere in this textbook.
B. Mitral isthmus–dependent atrial flutter The advantage of knowing these common sites is that the
C. Pulmonary vein tachycardia level of suspicion for automatic atrial tachycardia is higher
D. A and B are possible if the P-wave morphology during tachycardia is consistent
E. All of the above with an origin in one of these locations. For example, if a
Answer: D—A and B are possible. biphasic P-wave is observed in lead V1 (similar to that seen in
Case 18 563
sinus rhythm), with large positive P waves in leads II, III, and common site for automatic atrial tachycardia, that mecha-
aVF (inferior access) and a positive P wave in lead I, then a nism would also be suspected.
high crista terminalis site is suspected. Because it is a known
Table C18.1
Differentiating Between Automatic and Reentrant Atrial Arrhythmia
Characteristic Focal Tachycardia Reentrant Tachycardia
Inducibility Often difficult; highly dependent on sedation and Typically reliably inducible with extrastimuli
autonomic tone
Appearance on Activation maps suggest a unique origin with clear Continuous electrical activation can be visualized
3-dimensional outward propagation from that sitea throughout the entire cardiac cycle (cycle length of
mapping system the tachycardia)b
Unipolar potentials At the site of origin, the unipolar potential is No potential is specifically associated with reentrant
completely negative tachycardia
Propagation loop No loop is usually visualized, but it can manifest in Often visualized; however, passive activation of a
very diseased hearts because uniform outward protected zone should be excluded
propagation is not allowed
Pace map Pace map at the site of earliest activation usually Pace map replication may be seen at the exit site or
replicates the P-wave morphology of tachycardia close to the exit site (from the slow zone of the
circuit)
Entrainment Overdrive suppression will be seen; criteria for Remains the main diagnostic maneuver
entrainment (if strictly applied) will not be met
a
Not diagnostic in severely diseased hearts or if passive activation of another chamber (that does not contain the circuit) causes a pattern of outward propagation, even with
a primarily reentrant arrhythmia.
b
The entire cycle length should be accounted for; if it is not, mapping may be incomplete or may have been performed in a chamber not containing the circuit.
Unipolar recording of origin of the focal tachycardia. Figure C18.4 illustrates

the principle involved. With a unipolar recording electrode
Recording (widely spaced bipolar or true unipolar recording electrode),
electrode if the activation wave front is traveling toward the recording
+ electrode, then a positive deflection on the unipolar electro-
gram is seen. After the wave front passes through and travels
beyond the recording electrodes, a negative deflection is seen.
When the electrode is exactly at the site of origin of the tachy-
+
cardia, there is no positive deflection and a completely nega-
tive QRS complex is observed.
+ With 3-dimensional mapping, the unipolar electro-
grams can also be analyzed to further confirm the loca-
tion of earliest activation site (origin of the tachycardia), as
suggested by the activation map. Several important cave-
ats, however, should be kept in mind. First, if an epicardial
origin of the tachycardia is seen, an R wave (initial positive
deflection) may be seen on the unipolar signal at multiple
sites close to the origin of the tachycardia. Second, these
Figure C18.4 (Courtesy of William G. Stevenson, MD, Harvard findings are less sensitive if very large electrodes are used
Medical School, Boston, Massachusetts. Used with permission.) and if true unipolar recordings (or widely spaced bipolar
recordings) are used. Third, reentrant tachycardia may
Table C18.1 outlines the differences between a focal origin also show an all-negative QS deflection if the catheter is
automatic atrial tachycardia and reentrant atrial tachycardia. at the site of breakthrough from one atrium to the other
During point-to-point mapping, one feature that can suggest a (Bachmann bundle) or close to the exit of the tachycardia,
good ablation site for automatic tachycardia is an all-negative where widespread activation from that point mimics an
reflection (QS complex) on the unipolar recording at the site automatic arrhythmia.
Figure C18.5
Just as some sites of origin for an automatic atrial tachy-

cardia are statistically more prevalent (and allow electrophys-
iologists to judge whether a particular P wave morphology
suggests an automatic arrhythmia), so are some circuits
involved in macroreentrant arrhythmia. Figure C18.5 illus-
trates the possible circuits for left atrial macroreentry,
including after wide-area circumferential ablation. The elec-
trophysiologist should always think from first principles of
where the scars and electrically inert anatomic boundaries
are located. For example, the pulmonary vein, mitral annu- Figure C18.6
lus, and fossa ovalis are natural boundaries to a circuit.

If a scar has been identified or is known from previous The multiplicity of possible circuits in patients with mac-
surgical procedures, a number of potential circuits should be roreentrant atrial arrhythmias makes it very difficult to per-
immediately visualized and remembered for further entrain- form detailed entrainment mapping, identify the slow zones,
ment mapping or when developing a strategy to find the opti- and ablate each of these circuits. Alternatively, an adjunct to
mal ablation line. For example, a tachycardia circuit with a entrainment mapping is to map regions of atrial scars and
slow zone just superior to the right upper pulmonary vein may areas in the primary macroreentrant tachycardia circuit that
be identified. To transect that circuit, an ablation line could be produce fractionated or double potentials. In Figure C18.6,
drawn from the right upper pulmonary vein (near the roof) the grey area represents scar, the pink dots indicate fraction-
to the mitral annulus or sometimes to the tip of the left atrial ated potentials, and the blue dots indicate double potentials.
appendage. However, if ablation was performed previously on The map was created during an atrial flutter with a cycle
the roof of the left atrium or if the patient had a scar in that length of 290 milliseconds.
region, a more appropriate ablation line would extend from
the right upper pulmonary vein to the scar. Because of the Which statement is true with reference to the electroana-
possible multiplicity of these circuits, particularly for patients tomic map in Figure C18.6?
who have undergone prior procedures, and the high number A. An automatic tachycardia arising in the inferior poste-
of electronically inert anatomic boundaries in the left atrium, rolateral right atrium (red area) is possible
the scarred regions in the heart must be defined accurately B. The left atrium is unlikely to house a significant portion
when mapping the reentrant flutter. of the tachycardia circuit
C. Ablation from the scar to the inferior vena cava (IVC)
will likely terminate the flutter
D. Ablation from the scar to the SVC will likely terminate
the flutter
E. Further mapping is indicated
F. All of the above
Answer: F—All of the above.
Case 18 565
If this is a macroreentrant tachycardia, has the entire cir-

cuit been mapped? Consider that the flutter cycle length was
290 milliseconds and the activation sequence in this map had
a cycle length of 284 milliseconds (+212 to –72 milliseconds).
Thus, it is highly unlikely that a large portion of the tachycar-
dia circuit is located outside of the right atrial region shown
in this map. However, the possibility that an automatic tachy-
cardia arising in the posterolateral inferior right atrium (red
region) cannot be excluded. Although symmetric propaga-
tion of the wave front from that site is expected, unidirec-
tional block between the scar and the IVC may occur in a
scarred atrium and cause the propagation wave front shown
in the map. Entrainment maneuvers will identify the mecha-
nism of the tachycardia.
If a macroreentrant tachycardia is propagating around
this scarred zone, then this arrhythmia likely can be elimi-
nated successfully by various ablation lines such as from the
scar to the IVC, from the scar to the SVC, from the scar to the
tricuspid annulus anteriorly, and likely from the scar to the
region of double potentials shown more posteriorly. Which
ablation line should be drawn? Generally, the shortest abla-
tion line that does not involve regions near critical structures Figure C18.7
(eg, coronary artery, atrioventricular [AV] node, etc) should
be drawn. Most ablationists would draw the line from the scar With further points taken in the lateral wall (Figure C18.7),
to the IVC. If drawing a line to the SVC, care must be taken the scar and propagation wave front are better defined. Note
to avoid damage to the phrenic nerve. Finally, note that very the dark red region (arrow) shown between the sites of early
few mapping points have been taken around the region of the activation (relative to a reference) and late activation (purple
scar. It is unusual for an arrhythmogenic scar to be so small region). This is a programmable feature that points out where
and discrete; therefore, further mapping is indicated. early meets late activation. Care must be taken in interpreting
this type of annotation. In macroreentrant arrhythmias, the
red-colored region depends on the reference point selected
and the setting of the windows (number of milliseconds before
and after the reference); it has no specific or inherent mean-
ing. Despite this, however, quick visualization of the circuit is
sometimes facilitated by such programmed options.
A second reason to carefully map out the scars in their
entirety is because scars may be heterogenous. In this situ-
ation, multiple scars may have coalesced, but intervening
viable tissue can form arrhythmogenic channels for many
other macroreentrant circuits. If this has occurred, then
those channels should be ablated. Alternatively, the scar can
be encircled and anchored to an anatomic obstacle such as the
tricuspid annulus or IVC.
Figure C18.8
For this patient, ablation was performed from the scar

to the IVC, with termination of the flutter during ablation
and subsequent noninducibility of that flutter. Figure C18.8
shows termination of the tachycardia during radiofrequency
ablation. Note that even with the multielectrode catheter
(IS 1,2–IS 19,20), the mechanism of tachycardia (automatic
vs reentrant) cannot be determined. Thus, the mechanism
of tachycardia cannot be determined with any type of map-
ping; it must be defined with pacing maneuvers, specifically
entrainment.
Figure C18.9
An electroanatomic map (Figure C18.9) was obtained

from a patient with atrial tachycardia after a pulmonary vein
isolation procedure. The right atrial map is shown. The cycle
length of the tachycardia was 310 milliseconds.
Case 18 567
Which diagnostic possibility can be excluded on the possibility of a macroreentrant tachycardia exclusively in
basis of this high-density map of the right atrium during the right atrium can be excluded. The second observation
tachycardia? would be that the earliest site of activation is in the supe-
A. A macroreentrant atrial tachycardia in the right rior septal right atrium, near the Bachmann bundle. Early
atrium activation is also seen more posteriorly in the fossa ovalis–
B. A macroreentrant atrial tachycardia in the left atrium coronary sinus region. Th is fi nding also makes an auto-
C. An automatic tachycardia in the left atrium matic tachycardia from the right atrium unlikely because
D. An automatic tachycardia in the coronary sinus it is difficult to explain 2 nearly simultaneous and early
musculature beats from spatially separated sites. The electrophysiologist
E. All of the above should consider a left atrial tachycardia (macroreentrant or
automatic) that passively activates the right atrium. In gen-
Answer: A—A macroreentrant atrial tachycardia in the
eral, if multiple sites in the right atrium appear early, or if
right atrium.
the earliest site is on the intra-atrial septum, the left atrium
Upon examination of the electroanatomic map shown in should be mapped before attempting ablation. Note also, in
Figure C18.9, the fi rst main observation is that the tachycar- the peritricuspid annular atrium (isthmus), there is a fusion
dia cycle length far exceeds the mapped activation interval. of activation wave fronts on the lateral wall; this shows that
With a macroreentrant tachycardia that is confi ned to the the tachycardia is not an isthmus-dependent flutter and also
right atrium, a high-density map of the right atrium should shows that the IVC tricuspid valve isthmus was not blocked
include nearly all of the cycle length; thus, in this case, the by prior ablation.
Vent. rate 131 bmp

PR interval 96 ms
QRS duration 152 ms
QT/QTc 384/567 ms
P-R-T axes * 102 81
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure C18.10
The electrocardiogram in Figure C18.10 was obtained previously emphasized, an automatic atrial tachycardia could
from a patient with easily induced sustained atrial flutter not be completely excluded, either. Entrainment maneuvers
after a pulmonary vein isolation procedure. The flutter wave were performed, and the mechanism of the arrhythmia was
morphology is not typical of isthmus-dependent flutter. As confirmed to be macroreentrant.
(A) (B)
Figure C18.11
A detailed electroanatomic map of the left atrium was highly unlikely. If the cavotricuspid isthmus flutter was coun-
obtained (Figure C18.11). Panel A shows the posteroanterior terclockwise in activation, then after exciting the slow zone
view, panel B shows the inferior view. The black dots on the in the isthmus, activation should proceed either via the coro-
posterior left atrium are esophageal points. Note especially nary sinus or through the fossa ovalis and Bachmann bun-
the activation pattern around the mitral annulus in the infe- dle region to activate the left atrium with a septal-to-lateral
rior view. The dark red dots represent ablation points, which sequence. If clockwise isthmus-dependent atrial flutter was
were created in a wide-area circumferential manner around present, then activation via the Bachmann bundle would
the pulmonary vein. The circumferential lesion around the be expected to occur, even before exit through the isthmus
left-sided vein was anchored to the mitral annulus by linear slow zone to the lateral wall of the right atrium. Thus, typical
ablation. cavotricuspid isthmus–dependent flutter can be reasonably
excluded.
Which observation is supported by the map shown in
Automatic tachycardia cannot be excluded, although the
Figure C18.11?
cycle length of the mapped tachycardia is fairly close in its
A. Cavotricuspid isthmus–dependent flutter can be
approximation of the cycle length of the tachycardia itself.
excluded
Just because an ablation line was created does not indicate
B. Mitral isthmus–dependent flutter can be excluded on
whether transmural lesions have been placed all across the
the basis of the prior ablation
line, with resulting desirable conduction block. A draw-
C. An automatic atrial tachycardia can be excluded
back of mapping systems is that ablation points often are
D. A flutter circuit on the left atrial roof between the supe-
cataloged on the basis of operator preference, rather than
rior veins is possible
on objective data (eg, tissue contact and a transmural lesion
Answer: A—Cavotricuspid isthmus–dependent flutter can
being made). With further entrainment mapping, a perimi-
be excluded.
tral valve isthmus flutter was diagnosed, with a gap in the
The cycle length of the mapped flutter was 210 millisec- ablation line between the left-sided ablation circle and the
onds, making cavotricuspid isthmus–dependent flutter mitral annulus.
Case 18 569
Figure C18.12
With further ablation at the region between the left infe- circuits around the mitral annulus, as is often done around
rior pulmonary vein and the mitral valve, tachycardia was the tricuspid annulus. However, multielectrode catheter
terminated (Figure C18.12 shows flutter termination). Note stability is more difficult on the left side because portions
how the highly fractionated signals after ablation show of the catheter may prolapse into the left atrial appendage
slowing of conduction through this left-sided isthmus. or a pulmonary vein, or the catheter may slide into the left
Multielectrode catheters (IS 1,2–IS 19,20) can be used to map ventricle.
Figure C18.13
Although ablation between the mitral annulus and the be present in the coronary sinus musculature but not the left
left lower pulmonary vein terminated the tachycardia, bidi- atrial mitral isthmus. At other times, block may be present in
rectional conduction block across this ablation line should the atrial tissue between the left lower pulmonary vein and
be ensured. Presently, no studies have clearly shown that the mitral annulus, but conduction is still present in the cor-
bidirectional block is a required end point for ablation at onary sinus musculature because of these multiple connec-
this site, but the situation is analogous to cavotricuspid isth- tions. Thus, it is best to analyze both the left atrial endocardial
mus ablation. For the latter situation, there are data show- signals and the coronary sinus activation sequence by using a
ing that recurrence is less common when bidirectional block multielectrode catheter.
is obtained. To demonstrate the necessity for obtaining Another important cause of difficulty in demonstrating
bidirectional block for the mitral isthmus ablation line, a bidirectional block with the left atrial isthmus is the relatively
closely spaced multielectrode catheter (IS 1,2–IS 19,20) was rapid conduction that can occur from the pulmonary vein to
placed along the mitral annulus, straddling the ablation line more proximal portions of the mitral isthmus, via the poste-
(Figure C18.13). In this example, pacing is from electrodes rior left atrium. Thus, if pacing from the mitral annulus lateral
IS 19,20. Note that electrodes IS 1,2 through IS 5,6 show a to the ablation line, conduction may proceed around the pul-
reversed activation sequence. This strongly suggests that monary veins to the more medial portions of the mitral annu-
lateral-to-medial conduction block is present. A similar lus; the wave front at these locations proceeds from the mid
maneuver can be repeated with pacing from electrodes IS 1,2 left atrium and coronary sinus to the proximal left atrium and
and checking for reversal of wave front in electrodes IS 19,20 coronary sinus, giving the appearance of continued conduc-
through IS 13,14. However, it can be difficult to position the tion. This phenomenon is analogous to lower-loop conduc-
multielectrode catheter in this location and maintain stable tion giving rise to the appearance of continued conduction
contact without prolapsing into the ventricle or one of the across the cavotricuspid isthmus, even when blocked by abla-
pulmonary veins. tion. This concept is worth understanding fully because it is
It is also important to appreciate that the CS catheter applied to various situations, including left atrial ablation. For
alone is inadequate for demonstrating conduction block. This example, appreciating conduction around or into and out of
is because of the multiple connections between the coronary the pulmonary veins affects how to determine whether block
sinus musculature and the left atrium. Sometimes, especially is present across a line placed between the pulmonary veins
for ablation within the coronary sinus, conduction block may and the mitral isthmus.
Case 18 571
Figure C18.14
In Figure C18.14, a multielectrode catheter (IS 1,2 IS 19,20) the lateral wall of the cavotricuspid isthmus. Before ablation,
has been placed across the cavotricuspid isthmus; poles 1,2 pacing from the proximal coronary sinus resulted in a clear
are just engaging the coronary sinus and poles 19,20 are on medial-to-lateral propagation sequence on the IS catheter.
Figure C18.15
The tracing shown in Figure C18.15 was obtained further ablation is required. However, IS 9,10 through IS 1,2
after ablation of the cavotricuspid isthmus. Again, pac- show lateral-to-medial activation (reversal of activation), sug-
ing is from the mid or proximal coronary sinus. Note that gesting conduction block without the need for further abla-
IS 11,12 through IS 19,20 show a medial-to-lateral propagation. The reason for this discrepancy is because of lower-loop
tion sequence, consistent with continued conduction. Thus, conduction.
Crista terminalis
Lower-loop reentry
TV
IVC Typical
flutter
CS CS
Pacing Pacing
site site
IVC IVC
Figure C18.16
In Figure C18.16, the left-side schematic shows pseudocon- (pulmonary vein in the case of the mitral isthmus) occurs
duction. True block is present in the cavotricuspid isthmus, rapidly and then conducts in a lateral-to-septal direction,
but the pacing wave front propagates posterior to the IVC, fairly close to the ablation line, giving rise to the appear-
reaches the lateral wall, and proceeds in an inferior-to-superior ance of block (reverse activation sequence). High-density
direction in the lateral wall. Thus, if electrodes were placed mapping, perhaps with the aid of electroanatomic mapping,
only on the lateral wall, conduction would still appear. The can be used to detect at least a partial wave front conducting
same phenomenon can occur elsewhere (eg, around the left across the ablation line. Differential site pacing can also be
lower pulmonary vein). Thus, multielectrode catheters must performed to determine whether conduction is still present.
straddle the ablation line. If 2 pacing sites medial to the ablation line are chosen and if
The right-side schematic of Figure C18.16 shows pseudo- the local interval across the ablation line is unchanged, con-
block. This phenomenon can also occur around the pulmo- duction is still present. In contrast, if the interval across the
nary vein. Here, conduction is still occurring, albeit slowly, ablation line decreases as the distance between the pacing site
across the ablation line; however, conduction around the IVC and ablation line increases, then block is likely present.
Case 18 573
Figure C18.17
In Figure C18.17, note that during ablation, the first 2 a left atrial ablation line, a multielectrode catheter should be
beats show an activation sequence suggestive of conduction placed across the ablation line so the transition in activation
across the ablation line, but the mechanism of this activation sequence can be seen during ablation. This helps distinguish
sequence remains unclear. Note the transition on the third between slow conduction, pseudoconduction, pseudoblock,
beat to a clear reverse sequence. This transition is easy to true block, and other mechanisms.
observe and is diagnostic of block. Thus, to check block across
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure C18.18
Return to the initial tracing that started the discussion to entrain the tachycardia, overdrive suppression was clearly
about automatic and reentrant arrhythmias after atrial fibrilla- evident. The extent of the suppression varied with the rate of
tion ablation and review again the 12-lead electrocardiogram atrial pacing, with faster pacing rates resulting in more sup-
of the observed tachycardia (Figure C18.18). During attempts pression. None of the criteria for entrainment were met when
pacing faster than the tachycardia. The tachycardia was faster

but with a P-wave morphology identical to that when isopro-
terenol was used. Together, these findings strongly suggest
that the tachycardia was caused by enhanced automaticity.
DCS
Unlike the situation with macroreentry, analysis of the
P-wave morphology can be quite useful for automatic tachy-
cardia. The P-wave vector allows a reasonable guess regarding
the site of origin of the tachycardia and thereby simplifies the
mapping procedure.
For the electrocardiogram shown in Figure C18.18, which
site of origin is least likely for this automatic tachycardia?
Vein of
A. High crista terminalis Marshall
B. Left lower pulmonary veins
C. Right lower pulmonary veins
D. Mid coronary sinus
E. Vein of Marshall
Answer: A—High crista terminalis. CSO
Careful analysis of the P-wave morphology during this
automatic atrial tachycardia allows reasonable exclusion
of several areas that are known as more common sites of
automatic atrial tachycardia. The P wave is all positive in Figure C18.19
lead V1. This strongly suggests an origin in the left atrium.
Occasionally, tachycardias arising in the posterior wall of the Figure C18.19 shows the ablation site that successfully
right atrium will be predominately positive in lead V1 (vector terminated the tachycardia shown in Figure C18.18. Careful
moving from posterior to the anteriorly placed V1 lead); how- electroanatomic mapping was performed in the coronary
ever, the later left atrial activation that moves away from V1 sinus, the vein of Marshall, and the ostia of other smaller
will produce at least a small negative terminal component to atrial veins. The activation sequence timing from sites at or
the P wave in lead V1. Leads II, III, and aVF show a predomi- near the inferior pulmonary vein ostia was compared with
nantly negative P wave, which suggests that the origin of the that from the inferoposterior left atrium. Note that ablation
tachycardia is close to the base. Leads aVR and aVL show a points (red dots) are also seen around the coronary sinus
positive P wave, again suggesting an origin in the posteroin- ostium. The earliest site of activation was recorded in a cath-
ferior region of the left atrium. eter placed within this vein. When the vein of Marshall is the
A high crista terminalis site would typically produce a site of earliest activation, options for ablation include encircl-
biphasic P wave in lead V1, with an early positive component ing the ostium of the vein of Marshall, ablation within the
and a terminal negative component. Further, the P waves vein of Marshall, ablation in the left atrium on the ridge that
would be strongly positive and upright in leads II, III, and separates the left-sided pulmonary veins from the left atrial
aVF (vector proceeding from the superior to the inferior appendage, and in some instances, isolation of the coronary
leads). The posteroinferior left atrium is anatomically com- sinus musculature. In this patient, isolation at the ostium of
plex, with the musculature of both inferior pulmonary veins, the vein of Marshall successfully eliminated the tachycardia.
the posteroinferior left atrium itself, the coronary sinus, and
one of the epicardial atrial veins (including possibly the vein In Figure C18.19, the circumferential ablative lesions (red
of Marshall). All are possible sites of origin for this tachycar- dots) have been placed at the coronary sinus ostium. Which
dia. Thus, among the choices presented, the one that can be potential complication(s) may occur after isolation of the
excluded most easily is an origin in the high crista termina- coronary sinus ostium?
lis. Given the isoelectric nature of the P wave in lead I, an A. AV block
origin for the tachycardia in the left lower pulmonary vein is B. Coronary sinus stenosis
unlikely. Because the tachycardia was seen after pulmonary C. Ventricular diastolic dysfunction
vein isolation and because there was no evidence of conduc- D. Posterior coronary arterial damage
tion into the vein when this tachycardia was induced, both E. All of the above
lower veins can be excluded as potential sites. In this situ- Answer: E—All of the above.
ation, it is important to consider the vein of Marshall as an
origin for the tachycardia. The vein of Marshall is a remnant Ablation at the roof of the coronary sinus can injure the
of the left SVC and typically drains into the coronary sinus in compact AV node. The compact AV node is located in the
the plane between the left lower pulmonary vein and the left triangle of Koch, which is immediately superior to the roof
atrial appendage. of the coronary sinus ostium. Thus, when performing a
Case 18 575
circumferential ablation around the coronary sinus ostium, Another rare situation in which the coronary sinus may be
the roof lesions must be placed more left ward. Coronary completely isolated from the right and left atria occurs when
sinus stenosis also has been observed. Typically, these lesions an epicardial (vein-related) bypass tract connects the atrium
are well tolerated and found incidentally when trying to place to the ventricle via the coronary sinus musculature. Ablation
left ventricular pacemaker leads. However, complete occlu- may not be possible or recommended at the site of ventricular
sion of the coronary sinus can increase ventricular edema insertion because of the proximity of the posterior descending
(venous subfusion) and cause diastolic ventricular abnormal- artery or other arterial branch. The atrial insertions to these
ities. Branches of the right coronary artery and the posterior “epicardial pathways” may occur at multiple sites, including
descending artery itself may be damaged when ablating at the the right atrium via the coronary sinus ostium and the left
floor of the coronary sinus ostium, especially if the catheter atrium via the multiple left atrial coronary sinus connections.
inadvertently enters the middle cardiac or posterior cardiac Thus, one ablation technique in this situation is to isolate the
vein. coronary sinus. This procedure is exceedingly difficult and
Why is isolation of the coronary sinus desirable? The most involves circumferential ablation at the ostium, with map-
common reason for performing this type of ablation is to ping and ablation of each left atrial–coronary sinus connec-
ablate interatrial flutters. tion. If it is accomplished successfully, preexcitation will be
lost and reentrant tachycardia will be uninducible. However,
automatic atrial tachycardias arising from the coronary sinus
muscle will still show a preexcited pattern and can conduct
rapidly to the ventricle via these pathways.
Figure C18.20
LS
RS
The coronary sinus is one of the main interatrial connec-
tions. The left atrium and right atrium are electrically con-
nected, primarily via the Bachmann bundle, but muscular
connections also occur through the fossa ovalis and consis-
tently via the coronary sinus. As shown in Figure C18.20, the LI
RI
coronary sinus can form an important limb for the circuit of
macroreentrant tachycardias; in addition, the musculature of
this vein or the vein of Marshall can be a source of automatic
tachycardia. (The white arrow in Figure C18.20 signifies the
activation sequence.) The musculature of the right atrium
is continuous with the coronary sinus musculature, which
MVA
interdigitates with the left atrial musculature through the left
atrial coronary sinus connections. Thus, a large macroreen-
Figure C18.21
trant flutter loop may be created by right atrial activation that
proceeds to the left atrium via the Bachmann bundle, with
left atrial conduction coming back to the right atrium via the Figure C18.21 is an electroanatomic map after wide-area
coronary sinus muscles. In this situation, one option is to iso- circumferential ablation of tachycardia. This tachycardia also
late the coronary sinus. showed overdrive suppression that could not be entrained.
The coronary sinus may also serve as a conduit for con- Another common site for automatic tachyarrhythmias in the
duction across an ablation line that connects the lower pul- left atrium is the perimitral annular atrial myocardium; these
monary veins to the mitral annulus. Thus, even if complete tachyarrhythmias may occur even after pulmonary veins are
bidirectional block in the atrial tissue is obtained, conduc- isolated. For reasons that are not entirely understood, the
tion into the musculature of the coronary sinus (from the atrial tissue near the mitral annulus has an increased propen-
left atrium distally and then exiting more proximally) allows sity for atrial tachycardia, and the ventricular tissue around
the wave front of conduction to proceed back into the atrium the mitral annulus, particularly in the region of the aortic
with maintenance of a macroreentrant circuit (Figure C18.20, mitral continuity, has an increased propensity for premature
green, yellow, and blue circles). ventricular contractions and ventricular tachyarrhythmia.
Figure C18.22
Frequent premature atrial contractions (PACs) occurred the P-wave morphology during tachycardia. Radiofrequency
from the atrial aspect of the aortic-mitral continuity. Figure energy delivered at this site successfully eliminated the
C18.22 shows complex and early activation on the ABL d cath- tachycardia.
eter. The P-wave morphology of these PACs was identical to
LS
RS
LI
RI
Figure C18.23
As shown in Figure C18.23, energy delivery during the after ablation of atrial fibrillation cannot be assumed to be
tachycardia resulted in brief acceleration of the arrhyth- macroreentrant from gaps in the ablative line, and auto-
mia and then termination (arrow and blue dot indicate the matic tachycardia (if that mechanism is shown with pacing
successful ablation site). Additional ablative lesions (red maneuvers) should be mapped and ablated at the site of earli-
dots) were delivered around this site. Tachyarrhythmias est activation.
Case 18 577
Vent. rate 96 bmp

PR interval * ms
QRS duration 92 ms
QT/QTc 342/432 ms
P-R-T axes 78 140 107
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure C18.24
The electrocardiogram in Figure C18.24 was obtained flutter is far more complex than mapping and ablation of a
from a patient with inducible atrial tachycardia after ablation focal automatic tachycardia.
for atrial fibrillation.
Which method is useful for ablating macroreentrant atrial
Which diagnosis can be excluded after considering this tachycardia?
electrocardiogram? A. Map and ablate at the site of earliest atrial activation
A. Macroreentrant right atrial flutter B. Use a 3-dimensional mapping system and ablate at the
B. Macroreentrant left atrial flutter “red” area (the earliest activation relative to a reference
C. Interatrial flutter potential)
D. Atrial fibrillation C. Use a noncontact mapping system and ablate at the site
E. None of the above of first recorded activation in that flutter cycle
Answer: E—None of the above. D. Use entrainment mapping to define the slow zone and
circuit of the tachycardia; perform linear ablation to
Highly complex P wave or flutter wave morphology may transect the slow zone
be seen after multiple linear or circumferential ablations for E. None of the above
atrial fibrillation. A portion of the atrium could be fibril-
Answer: D—Use entrainment mapping to define the slow
lating, and another portion of the atrium or atrial chamber
zone and circuit of the tachycardia; perform linear ablation
could have organized flutter. Because of the nearly continu-
to transect the slow zone.
ous electrical activity seen on the electrocardiogram, the
start and end of the flutter wave are difficult to discern, as Macroreentrant tachycardias do not have an early site of
is the exit from the flutter circuit. Sometimes, even typical activation; that is, electrical activity occurs throughout the
atrial flutter will look highly atypical if the left atrium previ- cardiac cycle. If an electrode is placed anywhere in the atrium
ously was extensively ablated. This is because the flutter-wave and the timing of the potential at that site is, for example,
morphology in right atrial typical flutter is dependent on the 60 milliseconds before the onset of the flutter wave, there
method of left atrial activation. will always be another site that is 70 (or 80, or 100, etc) mil-
Although automatic atrial tachycardia is sometimes liseconds ahead. Thus, to map and ablate at the site of earliest
seen in patients with atrial fibrillation after ablation, by far activation is meaningless. With a 3-dimensional electroana-
the most common arrhythmia seen after a pulmonary vein tomic mapping system, a visual representation of the timing
isolation procedure is macroreentrant atrial tachycardia or of potentials relative to a reference (eg, coronary sinus poten-
atypical atrial flutter. Mapping and ablation for atypical atrial tial, P wave, etc) is created. Thus, an arbitrary site of early
activation (red area) is also of no particular significance when It sometimes is difficult to know where detailed entrain-
deciding the site of ablation (see Chapter 3). Similarly, with ment mapping should be performed. A meticulously per-
noncontact mapping, ablating at the site of the first recorded formed, high-density electroanatomic map may give visual
potential in a flutter cycle is fundamentally the same as ablat- clues about the flutter circuit location (on the basis of the
ing an even earlier or later site. mapped cycle length and propagation sequence) and allow
The only established method to define a macroreentrant targeted entrainment mapping. This technique is discussed
tachycardia circuit is entrainment mapping (see Chapter 5). in Chapter 3.
However, when an atrium has multiple scars, shows highly
fragmented potentials because of previous ablation for atrial
fibrillation, and has a propensity for multiple atrial flutter cir-
Box C18.2
cuits, entrainment mapping can be extremely difficult. First,
Method of “Pinging”
when attempting to entrain a particular flutter, the flutter
may terminate or change morphologically. Second, because Sites to attempt entrainment
Cavotricuspid isthmus
of the highly fractionated potential, it can be very difficult to
Proximal coronary sinus
know which signal should be taken for exact measurements Distal coronary sinus
to determine whether the pacing catheter is within the flutter Left atrial dome
circuit. Finally, complete mapping of the circuit and ablation Left atrium, across the coronary sinus
is time consuming, and in a patient with 6 or more induc- High right atrium near the superior vena cava
Intervals to measure
ible flutters, entrainment mapping is impractical if used as
Difference between tachycardia cycle length and postpacing
the sole method to map and ablate a particular tachycardia. interval
Thus, in modern ablation practice, empiric linear ablation Interval between stimulus and onset of flutter wave (STIM –
(connecting scars or electrically inert structures [eg, pul- P wave – local electrogram near the pacing electrode to
monary veins, prior ablation scars, prior surgical atriotomy onset of the flutter/P wave [EGM-P wave])
Premise
scars, mitral valve, and tricuspid valve]) is combined with
The shorter the differences in these intervals, the closer the
brief entrainment mapping at sites between such obstacles mapping catheter is to the flutter circuit
before ablation.
A second technique involves brief attempts at entrainment,

checking the difference between the postpacing interval and
Box C18.1 tachycardia cycle length and the difference between the stim-
Steps for Entrainment Mapping ulus–to–P-wave interval and local potential–to–P wave inter-
1. Pace the atrium at a slightly faster rate than the macroreen-
val. Entrainment at various sites in the right and left atria and
trant tachycardia comparing the results from these sites may indicate a likely
2. Ascertain atrial capture location for the circuit. This technique, sometimes termed
3. Upon cessation of pacing, determine whether the last paced pinging, involves empiric attempts to entrain at the tricus-
beat is entrained but not fused (using activation sequence of pid annulus, high right atrium, roof of the left atrium, mitral
intracardiac potentials in the case of atrial arrhythmia)
4. After establishing the diagnosis of macroreentry, repeat
annulus, coronary sinus, and near the atrial appendage. The
entrainment maneuvers at different sites in the atrium to premise of pinging is that as the pacing catheter gets closer
assess whether the postpacing interval approximates the to the circuit, the differences between the tachycardia cycle
tachycardia cycle length (pacing electrodes are within the length and postpacing interval minimize, as does the differ-
circuit) ence between the stimulus to the onset of the P wave and the
5. Ascertain whether concealed entrainment or manifest
entrainment (fused activation sequence) is present
local potential to the onset of the P wave (Box C18.2).
6. Assess the difference between 1) the interval from the pacing Before starting the pinging or classical entrainment map-
stimulus to the onset of the surface P wave; and 2) the inter- ping, it is important to exclude continued activity from a
val from the local potential at the site of the pacing catheter pulmonary vein that may not yet be completely isolated.
during tachycardia to the onset of the P wave Otherwise, frequent changes in flutter morphology will be
seen as the more rapid “driver” that continuously terminates,
reinduces, and changes one flutter to another.
A single macroreentrant atrial flutter can sometimes per-

sist after pulmonary vein ablation and empiric linear abla-
tion. In this situation, the entire procedure would be a failure
if the ablationist is unable to map and ablate the remaining
persistent flutter. In this situation, entrainment mapping can
be extremely helpful. The steps to entrainment mapping are
listed in Box C18.1 and discussed in Chapter 5.
Case 18 579
RS LS
RI LI
Figure C18.25
Figure C18.25 shows circumferential catheter mapping in are late, suggesting passive activation of the pulmonary veins.
various pulmonary veins during flutter. Note in each instance Thus, further ablation in or around the pulmonary vein is
that either no activity is noted within the pulmonary vein unlikely to treat the sustained flutter.
(absent pulmonary vein potential) or the near-field potentials
RA HIS LA
CS
IVC
Figure C18.26
After an automatic driver is excluded, then the entrain- spaced areas and measuring the important intervals enumer-
ment procedure can begin. Figure C18.26 is a schematic ated above.
(left anterior oblique view) that illustrates catheter posi- Entrainment principles were applied to the arrhythmia
tioning and the likely areas for circuits. Essentially, the cir- shown in Figure C18.24. Various sites in the right and left
cuit must be bounded either by an ablation-induced scar, 2 atrium all showed the classical features of entrainment. After
ablation-induced scars (gap in linear ablation), 2 anatomic the reentrant nature of this arrhythmia was firmly estab-
obstacles (left lower pulmonary vein and mitral annulus), or lished, the attempts at entrainment from various sites were
an anatomic obstacle and a non–ablation-induced scar (atri- compared (pinging) when pacing in the high right atrium
otomy, atrial myopathy, etc). If multielectrode catheters are or tricuspid valve annulus region. There was marked fusion
placed, it is reasonable to place them in the cavotricuspid in the activation sequence, both on the tricuspid annulus
isthmus; if a dual transseptal puncture approach is used for and the coronary sinus. Further, the postpacing intervals
atrial fibrillation, they can be placed in the left atrial isthmus exceeded the tachycardia cycle length (280 milliseconds) by
(between the left-sided pulmonary vein and mitral annu- at least 90 milliseconds.
lus). Now the pinging maneuver can begin by pacing widely
Case 18 581
Figure C18.27
Figure C18.27 shows the results of entrainment mapping Several important features should be noted on this tracing.
(pacing) in the distal left atrial appendage. The TVI catheter First, when pacing at a cycle length of 240 milliseconds, there
is located on the tricuspid valve annulus, in the region of the is clear evidence of capture, and the tachycardia cycle length
cavotricuspid isthmus. TVI 1,2 is located close to the coro- is 140 milliseconds during pacing. Second, there is very little
nary sinus ostium, and TVI 19,20 is on the right atrial free fusion in the activation sequences of the available and dis-
wall, near the annulus. The CS catheter is located within the played potentials between the beats that are paced during
coronary sinus, with CS 1,2 being the distal electrode in the tachycardia and the tachycardia itself; this feature may sug-
anterolateral mitral annular region. The LAA prox catheter is gest concealed entrainment but may also be indicative of a
the pacing catheter. similar activation wave front at electrode sites distant from the
tachycardia exit and pacing sites. Third, the last paced-beat P
In Figure C18.27, what is suggested by the interval from
wave occurs after the pacing stimulus, after an interval of 100
the electrogram to P wave (egm–P) being shorter than the
milliseconds, and during tachycardia. When measured from
interval from the pacing stimulus to P wave (St–P)?
the pacing electrode, the local potential precedes the P wave
A. The pacing site is in the tachycardia circuit
of tachycardia by 40 milliseconds. Fourth, the postpacing
B. The pacing site is within the slow zone
interval exceeds the tachycardia cycle length (318-280 milli-
C. The pacing site is the exit point of the reentrant
seconds) by 38 milliseconds. Fift h, after cessation of pacing,
tachycardia
the tachycardia continues, with an unchanged flutter-wave
D. The pacing site is not in the tachycardia circuit
morphology and intra-atrial activation sequence.
E. The arrhythmia is not reentrant
Answer: D—The pacing site is not in the tachycardia
circuit.
electrode (labeled “Pacing”) is placed in the left atrial append-

age and the tachycardia circuit is in the left atrium (as later
determined). The circuit involves the myocardium on the roof
AFL x of the atrium and lateral to the pulmonary veins. The pac-
ing wave front must exit from the left atrial appendage to get
x Pacing
into the circuit and entrain the tachycardia. The stimulus–
to–P-wave interval is the sum of the conduction time from the
pacing site into the circuit (labeled “x”) and the conduction
y time from when the circuit is entered to when it exits from the
protected isthmus to the rest of the atrium (labeled “y”). In
contrast, during tachycardia, the pacing site is activated by the
Potential − P = y − x circuit exit to the left atrial appendage, while the circuit contin-
St − P = y + x ues to propagate toward its exit; thus, the potential–to–P-wave
interval is the difference between y and x. If the pacing site
Figure C18.28
is even further from the circuit, the difference between the 2
intervals will be even more marked. If the pacing site, however,
The reason for the difference in intervals when compar- is within the circuit, these 2 measured intervals are the same.
ing the stimulus to P wave and the local potential to P wave is Although subtle differences exist, the difference in these inter-
because the pacing electrode is not in the tachycardia circuit. vals are analogous to the differences between the tachycardia
This is shown schematically in Figure C18.28. Note that an cycle length and postpacing intervals (see Chapter 5).
Figure C18.29
The results of entrainment mapping from the mid left interval is virtually the same. Both features strongly suggest
atrial roof in the region of the Bachmann bundle are shown that the pacing site is within the tachycardia circuit. Further,
in Figure C18.29. Here, the postpacing interval is identical to there is no discernible difference in the intra-atrial activa-
the tachycardia cycle length (280 milliseconds). The stimu- tion sequences during tachycardia and during the tachy-
lus–to–P-wave interval and the local potential–to–P-wave cardia beats that were entrained by pacing, which suggests
Case 18 583
concealed entrainment. This means that the pacing site not 39%
only is in the circuit but also is either in the slow zone of the 90% 29%
circuit or close to the exit from the slow zone; further, there is
little (if any) fusion of the antidromic wave front from pacing
(see Chapter 5).
All of these features strongly suggest that the pacing
electrode is within the circuit, but the ablationist must still 36%
determine whether this a good site for ablation. Consider 17%
the possibility that a fairly large portion of the atrium near 132%
the Bachmann bundle may be part of this large reentrant 6% 9%
loop circuit. Point ablation at this site is unlikely to be effec-
tive, and a region of slow conduction (if discrete) should be Figure C18.30
found, or a long linear ablation that transects this region of
the left atrium could be considered if lesions were anchored
to either another ablative lesion or an anatomic obstacle The information obtained with the entrainment and
such as the mitral annulus. Here, linear ablation is difficult, pinging technique discussed above can also be obtained by
and obtaining a long linear transmural lesion near the roof determining the interval from stimulus to P-wave onset at
of the left atrium is challenging and potentially may cause the interrogation site and referencing this as a percentage
perforation. of the tachycardia cycle length. In Figure C18.30, note that
How can one determine whether the pacing site is within sites close to the coronary sinus show a very short stimulus–
the circuit and also within the slow zone? Previously, the to–P-wave interval, suggesting that they are close to the exit of
differences in intervals from the stimulus to P wave and the the tachycardia. In contrast, sites near the medial portion of
potential to P wave were considered. However, after a system- the Bachmann bundle, close to the septal ostium of the right
atic approach shows that this is a reentrant tachycardia and upper pulmonary vein, show that the stimulus–to–P-wave
that the pacing site is within the circuit, consider the abso- interval constitutes a large percentage of the tachycardia cycle
lute value of this interval. The absolute value of the stimu- length (suggesting an entrance site). Understand that measur-
lus–to–P-wave interval indicates whether the pacing site is ing these intervals and calculating percentages are meaning-
proximal to the slow zone (long interval) or closer to the exit less if the tachycardia is not already established as reentrant
(short interval). A given stimulus–to–P-wave interval is com- and if the pacing electrodes are not within the tachycar-
pared with the tachycardia cycle length to judge its relative dia circuit. This order of approach to entrainment must be
length. In this instance (pacing at the mid left atrial roof), remembered: first, determine the mechanism; second, deter-
the stimulus–to–P-wave interval was 39% of the tachycardia mine if the mapping catheter is in the circuit; and third, focus
cycle length. on determining whether it is a good ablation site.
Figure C18.31
Figure C18.31 shows entrainment mapping from the lat- the tachycardia exit site or the slow zone entrance. In addi-
eral left atrial roof. Again, the postpacing interval closely tion, analysis of the potential at the pacing site (LBB prox)
approximates the tachycardia cycle length, and the inter- showed a fragmented signal that could be entrained during
vals during tachycardia from the stimulus to P wave and pacing and likely represented a region with slow conduction.
local potential to P wave are nearly identical. The activation Ablation at this site successfully terminated the tachycar-
sequence is nearly identical to the tachycardia when pacing dia. If the tachycardia is no longer inducible and previously
from the entrained location. The main difference here is that was easy to induce, some operators would not ablate further.
the intervals for the stimulus to P wave and local potential However, as slow zones are rarely completely discrete, espe-
to P wave constitute about a quarter of the tachycardia cycle cially in chronically enlarged left atria, anchoring linear abla-
length, suggesting that the site is not particularly close to tion may still be required.
Case 18 585
Figure C18.32
At times, the distinction between focal or automatic The most common method used to identify the origin of
atrial tachycardias and macroreentrant flutters is difficult to a premature beat is point-to-point mapping and finding the
make because of overlapping mechanisms and because they earliest site of activation. Activation on the LASSO catheter
may occur simultaneously with atrial fibrillation. Figure occurs earlier than the atrial potential by the His bundle
C18.32 was obtained from a patient with symptomatic, region or the coronary sinus during the PAC. But on the basis
medication-refractory atrial fibrillation. Pulmonary vein iso- of this finding alone, the origin of the premature beat in the
lation already had been performed. In the electrophysiology SVC cannot be determined because sites in the right atrium
laboratory, episodes of atrial fibrillation and various atrial and elsewhere may show an even earlier signal. The critical
flutters continued to occur. The circumferential mapping finding in this tracing is the reversal of far- and near-field
catheter (LASSO 1,2-10,1) was placed in the SVC, approxi- potentials. In sinus rhythm, a far-field potential (LASSO
mately 1 cm distal to the SVC–right atrial junction. The first catheter) that times with the right atrial potential (hRA cath-
beat in Figure C18.32 shows sinus rhythm with right bundle eter) precedes the larger, near-field, venous potential spike.
branch block. The second beat is a PAC that was frequently That is, the far-field signal occurs before the near-field signal,
seen in this patient, particularly with the use of isoprotere- indicating passive activation of the vein during sinus rhythm.
nol, and sometimes preceded the onset of the various atrial With the PAC, the sharp near-field potential is now first and
arrhythmias. occurs considerably before the far-field right-atrial signal that
times with the right-atrial signal on the hRA catheter. This
Which statement is likely true regarding the PAC shown in
reversal of far- and near-field signals is virtually diagnostic of
Figure C18.32?
a PAC origin in the SVC musculature.
A. Venous potentials from musculature in the SVC are
When considering the coronary sinus activation, par-
seen, and this tissue is passively activated during the
ticularly when comparing it with coronary sinus activation
PAC
in sinus rhythm, a left atrial or right upper pulmonary vein
B. Venous potentials from musculature in the SVC are
origin for this PAC is highly unlikely. However, this possibil-
seen; this tissue is the origin for the PAC
ity cannot be excluded because during linear ablation in the
C. The ectopy cannot be arising from the left atrium
left atrium (ablation between the mitral annulus and the left
D. The ectopy cannot be arising from the right upper pul-
upper pulmonary vein), the coronary sinus musculature itself
monary vein
can be dissociated from the left atrium or at least markedly
delayed. Also, direct muscular connection between the right
Answer: B—Venous potentials from musculature in the upper pulmonary vein and the SVC may occur. Thus, ectopy
SVC are seen; this tissue is the origin for the PAC.
that originates in the left atrium (near the right superior pul- to isolate the right upper vein, pulmonary vein potentials
monary vein) or right upper pulmonary vein may exit to the occurring earlier distal in the vein rather than proximal, and
SVC almost immediately after activation. With a direct con- an unusual response to right atrial pacing (as discussed else-
nection, important clues would have been present during the where in this textbook).
pulmonary vein isolation procedure, including the inability
Figure C18.33
During atrial pacing (Figure C18.33), repeated spontane- with a different atrial activation sequence was seen (note the
ous nonsustained atrial tachycardia was observed from the coronary sinus activation in the last beat shown in Figure
musculature of the SVC. This SVC tachycardia was more C18.33). The morphology of the sustained arrhythmia on the
likely to occur with isoproterenol but also occurred sponta- surface 12-lead electrocardiogram suggested counterclock-
neously (rather than with programmed stimulation), which wise isthmus-dependent atrial flutter, and the diagnosis was
suggested an automatic tachycardia. In some of these tachy- confirmed with entrainment mapping in the cavotricuspid
cardia episodes, a sustained macroreentrant tachycardia isthmus.
Case 18 587
Figure C18.34
In some instances, after spontaneous initiation of an The result of entrainment mapping and other features that
SVC, automatic tachycardia was followed by tachycardia differentiate between these mechanisms would depend on
that initiated a macroreentrant flutter “degeneration” of when these maneuvers are performed relative to the actual
the arrhythmia into atrial fibrillation (Figure C18.34). Note arrhythmias present. For example, overdrive suppression
that the automatic atrial tachycardia with early near-field would have been observed in the early stage of the SVC tachy-
activation on the catheter continued in the SVC during the cardia, but if a stable atrial flutter was induced, entrainment
initial period of atrial fibrillation. Thus, simultaneous mac- would have shown the last paced beat being entrained but
roreentrant (atrial flutter) and automatic (SVC) tachycar- not fused. Even more complex responses during entrainment
dia, followed by atrial fibrillation, were seen in the same pacing are seen when simultaneous atrial flutter and a faster
patient. automatic atrial tachycardia are present simultaneously.
Figure C18.35
In Figure C18.35, during continuous atrial fibrillation, SVC may occur, with fragmentation of the signals within
a morphologic change in the SVC potential (LASSO cath- the SVC. Finally, continued entrance block from the rapid
eter) is noted. Several possible changes may occur. First, atrial fibrillation into the SVC may be seen with sponta-
a parasystolic arrhythmia (ie, continued automatic tachy- neous termination of the automatic tachycardia; loss of
cardia) may be observed in the vein; this may have both venous potentials on the LASSO catheter may be seen.
exit block to the atrium and entrance block from the atrial Thus, it is difficult to comment on isolation of a vein during
fibrillation. Conduction of the atrial fibrillation into the atrial fibrillation.
Figure C18.36
Case 18 589
During atrial fibrillation (Figure C18.35), organization into the 12-lead electrocardiogram, the P-wave morphology and
a stable tachycardia was observed (Figure C18.36). Note that the intracardiac atrial electrogram activation sequence were
during this tachycardia, the near-field signal on the LASSO distinctly different from any of the macroreentrant flutters
catheter occurred after the far-field signal that timed with previously defined. The tachycardia had a very short ventric-
right atrial activation. Thus, this tachycardia does not origi- uloatrial interval, with earliest atrial activation occurring on
nate within the SVC, and the musculature of the SVC is being the proximal His bundle electrode.
passively activated by some other arrhythmia mechanism. In
Figure C18.37
In Figure C18.37, note that a premature ventricular con- available in the invasive electrophysiology laboratory to dis-
traction, placed during the tachycardia before antegrade His tinguish between these mechanisms, but the potential for
bundle activation, preexcited the retrograde His bundle and, overlap also must not be overlooked. If an automatic mecha-
in doing so, preexcited the atrium with an identical atrial nism is identified, the procedure is usually straightforward,
activation sequence and reset the tachycardia. Spontaneous with point-to-point, multielectrode, or 3-dimensional map-
variation in the His-atrial interval (not shown) resulted in ping identifying the earliest site of activation, with ablation
subsequent changes in the atrial cycle length. All of these being targeted to that site. If a reentrant tachycardia is identi-
findings were strongly suggestive of typical AV node reen- fied, then entrainment mapping (and 3-dimensional mapping
trant tachycardia. A slow-pathway ablation was performed, in some cases) is used to identify the circuit of the arrhythmia
with no further induction of this arrhythmia. and the slow zone for that tachycardia circuit. Ablation then
Thus, the electrophysiologist must be intimately familiar is performed, either by targeting the slow zone or transecting
with the various mechanisms of tachycardia and the methods the circuit at a strategic site between 2 anatomic obstacles.
The electrophysiologist may note features of entrainment

and an apparent warm-up of the flutter circuit. This is because
of initial overdrive suppression of the faster automatic tachy-
Induces cardia, which then speeds up (shorter cycle length) while
entraining the macroreentrant circuit. Another complicating
factor may be spontaneous termination of a given flutter by
Resets the rapid atrial tachycardia, induction of a different flutter
Entrains (with a different, entrainment-diagnosed slow zone, etc), and
Passive eventual atrial fibrillation. Being alert to the possibility of a
single focal driver during complex arrhythmias is important
because it may facilitate a curative ablation.
Abbreviations
AACl, atrial arrhythmia cycle length [f]

AFL, atrial flutter [f]
Figure C18.38
CS, coronary sinus [f]
CSO, coronary sinus ostium [f]
As shown in Figure C18.38, when more than one arrhyth- DCS, distal coronary sinus [f]
mia occurs and differing mechanisms potentially are involved, egm, electrogram (potential) [f]
the clear-cut approach used with automatic or macroreen- HIS, His bundle [f]
trant tachycardias cannot be applied easily. For example, IVC, inferior vena cava
an automatic tachycardia in a pulmonary vein may be rapid LA, left atrium [f]
enough to serve as an induction mechanism for a sustained LI, left inferior [f]
macroreentrant flutter. When entrainment is attempted dur- LS, left superior [f]
ing the automatic tachycardia, the typical response with over- MVA, mitral valve annulus [f]
drive suppression may be seen (assuming no entrance block P, P wave [f]
during tachycardia into the vein). During the stable atrial PAC, premature atrial contraction
flutter, typical entrainment findings for this arrhythmia PPI, postpacing interval [f]
will be seen. However, if both arrhythmias occur simultane- RA, right atrium [f]
ously and if the atrial tachycardia is faster, it would induce RI, right inferior [f]
the arrhythmia and continuously entrain the macroreentrant RS, right superior [f]
flutter. Thus, when attempting entrainment mapping, a com- St, stimulus [f]
plex response with overdrive suppression of the automatic SVC, superior vena cava
focus and flutter entrainment will occur. TV, tricuspid valve [f]
Case 19
Figure C19.1
The complex tracing shown in Figure C19.1 was obtained this is a sinus beat with a very short atrial-His interval, sug-
from a patient after incessant atrial tachycardia had been diag- gesting fusion with a junctional beat. The next beat shows a
nosed and ablative therapy delivered. The basic pattern after more physiological atrial-His interval, and then a junctional
ablation showed competing sinus and junctional rhythms. beat is seen again. After termination of tachycardia, under-
With the first junctional beat, note the retrograde activation lying mild sinus node dysfunction (with junctional escaped
of the atrium and then an antegrade capture beat. Following beats) was seen.
In this case, the nature of this atrial arrhythmia and where
ablation was performed will be discussed in detail. However,
Abbreviations are expanded at the end of this chapter. before that discussion, note the unusual potentials seen on
Terms with “[f]” denote abbreviations that appear in the figures only. the ABL d catheter (Figure C19.1, white arrow).
591
In Figure C19.1, the ABL d catheter was placed in the left catheter would be caused by mechanical interaction with
atrium after single transseptal puncture. The HBE1-HBE4 another catheter. Note the signals seen on the HBE 2 catheter
electrodes and the CS catheter are in their usual locations. (yellow arrows). In this case, an identically timed unusual sig-
What is the likely origin of the potential seen on the ABL d nal on the RVp catheter is seen (green arrow). These catheters
catheter (white arrow)? often are positioned close to the right ventricular outflow
A. Artifact from catheter-to-catheter mechanical interac- tract, and if they bump into each other, noncardiac signals
tion (catheter “banging”) (mechanical artifacts) are generated. Although external elec-
B. An electrical signal that is dissociated from other atrial tromagnetic fields may produce noise on the intracardiac sig-
signals nals, these are usually high-frequency signals and are seen on
C. Noise from an external electromagnetic source the surface electrocardiogram and on multiple intracardiac
D. Noise from possible fracture of the mapping-ablation channels. Finally, note that the regular potential seen on the
catheter ABL d catheter in the left atrium is likely physiological (not
an artifact).
Answer: B—An electrical signal that is dissociated from
After ablation or a maze procedure, portions of the atrium
other atrial signals.
(pulmonary veins, superior vena cava, vein of Marshall, etc)
Artifacts are among the most confusing signals in terms of may show local electrical activation that is completely dissoci-
identification and interpretation. In this patient, the ablation ated from the rest of the atrium. Such isolation procedures typi-
catheter was placed somewhere in the left atrium, where no cally are performed when treating atrial fibrillation, but in some
other catheters were present. It is therefore highly unlikely unusual circumstances, it may be required for atrial tachycar-
that the regular and reproducible potential on the ABL d dia, ventricular tachycardia, or accessory pathway ablation.
Figure C19.2
Returning to the case, begin by analyzing the presenting was otherwise healthy and was athletic before the onset of fre-
arrhythmia (Figure C19.2) and determining which isolation quent (and at times incessant) tachypalpitation. Preliminary
procedure was required. Then, revisit the intracardiac elec- assessment included an echocardiogram that showed a grad-
trogram obtained after ablation (Figure C19.1). ual decrease in ventricular function, with an ejection fraction
A 16-year-old male had palpitation that occurred at rest of 35%. During typical symptoms at rest, a 12-lead electrocar-
but was most prominent with exercise. He had noticed this diogram was obtained (Figure C19.2).
for about 3 years but recently was increasingly fatigued. He
Case 19 593
Which diagnosis is least likely on the basis of the 12-lead however, is strongly positive. In addition to being an inferior
electrocardiogram obtained during a symptomatic period lead, lead III is a rightward lead relative to the other inferior
(Figure C19.2)? leads. Thus, when the origin of an automatic tachycardia is
A. Sinus tachycardia from the left atrium, even if not from a very superior location
B. Atrial tachycardia because of the left-to-right orientation of the vector, lead III
C. Mobitz I atrioventricular (AV) block at the level of the may be the only inferior lead that shows a positive P wave.
compact AV node Altogether, these findings argue against a sinus mechanism
D. AV reentrant tachycardia and point to a left atrial origin for the tachycardia. Note how
E. Pulmonary vein tachycardia in lead I, the P wave is isoelectric and negative, which also is
consistent with a left atrial origin.
Answer: A—Sinus tachycardia.
The mechanism of the arrhythmia cannot be deduced from
Figure C19.2 shows a slow supraventricular tachycardia, with the electrocardiogram, only the likely exit (the earliest site of
a gradual prolongation of the PR interval, consistent with decre- activation) can be defined. Thus, a decrementally conducting
ment at the level of the compact AV node (Mobitz I AV block). accessory pathway located on the lateral mitral annulus may
The P-wave morphology gives important clues about which diag- present with this P-wave morphology. The mechanism under-
noses can be excluded; in lead V1, the P wave is predominantly lying changes in the R-P and PR interval with AV tachycardia
negative. Because the sinoatrial node is posterolaterally located, is more complicated. Hypothetically, the retrograde pathway
the initial vector of the P wave in lead V1 is positive (moving could have progressively less decrement, resulting in a pro-
toward the anteriorly placed electrode) in sinus rhythm. With gressively shorter R-P interval, which stresses the AV node and
left atrial enlargement, a predominantly negative P wave some- gradually increases the PR intervals. Finally, AV node reentry,
times is seen in lead V1, although in that situation, a strongly although unlikely, cannot be excluded because the entire cir-
positive P wave is expected in leads II, III, and aVF. The sino- cuit for AV node reentry or the exit of the slow (rarely fast)
atrial node is located at the junction of the superior vena cava pathway may be via the coronary sinus musculature and into
and the right atrium. Thus, based on this exit, a strong inferior relatively lateral portions of the left atrium. Therefore, although
axis with positive P waves in the inferior leads should be seen. several diagnoses are possible, sinus tachycardia as a potential
In this patient’s electrocardiogram, the P wave is iso- cause of this patient’s slow tachycardia can be excluded on the
electric in lead II and mildly positive in lead aVF. Lead III, basis of the analysis of the P-wave morphology.
Figure C19.3
In Figure C19.3, the patient’s tachycardia is shown on the degree of positivity of the P wave is relatively low in lead III,
left, whereas another patient’s electrocardiogram with typi- reflecting the right-sided origin from the sinus node, with the
cal P-wave morphology in sinus rhythm is on the right. (The vector proceeding from superior to inferior and also slightly
right panel shows a predominantly positive P wave in lead V1 from right to left.
and positive P waves in leads II, III, and aVF). Note that the
Figure C19.4
During onset of tachycardia in the electrophysiology labo- changes; specifically, in the tachycardia (second) beat, there
ratory (before transseptal puncture), the intracardiac electro- is fairly clear distal-to-proximal activation, whereas with the
grams shown in Figure C19.4 were obtained. Note the subtle first beat, there is a fused sequence, with the mid coronary
change in the P-wave morphology between the first and sec- sinus appearing earliest. Note also that the earliest intracar-
ond beat. In the first beat, the P wave in lead III becomes more diac potential is on the HBE catheter and appears to precede
positive, and the P wave in lead V1 becomes almost entirely the P-wave onset on the surface electrocardiogram.
negative. In the second beat, the P-wave morphology is exactly Is this then a likely site of origin for the tachycardia?
the same as the P-wave axis during tachycardia. The first beat Would ablation near the His bundle possibly risk AV block?
represents fusion between sinus rhythm and tachycardia. Just On closer inspection, although the atrial potential (on the His
as slow sinus rhythm may be competing with a junctional electrode) is the earliest of the intracardiac electrograms, the
escape or junctional tachycardia, similar competition (iso- early part of the deflection is far field (low-frequency blunted
rhythmic dissociation) may occur between sinus rhythm and deflection). This suggests that the true early site of activation
atrial tachycardia. is somewhere near (but not exactly) at this His bundle record-
Although the intracardiac activation sequence appears ing site. Whenever a catheter placed on the septum shows an
fairly similar between these 2 beats, there are some impor- early far-field deflection, the left atrium (and possibly aortic
tant differences. Note that the hRA potential (arrow) is valve) must be mapped to find the true earliest site of acti-
nearly simultaneous with the atrial potential recorded vation. Note also, on the second beat of the coronary sinus
on the His bundle catheter, but on the second beat (tachy- electrograms, the early deflection in the mid coronary sinus
cardia), the atrial potential on the His bundle catheter is again far field. This suggests that if a left atrial tachycardia
markedly precedes activation of the high right atrium. is diagnosed, the origin is not the coronary sinus musculature
The coronary sinus activation sequence also shows subtle but the left atrial myocardium.
Case 19 595
Figure C19.5
With administration of isoproterenol (1 mcg/minute), the D. Crista terminalis tachycardia

rate of the tachycardia increased. Further mapping of the E. A and C
right interatrial septum was undertaken using a deflectable F. B and D
mapping-ablation catheter (ABL d, ABL p). When manipulat- Answer: E—Left atrial roof tachycardia and AV node
ing the catheter just above and posterior to the compact AV reentry.
node, close to the site of the fast pathway, the intracardiac
electrogram shown in Figure C19.5 was obtained. Tachycardia continued, despite AV block likely caused
by mechanical trauma near the compact AV node during
Which diagnoses continue to remain likely possibilities? mapping. This would exclude any form of AV tachycardia.
A. Left atrial roof tachycardia However, AV node reentry can continue, even with supra-
B. Posterior mitral annular tachycardia hisian block, particularly if trauma occurred in the lower
C. AV node reentry common pathway proximal to the compact AV node.
Table C19.1
Potential Mechanisms of Multiple (Atrial or Ventricular) Sites of Near-Simultaneous Activation
Type of Activation Observation During Ventricular Pacing Possible Mechanism
True site of early Proximal His-atrial potential is simultaneous Right midseptal accessory pathway
activation is with a proximal coronary sinus atrial potential
somewhere between Proximal His-atrial potential is simultaneous Left midseptal accessory pathway
the simultaneously with a mid coronary sinus atrial potential
early recorded sites Distal coronary sinus atrial potential, proximal Right upper pulmonary vein origin of atrial tachycardia
coronary sinus atrial potential, and high right
atrium potential are nearly simultaneous
Bachmann bundle region, His bundle atrial Left atrial roof or anterior mitral annular tachycardia
potential, and proximal coronary sinus are
activated nearly simultaneously
Ostium of left-sided pulmonary vein and mid– Left pulmonary vein tachycardia with electrically active
coronary sinus are activated simultaneously vein of Marshall conduction
Near-field and far-field potentials occurring at Consider tachycardia from a left-sided pulmonary vein, with
about the same time within the right upper simultaneous activation of the right atrium (cause of the
pulmonary vein far-field potential) and the right upper pulmonary vein
musculature
More than one method Early activation in the mid coronary sinus and Two accessory pathways: left posterior and right
to activate the His bundle region anteroseptal; also consider fusion between a left posterior
cardiac chamber pathway and fast pathway of the atrioventricular node
(atrium or ventricle) Simultaneous activation of the His bundle atrial Two accessory pathways: right lateral and right anterior; also
potential and high right atrium consider fusion between a right lateral accessory pathway
and the fast pathway of the atrioventricular node
During wide complex tachycardia, multiple A fascicular tachycardia with multiple connections to the
early sites on the right or left interventricular ventricle via the Purkinje network; also consider a His
septum bundle tachycardia, supraventricular tachycardia, or
Mahaim pathway inserting into the right bundle, with
the ventricle being activated via multiple Purkinje exits
Short R-P tachycardia with early activation of Atrioventricular node reentry or junctional tachycardia,
the proximal His region and the proximal with exits to the atrium via bystander left-sided fast
coronary sinus after His bundle activation pathways or the slow pathway
On detailed examination of the activation sequence, the An atrial tachycardia that originates in the left atrium,
atrial potential near the His bundle catheter and the coronary about equidistant from the His bundle and the posteriorly
sinus are being activated nearly simultaneously (His signal is located coronary sinus region, remains a strong possibility.
slightly ahead). When 2 sites of considerable spatial separation Sites that should be mapped with particular attention would
are activated simultaneously, either 2 mechanisms are acti- be the left atrial roof and the ostia of the pulmonary veins.
vating the atrium or the true early site of activation is some- This tracing (Figure C19.5) further shows that the hRA cath-
where between them, equidistant in terms of conduction time eter, now placed in the region of the right atrial appendage, is
(Table C19.1). With this reasoning, a crista terminalis tachy- also activated very close in timing to activation of the atrium
cardia can be excluded because the high right atrium should near the His bundle and the coronary sinus. Thus, 3 sites
be earlier and the His bundle should clearly show activation are activated almost at the same time. Such a finding early
earlier than the middle coronary sinus electrodes. Similarly, in an electrophysiology study can be useful for identifying
a posterior mitral annular tachycardia would be expected to regions of the heart that should undergo detailed mapping
have mid coronary sinus activation considerably earlier than and analysis.
the atrial activation near the His bundle.
Case 19 597
Figure C19.6
Transseptal puncture was performed and the left atrium fusion along with the T wave, it is difficult to know whether
was mapped (Figure C19.6). The ABL catheter was placed on a given site is being activated considerably earlier than the
the roof of the left atrium, close to the septum. Note how the onset of the surface P wave. For automatic atrial tachycar-
potential on the ablation catheter now clearly precedes atrial dias in a normal heart, a site at least 30 milliseconds ahead of
activation on the His bundle catheter. Note also that the ABL the earliest discernible onset of the P wave should be found.
catheter now has a near-field potential (recall that the earliest Importantly, a stable endocardial potential should be used as
potential on the His bundle catheter looked far-field [Figure a marker for further activation mapping. Thus, if the coro-
C19.4]). This suggests earlier activation of the left atrium nary sinus is in a stable position, use this as a reference for
compared with the right atrium. further point-to-point mapping, just as is done for electro-
Also in Figure C19.6, note the difficulty associated in try- anatomic mapping (see Chapter 3). However, remember that
ing to determine whether a given potential is earlier than the because the coronary sinus potential was occurring slightly
surface P wave. In the previous figures that showed slower later than the P-wave onset, a true early site using this refer-
tachycardia and no fusion with the T wave, the onset (and ence should be even more than 30 milliseconds ahead of the
morphology) of the P wave was fairly easy to recognize. With P-wave onset.
Figure C19.7
The mapping-ablation catheter was next moved to the ante- sites then should be mapped? Further mapping was undertaken
rior mitral annulus (Figure C19.7). Here again, note the diffi- with a circumferential multielectrode catheter in 4 pulmonary
culty in ascertaining the onset of the P wave because of fusion veins (right upper, right lower, left upper, and left lower), and
with the preceding T wave. The activation timing compared activation of the musculature of these veins was considerably
with the atrial potential recorded on the His catheter is similar late compared with the left atrial roof. For the right upper vein,
to that noted on the left atrial roof (not particularly early). What activation was later than that of the His bundle region.
Figure C19.8
Case 19 599
In Figure C19.8, during atrial extrastimulation, tachycar- pulmonary vein, then the catheter should be advanced fur-
dia is induced during the drive train. The ABL d electrode ther into the vein).
now records an atrial potential considerably earlier than the Other features that strongly suggest identification of a
ABL p electrode and about 40 milliseconds before the onset likely successful ablation site include earlier activation (with
of the surface P wave. In this young patient with an other- a near-field potential) of that site compared with surrounding
wise healthy heart, this site is expected to be very close to myocardial sites and a unipolar potential that is all negative
the origin of an automatic atrial tachycardia. Note that the (suggesting activation is proceeding away from that particu-
potential on the distal electrode is earlier than that of the lar site). In certain instances, if pacing at low output from that
proximal electrode. If the area is being mapped, the map- site reproduces the P-wave morphology and the intracardiac
ping catheter should be advanced further in the direction electrogram sequence, then ablation at the site will likely be
of the distal electrode (eg, if the mapping catheter is in a successful.
Figure C19.9
Figure C19.9 shows the location of the mapping-ablation the very tip of the appendage, activation sites were found
catheter at the site where the early potential in Figure C19.8 that preceded the surface P-wave onset by approximately
was obtained. Th is is a right anterior oblique (RAO) pro- 50 milliseconds.
jection. The ablation electrode (white arrow) is located in With this young patient, to avoid the high risk of perforat-
the left atrial appendage via transseptal puncture. As the ing the very thin tissue at the appendage apex, the case was
catheter was advanced further into the left atrial append- approached like a pulmonary vein tachycardia, by isolating
age very close to the tip (as judged by intracardiac ultra- the pulmonary vein. A circumferential ablation was per-
sonography; the yellow arrow indicates the ultrasound formed, just within the left atrial appendage, to isolate the
probe), even earlier potentials were noted. Eventually, at distal portion of the appendage.
Figure C19.10
The initial tracing shown at the start of this case discus- tachycardia, a prolonged sinus node recovery is seen, with
sion is reproduced here in Figure C19.10; it was obtained junctional escape beats (as explained above). The left atrial
after circumferential ablation within the left atrial append- appendage uncommonly can be the site of origin of atrial
age. Note that the potentials on the ABL d catheter continue tachycardia and sometimes atrial fibrillation. Targeted
to occur at exactly the same rate as the atrial tachycardia, ablation within the atrial appendage usually may be per-
even though this portion of the appendage has been iso- formed safely, but if doubts arise with regard to risk of per-
lated from the proximal left atrial appendage and the rest foration, the appendage can be successfully isolated, as in
of the atrial myocardium. With cessation of the incessant this patient.
Case 19 601
Figure C19.11
An interesting phenomenon was observed during tachy- inscribed. Therefore, at first glance, there are 2 obvious expla-
cardia when placing sensed premature ventricular contrac- nations for this phenomenon. One, a retrograde decremental
tions (PVCs) (Figure C19.11). After the PVC, there was no pathway (with a long ventriculo-atrial interval) and the PVC
change in the atrial cycle length or activation sequence (no produce further decrement and cause postexcitation of the
preexcitation of the atrium). Subsequently, the tachycardia next atrial potential. Two, the PVC penetrates into the lower
slowed for one beat but then resumed a cycle length similar to common pathway and postexcites the atrium.
that observed previously. However, from the discussion above, know that neither
of these explanations is correct because AV dissociation was
Which is a likely explanation for the slowing of the tachy-
noted during the arrhythmia and retrograde activation dur-
cardia subsequent to the PVC?
ing the arrhythmia, and retrograde activation during ven-
A. The PVC preexcited the atrium via the AV node and
tricular pacing was completely different from the activation
caused overdrive suppression of the atrial tachycardia
sequence of this arrhythmia. This tracing (Figure C19.11)
B. The PVC preexcited the atrium via an accessory path-
underscores the importance of not relying on a single obser-
way and caused overdrive suppression of the atrial
vation to make a diagnosis.
tachycardia
What is the explanation for this clear change in the atrial
C. The PVC penetrated an AV node reentry circuit and
cycle length subsequent to the PVC with atrial tachycardia? If
caused subsequent postexcitation
this finding was not seen repeatedly, it could be a coincidental
D. A form of ventriculophasic arrhythmia is present
variation in the atrial cycle length; nevertheless, for a given
E. The PVC is causing postexcitation of the atrium via an
level of isoproterenol, the atrial cycle length was very stable,
accessory pathway, with long conduction time
which makes coincidental variations unlikely. Atrial tachy-
Answer: D—A form of ventriculophasic arrhythmia is cardias, like sinus tachycardia and sinus rhythm, can be quite
present. sensitive to autonomic tone. In sinus rhythm, when patients
The first step in analyzing this complex phenomenon is to have 2:1 AV block or AV dissociation, the sinus cycle length
ascertain whether ventriculoatrial conduction occurred after can vary considerably, depending on whether a conducted
the PVC. Note 2 important findings. First, the cycle length of beat is present before that sinus beat (ventriculophasic sinus
the tachycardia in the atrium is unchanged following the PVC arrhythmia). When this PVC was placed, ventricular and atrial
and the activation sequence does not change. Thus, the atrial activation occurred near-simultaneously, which can produce a
potentials seen after the PVCs have not been reset (preexcited cannon atrial potential wave and affect autonomic tone via the
or postexcited). Second, the arrow points to a retrograde His carotid body–mediated baroreflex. This is the likely explana-
bundle deflection showing that the PVC did penetrate into tion for this finding, particularly in the context of all the other
the AV node but not to the atrium, as atrial activation has findings and the successful ablation site described above.
commenced even before the retrograde His bundle had been
Figure C19.12
Having now recognized the origin and appropriate

treatment for this patient’s unusual atrial tachycardia, it is Bachmann
important to review some of the key tracings to verify that bundle
the information from the earlier tracings fits the facts that
were learned later in the case. For students of electrophysi- LAA
ology, this is a very important exercise. Often, much more
may be learned from the case than just the diagnosis and
the knowledge of the correct ablation site. For example, as His
noted earlier in the case (and shown in Figure C19.12), when
only right-sided catheters and the coronary sinus catheter
were placed, nearly simultaneous activation was seen on
the His bundle, mid coronary sinus, and high right atrial
regions, with the earliest of these 3 sites being in the His
bundle region. In fact, as mentioned above, signals found
when mapping in the right upper pulmonary vein were
much later than activation of the His bundle region. How
do these facts fit with the later knowledge of the tachycardia
originating in the left atrial appendage?
Figure C19.13
The autopsied heart section (Figure C19.13) illustrates

the anatomic basis for these electrophysiologic phenomena.
The primary site for interatrial conduction (right atrium
to left atrium or left atrium to right atrium) occurs via the
Bachmann bundle. Earlier, this bundle was thought to be
specialized conducting tissue, but it is now known that the
Bachmann bundle is simply the transverse atrial myocardial
fibers on the roof of the left and right atria (connecting the
2 atrial appendages). Because of the transverse orientation
of these fibers, conduction velocity is fairly rapid, parallel to
Case 19 603
the fiber orientation. Activation of the left atrial roof, anterior vein, conduction must now travel perpendicular to the fiber
mitral annulus, or the left atrial appendage will proceed fairly orientation on the roof of the left atrium (Bachmann bundle);
quickly across the Bachmann bundle to the high anterior sep- in addition, it must traverse the ostium of the right upper vein
tum of the right atrium, which is close to the region where (typically an area of slow conduction) to activate the muscu-
the proximal His bundle catheter recorded atrial potentials. lature of the right upper vein. Thus, if right upper pulmonary
Activation of the right atrial appendage occurs very soon after vein activation is much later than the His bundle region,
activation of this site. Why was it that activation of the right this does not necessarily mean that the patient has a right
upper pulmonary vein was much later than that of the His atrial tachycardia, as was demonstrated in this case discus-
bundle region? In crossing from the anteriorly located atrial sion. Why then was the coronary sinus region fairly early in
appendage to the posteriorly located right upper pulmonary activation?
Sinus
node
Bachmann
bundle
RSPV
LSPV LAA
44±9 ms 50±7 ms
18±11 ms
LAA
RA LA LA
79±12 ms
20±4 ms
40±11 ms
RIPV LIPV
CS
Proximal Distal
Figure C19.14 (Adapted from the 21st Annual Scientific Session of the North American Society of Pacing and Electrophysiology,
Washington, DC, May 17–20, 2000 [poster presentation].)
To understand why the coronary sinus is activated fairly the coronary sinus, an activation pathway occurs anteriorly
early with a left atrial appendage tachycardia, first determine in a circumferential manner, just behind the mitral annulus
the normal activation patterns within the left atrium itself. and anterior to the plane of the pulmonary veins. Therefore, a
Again, the Bachmann bundle is the main entrance point via left atrial appendage tachycardia is anticipated to activate the
the right atrium into the left atrium and vice versa, but after atrium, near the coronary sinus, fairly early; in addition, the
this site is activated, further propagation of the wave front in His bundle region would be activated relatively quickly via
the left atrium is not uniform. In Figure C19.14, the left panel the Bachmann bundle. Then, depending on the location of the
shows activation times at various points in the left atrium connections between the left atrium and the coronary sinus
during sinus rhythm. Note that the posterior left atrium (and musculature, the earliest sites of activation within the coro-
thus the pulmonary veins) are activated fairly late. Because nary sinus will not be far behind activation of the His bundle
of the fiber orientation around the Bachmann bundle into region and will be much ahead of activation of the posteriorly
the left atrial appendage and the posterior left atrium near located pulmonary veins (Figure C19.14, right panel).
Figure C19.15
After circumferential ablation within the left atrial append- ablation could be activation of the left atrial appendage dis-
age, the intracardiac electrograms shown in Figure C19.15 tal to the site of ablation. Alternatively, the atrial potentials
were obtained. Competing sinus and junctional rhythms around the ablation site could be fragmented because the
are present. The ABL d catheter is located about 1 cm within ABL d catheter (in this case, an 8-mm tip electrode) is strad-
the left atrial appendage. Which statement is true? dling the ablation line. However, if entrance into the “iso-
A. Entrance block into the appendage is definitely present lated” portion of the appendage is occurring, there should
B. Exit block from the appendage is definitely present be suppression of the left atrial appendage focus. This is not
C. Entrance and exit block into and from the left atrial seen because the appendage firing cycle length is unchanged,
appendage are definitely present which strongly suggests that entrance block into the append-
D. Neither entrance block into the appendage nor exit age is also present. Nevertheless, automatic tachyarrhythmias
block from the appendage is present sometimes may exhibit entrance block into the focus (para-
systolic rhythm). Further mapping and maneuvers (eg, mov-
Answer: B—Exit block from the appendage is definitely
ing the catheter deeper into the appendage) need to be done
present.
before entrance block can be ascertained.
As discussed earlier, the potentials recorded by the ABL d Does it make a difference whether entrance block is pres-
catheter have the same cycle length of the observed atrial ent? Unidirectional conduction occurs in various electro-
tachycardia, and after ablation, these potentials continue to physiologic scenarios, including accessory pathways that
be seen, although the proximal left atrial appendage and the conduct retrograde but not antegrade or when unidirectional
rest of the atria are not activated. Because the potentials occur block occurs across the cavotricuspid isthmus. Perhaps most
at a stable cycle length, with some occurring long after sinus importantly, exit block from the pulmonary veins can occur
activation of the neighboring atrium (considerably later than without entrance block into the vein, as evident by imped-
the expected refractory period of the neighboring tissue), exit ance mismatch between the source and the sink for electri-
block certainly is present. It is difficult to predict whether exit cal conduction (see Chapter 7), although the significance of
block would be present in the days and months after ablation, this with regard to the pulmonary vein or atrial appendage
although for this patient, tachycardia did not recur for several is unknown. In our practice, during ablation of pulmonary
years. veins for atrial fibrillation, we have used loss of conduction
With regard to entrance block, the situation is more com- into the pulmonary vein as an end point for ablation. This
plex. During sinus rhythm (Figure C19.15), a far-field potential patient had clear and persistent exit block, including after
followed by a near-field potential was recorded on the ABL d waiting for more than an hour and with administration of
catheter (arrow). The far-field potential is probably atrial isoproterenol; thus, exit block was considered a sufficient end
activation proximal to the ablation line, and the near-field point for ablation.
Case 19 605
If a catheter within the atrial appendage is advanced fur-

ther, a large near-field atrial potential will be observed, and
care should be taken to avoid perforation. If a catheter is
advanced in a branch of the left upper pulmonary vein, the
atrial and pulmonary vein potentials become less promi-
nent, and signals are eventually lost. Finally, if the catheter
is located on the mitral annulus and prolapsing into the
anterior portion of the ventricle, then the atrial potential is
lost but a large ventricular near-field potential then will be
observed.
Figure C19.16
The fluoroscopic image shown in Figure C19.16 is an RAO

projection. The ablation catheter (arrow) is likely to be
located in what region of the heart?
A. The left atrial appendage
B. The left upper pulmonary vein
C. The anterior mitral annulus
D. Any of the above
Answer: D—Any of the above. Figure C19.17
Although in this case discussion, an atrial appendage

tachycardia was successfully ablated, this RAO image shows In addition to the obtained potential, the left anterior
the transseptal (ablation) catheter “breaking the plane” of the oblique projection can be useful, particularly when distin-
annulus. The coronary sinus in the RAO projection defines guishing between a catheter deep in the left atrial appendage
the annulus (see Chapter 1). If a catheter is located ventricular vs in a branch of the left upper pulmonary vein. In Figure
to the plane of the coronary sinus after transseptal puncture, C19.17, note that the ablation catheter (arrow) is relatively
it is in the ventricle itself, in the left atrial appendage (which more septal than would be expected from a pulmonary vein
drapes over the ventricle), or in the left upper pulmonary vein. location. If the catheter has advanced well outside the pul-
The ostium of the left upper pulmonary vein is fairly poste- monary vein, it should be lateral and outside the cardiac sil-
rior and typically is further away from the annulus than the houette. A quick examination of the electrograms and the left
ostium of the left lower pulmonary vein. However, the major anterior oblique projection can allow the operator to imme-
tributary of the left upper pulmonary vein drains the anterior diately recognize when the catheter is being advanced deep in
portion of the left upper lobe, and a catheter placed in this the appendage and to pull back to avoid perforation.
vein or branch will also break the plane of the coronary sinus The concept of electrical isolation of an arrhythmogenic
and be located in a ventricular orientation. structure is seen in various anatomic locations in cardiac
From this view alone, the true position of the catheter electrophysiology. The most common isolation maneuver
is difficult to determine. It is important to monitor elec- in electrophysiology practice is isolation of the pulmonary
trograms when maneuvering catheters in these locations. veins.
Figure C19.18 (Adapted from Gurevitz O, Friedman PA. Pulmonary vein exit-block during radio-frequency ablation of paroxysmal atrial
fibrillation. Circulation. 2002;105:e124–e125. Used with permission.)
In the intracardiac electrogram shown in Figure fibrillation) continued. Therefore, this patient had electri-
C19.18, atrial fibrillation is easily diagnosed from the left cal disarticulation or isolation of the pulmonary vein. Exit
side of the tracing (HRA, PV, and CS electrodes). During block during this rapid arrhythmia clearly is present, but
circumferential ablation of the right upper pulmonary on the basis of this tracing alone, we cannot comment on
vein, sinus rhythm was restored and is clearly evident on entrance block into the vein until the arrhythmia within
the surface leads and the intracardiac CS and HRA elec- the vein has subsided. Also, this tracing alone does not
trodes. However, within the pulmonary vein, rapid irreg- show whether exit block with a slower tachycardia arises
ular arrhythmias (pulmonary vein tachycardia or atrial from within the vein.
Case 19 607
Figure C19.19
With administration of isoproterenol approximately an tachycardia in the pulmonary vein, which presumably
hour after ablation, rapid intermittent arrhythmia is seen would have caused fibrillation throughout the atrium. It is
within the pulmonary vein, again with exit block during currently unknown how long such isolation can continue
arrhythmia (Figure C19.19). In addition, entrance block into after ablation and whether entrance block into the vein
the vein with absence of pulmonary vein potentials was noted promotes or impedes initiation of arrhythmias within the
when the paroxysms of atrial arrhythmia were absent from isolated vein. Consider also the possibility that the catheter
the vein. Although the clear conversion to sinus rhythm and (used to document isolation of the vein) itself may promote
isolation of atrial fibrillation or rapid tachycardias within the arrhythmia by causing mechanical trauma. Nevertheless,
vein are uncommonly seen during ablation, they likely repre- when an arrhythmogenic source is found and, for various
sent a favorable result in terms of prognosis. clinical or electrophysiologic reasons, direct ablation of
Also apparent on analysis of Figure C19.19 is that sinus the arrhythmogenic substrate is not advisable, isolation of
rhythm continued as a result of circumferential isolation that segment should be considered an option for ablative
of the pulmonary vein, despite the paroxysms of rapid therapy.
Table C19.2
Isolation Procedures in Cardiac Electrophysiology
Arrhyth mogenic Reason for Difficulty With Rationale for Isolation Technique of Isolation Outcome
Substrate Direct Ablation of the
Arrhythmogenic Substrate
Pulmonary vein Ablation of the pulmonary Ablation at the ostium of the pulmonary Circumferential ablation is performed, The goal is to establish
vein musculature itself has vein isolates the entire portion of either at the ostium itself or by isolating a exit block during rapid
unacceptably high risk of the arrhythmogenic pulmonary vein “cuff ” of left atrial musculature proximal tachycardias arising from the
pulmonary vein stenosis musculature, with less risk of pulmonary (atrial to) a pulmonary vein ostium pulmonary vein musculature
Ablation of distal portions of vein stenosis However, block of conduction
this musculature have higher The larger circumference at the ostium into the vein (entrance block)
risk for collateral lung injury allows some fibrosis to occur without is typically chosen as the end
and perforation flow-impeding stenosis, and ablation point for circumferential
of the thicker musculature allows pulmonary vein isolation
“aneurysmal” remodeling and thereby
less narrowing
Distal (often Ablation distal (cranial) to a Circumferential ablation below the valve With fluoroscopy and intracardiac Exit block from the focus to the
supravalvar) semilunar valve (pulmonary has less risk of injuring the coronary ultrasonography, ablation is performed ventricle
ventricular outflow and aortic) may be associated artery and can isolate the arrhythmogenic approximately 1.5–2 cm below the ostia Entrance block may also be
tract tachycardia with risk of injury to the substrate distal to the ablation ring of the coronary artery, aiming to isolate observed in some patients
coronary arterial system the supravalvar muscular extensions and
Particularly, supra-aortic valve the distal portion of the outflow tract
ablation may inadvertently musculature
occur within a coronary
artery
Epicardial coronary The location of the accessory By isolating the musculature of the vein, The ostium of the venous branch (eg, middle For antegrade-conducting
vein–related pathway within the middle either at the ostium of the branch cardiac vein) can be circumferentially pathways, after the vein
accessory cardiac vein or other (or rarely, the entire coronary sinus), ablated, sometimes on the floor of the housing the pathway is
pathways in highly cardiac veins may be close reentrant arrhythmia is prevented coronary sinus, with a mapping catheter isolated, preexcitation
symptomatic to a major coronary artery The ablation is performed a considerable within the vein to assess for entrance will cease, and antidromic
patients (eg, posterior descending distance proximal to the actual pathway block and loss of preexcitation (with tachycardia and preexcited
artery, large posterolateral connection and avoids the coronary antegrade-conducting pathways) atrial fibrillation cannot
branches); thus, ablation at artery For pathways with multiple connections occur
the pathway location could into the coronary sinus musculature, However, automatic
have prohibitively high risk of ablate each connection between the tachycardias arising from the
myocardial infarction coronary sinus muscle and the left atrium musculature of the coronary
along the entire coronary sinus vein itself will still show
This difficult procedure requires meticulous preexcitation
ablation of the coronary sinus–left atrium
connection(s)
Left atrial appendage Ablation deep within the Ablation closer to the ostium of Because stenosis after ablation is not a During continued tachycardia,
appendage may have high risk the appendage may isolate the consideration, provided that the ablations there is exit block from the
of perforation arrhythmogenic focus or circuit without circle is performed proximal (atrial) to the distal atrial appendage, with
The atrial appendage may undue risk of perforation arrhythmogenic source, ablation can be or without entrance block
overlie the left circumflex performed within the appendage itself during sinus rhythm
coronary artery
Superior vena cava Potential phrenic nerve injury Circumferential ablation at the junction of Similar rationale as described for As with the pulmonary veins,
and superior vena caval the right atrium and superior vena cava in pulmonary vein isolation exit block and entrance
stenosis after ablation deep some cases may have less risk of phrenic Exception is when the phrenic nerve may block from and into the vein
into the vein nerve damage and, as with pulmonary be more easily damaged at the ostium; typically is desirable
vein isolation, less risk of postablative ablation further into the vein may be
stenosis required
Vein of Marshall Ablation within the vein, when Isolation of the vein of Marshall at its Smaller deflectable catheters are placed in Exit block for arrhythmogenic
recognized as a source of junction with the coronary sinus may the coronary sinus tachycardia and loss of
atrial fibrillation, may be be easier than advancing a catheter and Viewing the right anterior oblique conduction between a
difficult with small-caliber ablating the arrhythmogenic musculature projection, the course is followed with pulmonary vein into the
veins within the vein clockwise torque on the catheter (from coronary sinus (complete
Although endocardial ablation a femoral route) to enter the vein of isolation of the pulmonary
can be attempted on the ridge Marshall vein)
between the pulmonary veins The catheter is then withdrawn to an
and left atrial appendage, it is ostial location and circumferential
not always successful ablation performed; the catheter is then
re-advanced into the vein to document
entrance block
Other situations in which isolation rather than direct abla-

tion is an option to be considered include supravalvar ventric-
ular outflow tract tachycardia, superior vena caval origin for
atrial fibrillation, vein of Marshall or coronary sinus origin
for atrial fibrillation or tachycardia, and epicardial coronary
vein–related accessory pathways that are in the proximity of
a major coronary artery. Isolation procedures are shown in
Table C19.2.
Figure C19.21
Figure C19.21 shows the fluoroscopic RAO image of cath-

eter positioning during left ventricular outflow tract mapping.
This image does not allow direct identification of the catheter
in the left side of the heart (yellow vs white arrow). However, by
knowing that the aortic root lies posteriorly, the catheter by the
Figure C19.20
white arrow must be in the aortic root, whereas the catheter
by the yellow arrow must be in the right ventricular outflow
Figure C19.20 (left anterior oblique projection) shows the tract, likely near the pulmonic valve. With fluoroscopy alone
site of earliest activation in the right ventricular outflow tract (ie, without aortic root angiography), it is difficult to ascertain
in a patient with PVCs that had a left bundle branch block whether the catheter in the left ventricular outflow tract is
(negative in V1) and inferior axis (tall R wave in lead II), sug- above or below the aortic valve, nor can the distance between
gesting an origin in the right ventricular outflow tract. As the the catheter and a major coronary artery ostium be measured.
catheter was advanced distally and posteriorly in the right
ventricular outflow tract, the earliest sites of activation were
noted. However, the potential at the earliest site in this cham-
ber occurred simultaneously with the onset of the QRS com-
plex, suggesting that the true origin of the PVCs was located
elsewhere. As described in Cases 12 through 14, the left ven-
tricular outflow tract is posterior to the right ventricular out-
flow tract, and in posterior regions of the right ventricular
outflow tract that are close to the pulmonic valve, the imme-
diately posterior structure is the supravalvar portion of the
aortic root.
Figure C19.22
Figure C19.22 shows an intracardiac ultrasonogram

obtained with a linear, phased-array, imaging probe placed
in the right atrium. The arrow points to the catheter, which is
located just above the aortic valve, in the left coronary cusp.
Case 19 611
Figure C19.23
Low-output pacing was performed from the catheter concern for ablation in this region is potential injury to the
in the left coronary cusp (Figure C19.23). Note that a good left main coronary artery at its ostium or, with transmural
pace map was obtained from this site when compared with ablation through the aortic root, injury to the proximal por-
the spontaneous PVCs also seen in this tracing. The main tion of the left anterior descending artery.
Figure C19.24
During spontaneous PVCs (Figure C19.24), prepoten- be fraught with risk, including a potentially fatal acute occlu-
tials in the aortic cusp, close to the left main coronary artery sion of the left main coronary artery. Again, when ablation
ostium, were observed 70 to 80 milliseconds before the onset at the exact site of the arrhythmia focus is inadvisable, con-
of the surface QRS (arrow). Ablation at this site likely would sider isolating the arrhythmogenic site from the rest of the
eliminate these symptomatic PVCs, but the procedure would heart.
Figure C19.25
Figure C19.25 shows a circumferential mapping catheter cause the tip of the ablation catheter to engage a coronary
placed in the aortic root, just below the level of the left main artery.
coronary artery. Note that the ablation catheter, placed at the Complete circumferential isolation at the root level also
level of the circumferential catheter, will be moved about 1 can be difficult because of the proximity of the AV conduc-
cm lower to the left ventricular outflow tract, just below the tion system in the septal portion of the aortic root. Thus, if
level of the aortic valve before circumferential ablation occurs. an encirclement lesion is planned, AV conduction (junctional
Care should be used, even with ablation at this distance from beats) must be monitored carefully when ablating at the com-
the aortic root, because inadvertent catheter movement may missure of the right and left coronary cusps.
Figure C19.26
In Figure C19.26, the circumferential mapping catheter These indicate high-grade exit block to the rest of the ven-
(LS 1,2 to LS 10,1) was placed in the supravalvar portion of tricular myocardium, but occasional exits to the myocardium
the left ventricular outflow tract. Note the fairly frequent produce PVCs with a fi xed interval between the spike (local
spontaneous signals (arrows) indicating a rapid tachycardia. potential) and the onset of the QRS complex.
Case 19 613
Figure C19.27
As detailed elsewhere in this textbook (see Chapter 1), extensions above the base of the right coronary cusp. Similar
muscular sleeves of syncytial myocardium extend above the muscle “tongues,” although rare, may also extend above the
insertion of the aortic valve cusps into the aortic root. The noncoronary and left coronary cusps.
cardiac autopsy specimen shown in Figure C19.27 shows such
LPO
Circumferential catheter
in aortic root
Aorta
Posterolateral
left ventricle
Early MDP
Figure C19.28
Because there were early sites of activation, with partial aortic valve leaflet was able to isolate the supravalvar aortic
exit block above the valve at the level of the circumferential root (complete exit block), with no further recurrence of the
catheter (Figure C19.28), ablation just below the level of the previously symptomatic PVCs.
A 40 msec B 40 msec
+
I +
±
II ±
–
III –
R<S
Figure C19.29 (Adapted from Arruda MS, McClelland JH,

Figure C19.30
Wang X, Beckman KJ, Widman LE, Gonzalez MD, et al.
Development and validation of an ECG algorithm for identifying
accessory pathway ablation site in Wolff-Parkinson-White
syndrome. J Cardiovasc Electrophysiol. 1998;9[1]:2–12. Used with Figure C19.30 shows an inferior view of the heart. The
permission.)
arrow points to the junction of the middle cardiac vein into
Electrical isolation can occasionally be used to treat the coronary sinus. Even if the actual pathway connection to
supraventricular tachycardia such as that seen in patients the ventricle is located more distally in the vein, the muscu-
with Wolff-Parkinson-White syndrome and AV reentrant lature of the vein can be isolated by circumferential ablation
tachycardia, when the culprit accessory pathway is located at the ostium of the vein. Thus, automatic tachycardias gen-
epicardially relative to a cardiac vein. Figure C19.29 shows erally require targeted ablation at the earliest site of activa-
the classic electrocardiogram description by Arruda et al (J tion and reentrant tachyarrhythmias require ablation of the
Cardiovasc Electrophysiol. 1998 Jan;9[1]:2–12). Note particu- culprit slow zone responsible for the reentrant circuit, but
larly the initial delta wave axis in lead II. Although all poste- these approaches occasionally are unfeasible. This may be
rior accessory pathways will have a negative delta wave in the because of prohibitive risk of complications ablating at the
inferior leads (leads II, III, and aVF), when the initial deflec- site required.
tion in lead II is negative, a middle cardiac vein or posterior
cardiac vein accessory pathway should be considered.
Abbreviations
Several methods can be used to ablate middle cardiac vein
or posterior cardiac vein accessory pathways. Ideally, a path-
way potential within the middle cardiac vein should be tar- AV, atrioventricular
geted for ablation. However, these pathways may have broad CS, coronary sinus [f]
muscular connections into the venous system; even when a LA, left atrium [f]
discrete connection is found, an important coronary artery LAA, left atrial appendage [f]
may be adjacent to the pathway in the vein, making ablation LIPV, left inferior pulmonary vein [f]
difficult. In these situations, isolate either the middle cardiac LPO, left posterior oblique view [f]
vein or, more rarely, the coronary sinus itself. Complete isola- LSPV, left superior pulmonary vein [f]
tion of the coronary sinus is difficult, given the multiple con- MDP, middiastolic potential [f]
nections between this vein and the atria. If accomplished, AV PVC, premature ventricular contraction
reentrant tachycardia will no longer be inducible, and pre- RA, right atrium [f]
excitation will not be seen in sinus rhythm (although it may RAO, right anterior oblique
still be seen with ectopy or pacing from the coronary sinus RIPV, right inferior pulmonary vein [f]
musculature). RSPV, right superior pulmonary vein [f]
Case 20
When an electrophysiologist mentions encountering an atrioventricular (AV) node initiates AVNRT with the appear-
unusually difficult case in the electrophysiology laboratory, ance of junctional tachycardia. As mentioned elsewhere (see
the actual diagnosis may have been a common arrhythmia Chapter 4 and the case discussions), termination of a narrow
that occurred under unusual circumstances or with unusual complex tachycardia with an atrial potential argues against
characteristics. Just as the Oslerian dictum in internal medi- atrial tachycardia as the mechanism. Administration of
cine states that uncommon manifestations of common diag- adenosine that results in a prolonged A-H interval before
noses are more likely than a common manifestation of a rare termination of tachycardia would also exclude atrial tachy-
diagnosis, so is it also true in electrophysiology. Ablationists cardia. However, some automatic atrial tachycardias are sen-
must be thoroughly familiar with the protean manifesta- sitive to autonomic modulation or adenosine (or both), and
tions of common arrhythmias (eg, atrioventricular nodal during vagal stimulation, prolongation of the A-H interval
reentrant tachycardia [AVNRT], atrioventricular reentrant with AV block will occur with simultaneous termination of
tachycardia [AVRT], etc). Sometimes, the difficulty stems the atrial tachycardia. Although the rules of electrophysi-
from an unusual potential recorded during the electrophysiology must be mastered by the student electrophysiologist
ology study. These signals may be artifacts or bystanders that and ablationist, no phenomenon is without exception, and
obscure the actual tachycardia mechanism. For example, a all performed maneuvers and the clinical scenario must be
fragmented potential at the ostium of the middle cardiac vein considered when establishing the diagnosis.
during a narrow complex tachycardia may represent the path- Sometimes, unusual anatomy or physiology can cause
way potential (and thus be a suitable target for ablation) dur- difficulties. Patients with congenital heart disease, venous
ing orthodromic reciprocating tachycardia (ORT); or it may anomalies, abnormal hemodynamics that prevent adequate
simply arise from coronary sinus musculature extending into mapping of a tachycardia, and previous scars can make even
this vein, which has nothing to do with the circuit (unneces- the simplest arrhythmia difficult to understand and thus may
sary ablation at this site will be unsuccessful and potentially hinder identification of an appropriate ablation site.
risks injury to the arterial system). Particular difficulty occurs when more than one diagnosis
Other causes of difficulty may include strict adherence is present (eg, 2 or more accessory pathways, AVNRT with a
to the “rules” of electrophysiology and failing to recognize bystander accessory pathway, or competing atrial tachycar-
exceptions to these rules. For example, initiation of a tachy- dia and AVNRT [see Case 12]). Sometimes, one tachycardia
cardia with prolongation of the atrial-His (A-H) interval is may initiate another, and if these tachycardias have similar
typical of AVNRT and ORT. Yet a 2-for-1 initiation with intra-atrial activation sequences or ventriculoatrial (V-A)
antegrade fast and slow pathway conduction through the intervals, despite obvious changes in the QRS morphology,
the situation can be very challenging. Such scenarios include
AVNRT-initiating fascicular tachycardia with rapid retro-
Abbreviations are expanded at the end of this chapter. grade conduction, junctional tachycardia after ablation, and
Terms with “[f]” denote abbreviations that appear in the figures only. the use of isoproterenol in a patient with AV node reentry).
615
Table C20.1
The Difficult Case in the Electrophysiology Laboratory
Cause of Difficulty Examples Strategies to Minimize Difficulty
Difficult or unusual Coronary sinus muscle potentials Careful performance of pacing maneuvers (applying
potentials Bystander supravalvar great arterial potentials the concepts of association and dissociation between
Fragmented potentials from previous failed ablation of potentials)
an accessory pathway
Difficult or unusual 2:1 initiation of AVNRT Careful attempts to reproduce pattern of initiation
initiation Beat starting ORT or AVNRT Meticulous assessment of changes in intracardiac
Nonsustained ventricular tachycardia initiating ORT intervals (wobble) before and at initiation
with aberrancy
Difficult or unusual Atrial tachycardia with an atrial potential Careful analysis of variation in intracardiac intervals
termination Junctional tachycardia without an atrial potential (wobble) before termination
Reentrant ventricular tachycardia during catheter Attempts to reproduce mechanism of termination with
manipulation (mistaken for automatic tachycardia) pacing maneuvers
Difficult or unusual Post-Fontan status Knowledge of anatomic variance
anatomy Venous anomalies Imaging modalities
Conduction system anomalies Flexibility in applying established maneuvers in the new
setting
Difficult or unusual Hypertrophic cardiomyopathy Rapid termination of tachycardia and detailed analysis
physiology Hemodynamically unstable ventricular tachycardia of initiation and termination
Hemodynamically unstable narrow complex Supportive devices for maintaining blood pressure
tachycardia with a short R-P interval Advanced mapping systems (see mapping chapter)
Difficulty from Multiple accessory pathways Careful analysis of activation sequence
multiple diagnoses Bystander accessory pathway with AVNRT Importance of demonstrating reset of tachycardia in
Bystander fast pathway with ORT addition to preexcitation, etc
Induction of atrial flutter from an automatic
tachycardia that continuously resets the flutter
Truly unusual Nodoventricular tachycardia Experience with careful exclusion of common diagnoses
arrhythmia Tachycardia arising from a chamber or vein not
normally present
Automaticity from an accessory pathway without
preexcitation
Abbreviations: AVNRT, atrioventricular nodal reentrant tachycardia; ORT, orthodromic reciprocating tachycardia.
As an electrophysiologist gains experience and performs occur in an unfamiliar situation (Table C20.1). However, if a
important maneuvers consistently (see Chapter 4), he or she rare arrhythmia truly occurs, and if a systematic approach
becomes conversant with the exceptions to the rules of appli- is used to first exclude unusual manifestations of a com-
cation of these maneuvers and to the analysis of common mon arrhythmia, then the electrophysiologist will be better
arrhythmia, even in patients for whom the diagnosis seems equipped to confirm the diagnosis and formulate an ablation
apparent. Almost always, the difficult case will be a famil- strategy (eg, nodoventricular tachycardia, tachycardia from
iar arrhythmia, but it may have unfamiliar characteristics or conduction system remnants, etc).
Case 20 617
Figure C20.1
The intracardiac electrograms in Figure C20.1 were vena cava. The CS catheter was placed within the coronary
obtained from a 43-year-old woman with a previous diagno- sinus, with poles CS 13,14 located just within the coronary
sis of atrial fibrillation that was treated with pulmonary vein sinus ostium. The hRA catheter was located close to the usual
isolation. She had monomorphic atrial tachycardia that was sinus node location.
associated with clinically significant symptoms, and she was Marked variation in the cycle length (wobble) was noted.
referred to the electrophysiology laboratory for further man- The ablationist specifically noticed on multiple occasions that
agement. A circumferential catheter was placed in the supe- the V-A (His-atrial [H-A]) interval was longer (see the third beat
rior vena cava at the junction of the right atrium and superior of Figure C20.1) just before termination of the tachycardia.
Figure C20.2
Figure C20.2 shows variation in the H-A interval, as mea- Figure C20.3 shows that the A-H interval after the cycle
sured from the end of the His bundle deflection on the distal with the longer H-A interval was shorter (252 milliseconds)
HBE1 electrode to the earliest atrial potential on the proxi- than the A-H interval after the cycle with the shorter H-A
mal HBE3 electrode. Note the marked shortening of the H-A interval (297 milliseconds). This pattern was consistently
interval from 169 to 129 milliseconds. observed (ie, a short H-A interval was followed by a longer
Figure C20.3
Case 20 619
A-H interval, and a longer H-A interval was followed by a not affect the cycle length of the tachycardia. In comparison,
shorter A-H interval). in AV node reentry, the H-A interval is a close approximation
of conduction via the retrograde fast pathway, and because
Which diagnosis is verified by the consistent observation it is part of the AVNRT circuit, changes in the H-A interval
of a prolonged H-A interval subsequently causing a change would affect subsequent intervals (A-H interval, PR interval,
in the A-H interval of the next beat, as observed in Figure etc) and the rate of the tachycardia. Thus, the observation
C20.3? shown in Figures C20.1 through C20.3 helps exclude junc-
A. Junctional tachycardia tional tachycardia.
B. AV node reentry However, atrial tachycardia cannot be excluded as a possi-
C. ORT ble mechanism. Thus, if the H-A interval in the fourth beat of
D. Atrial tachycardia tachycardia (Figure C20.3) is short because of variation in an
E. None of the above automatic atrial tachycardia cycling (increasing tachycardia
rate), then the subsequent A-H interval may be long because
of greater stress on the compact AV node with the earlier
As detailed in Chapter 4 and in several of the case dis- beat of atrial tachycardia. Greater variability in the automatic
cussions in this textbook, variation in a specific intracardiac focus just before termination may also be why this phenom-
interval that causes a subsequent change in the tachycardia enon was observed close to termination of the tachycardia.
cycle length or another intracardiac interval can be diagnos- Even with ORT, the H-A interval can appear to be the driver
tic of certain arrhythmias. For example, in a patient with nar- of the circuit. With ORT, the H-A interval is a pseudointer-
row QRS tachycardia, a change in the His-ventricular interval val because no retrograde conduction is occurring via the
that subsequently changes the tachycardia cycle length (ie, AV node. The His bundle potential results from antegrade
resets the tachycardia) would strongly favor ORT rather than activation via the AV node, and the earliest atrial potentials
AVNRT or atrial tachycardia. If the H-A interval is clearly are from retrograde conduction via the accessory pathway.
demonstrated to be the “driver” of subsequent changes in the Nevertheless, if there is decremental retrograde conduction
tachycardia, AV node reentry is strongly favored as the cause via the accessory pathway, then the H-A and V-A intervals
of tachycardia. This observation is mainly relevant when dis- will vary. In addition, if the retrograde pathway is located
tinguishing between AVNRT and junctional tachycardia. in the septal region, AVNRT may be confused with the lon-
In junctional tachycardia, the rate of tachycardia is main- ger “H-A interval” being followed by a shorter A-H interval
tained by the periodicity of the automatic junctional focus, (facilitation of antegrade AV node conduction). Decremental
and the rate of tachycardia (His-His interval) will remain pathways on the anteroseptal or midseptal regions are rare,
unaffected by the presence or degree of retrograde conduction however, making AV node reentry much more likely than
to the atrium. Thus, marked changes or even block between ORT when the H-A interval change causes a subsequent
the His bundle and atrial potentials (H-A intervals) would change in the A-H interval.
Figure C20.4
In Figure C20.4, several important observations should be B. The tachycardia must be an atrial tachycardia because
noted. The arrow points to a beat with a markedly shortened the first beat occurs without apparent retrograde V-A
H-A interval. Note that the A-H interval for the next beat is conduction
longer and the next atrial sequence also comes later. Th is anal- C. The tachycardia is atypical AVNRT, as demonstrated by
ysis of several subsequent beats after a change in one particu- H-A and A-H interval dependence on the tachycardia
lar cardiac interval (ie, the H-A interval) is very important for and the long V-A interval
deducing the mechanism of tachycardia. Prolongation of the D. Typical AVNRT is the likely diagnosis
A-H interval that causes prolongation of the next atrial-atrial E. None of the above
(A-A) interval, despite shortening of the H-A interval in sub- Answer: D—Typical AVNRT is the likely diagnosis.
sequent beats, is strong evidence that the tachyarrhythmia is
dependent on the AV node. Although the tracing in Figure Remember that the distinction between typical and atypi-
C20.1 showed changes in the H-A interval and prompted cal AV node reentry is based on the site of earliest atrial
analysis of the subsequent beat, atrial tachycardia can be activation and not the V-A interval. Typical AVNRT may be
excluded because of the repeated finding of changes in the associated with a long V-A interval for several reasons, includ-
A-H interval determining the cycle length of the tachycardia ing 1) very quick retrograde fast-pathway conduction giving
(cycle length not affected by antegrade AV node conduction). rise to an atrial potential before the His bundle potential; 2)
Another important finding in Figure C20.4 pertains to slow antegrade AV nodal or infrahisian conduction resulting
initiation of tachycardia. It starts with the placement of a sin- in retrograde atrial activation before His bundle and ventric-
gle extrastimulus, which is associated with mild prolongation ular activation; or 3) slow retrograde fast-pathway activation
of the A-H interval. The first beat of tachycardia has an atrial causing the appearance of long V-A conduction times.
activation sequence that is similar to the subsequent beats of Because of the reciprocal relationship between the H-A and
tachycardia. The V-A interval for the first beat of tachycardia A-H intervals (dependence on AV node and retrograde atrial
is long and subsequently becomes shorter, as discussed above. activation), AV node reentry is strongly suggested. With the
The earliest atrial activation observed is in the region of the retrograde fast-pathway region (proximal His catheter being
proximal His bundle catheter. the usual surrogate for the fast pathway) being earlier than
the slow-pathway region (proximal coronary sinus electro-
Which statement is true? gram being the usual surrogate for the retrograde slow path-
A. The tachycardia cannot be typical AVNRT because of way), if this tachycardia is AVNRT, it is likely to have typical
the long V-A interval AV node reentry.
Case 20 621
Figure C20.5
Figure C20.5 shows termination of the tachycardia and patient, pacing the ventricles produced an atrial activation
marked variation in the H-A interval just before termination. sequence that was identical to that seen in tachycardia. It is
Again, note that when the H-A or A-H intervals are long, the highly unusual to have the focus of an atrial tachycardia aris-
subsequent A-A interval is also long (suggesting dependence ing at the exact same location of ventricular atrial activation
on AV node, etc). These findings strongly argue against atrial through the AV node or an accessory pathway. Thus, identi-
tachycardia as the mechanism of arrhythmia. To deduce the cal atrial activation sequences during tachycardia and ven-
mechanism of tachycardia, the most information on chang- tricular pacing strongly argue against atrial tachycardia. In
ing intervals can be obtained at initiation, termination, and this patient, ventricular activation could easily be dissociated
when placing extrastimuli during tachycardia. from the tachycardia; this effectively excluded ORT as the
A simple and useful maneuver for distinguishing between diagnosis. Thus, with exclusion of atrial tachycardia, ORT,
atrial tachycardia and AV node reentry is to assess the and junctional tachycardia, the remaining diagnosis was AV
atrial activation sequence during ventricular pacing. In this node reentry.
Figure C20.6
An important pitfall can occur when comparing the atrial Although the proximal His bundle atrial potential is used
activation sequence during rapid ventricular pacing with the as a surrogate for the fast pathway, the true fast-pathway exit
sequence during tachycardia. In Figure C20.6, there is retro- site is located behind the crest of the eustachian ridge. In the
grade V-A Wenckebach with an activation sequence in the left anterior oblique (LAO) projection, a catheter positioned at
atrium identical to that in tachycardia. However, closer exam- this site can be recognized by the left ward orientation of the
ination suggests that tachycardia was initiated earlier during catheter tip compared with the His bundle recording catheter
ventricular pacing; it continued throughout the tracing, with (see Chapter 4).
an identical atrial cycle length, and was dissociated from the In the patient being discussed, is further mapping nec-
rapid ventricular pacing. Thus, with this tracing alone, AVRT essary? Clearly, with the criteria established and explained
can be excluded, but conclusions cannot be drawn about the above, AV node reentry is the most likely diagnosis. The next
similarity of retrograde ventricular atrial activation and the step should generally be anatomic ablation at the slow-pathway
tachycardia atrial activation sequence. site. In this patient, however, a consistent finding was a rela-
tively long V-A interval, with the atrial potential on the His
To map the retrograde fast-pathway exit site, which strat-
bundle catheter only slightly preceding atrial activation in
egy is most exact?
the coronary sinus. Thus, to ensure that the retrograde fast
A. Use the proximal atrial potential on the His bundle
pathway was in fact the true earliest site of atrial activation, a
catheter
mapping catheter was placed at the anatomic location of the
B. Use the distal atrial potential on the His bundle
fast pathway, just behind the tendon of Todaro. The ABL d
catheter
catheter was placed there, but the atrial potentials at this and
C. Use the potential recorded by the proximal coronary
neighboring sites were later than that observed in the proxi-
sinus catheter
mal His bundle region and were in fact later than the atrial
D. Place a mapping catheter between the eustachian ridge
potential at the proximal coronary sinus region.
and the tricuspid annulus anteriorly
E. Place a mapping catheter behind the crest of the eusta-
chian ridge (tendon of Todaro)
Answer: E—Place a mapping catheter behind the crest of
the eustachian ridge (tendon of Todaro).
Case 20 623
Figure C20.7
In Figure C20.7, although the atrial potential on the proxi- right midseptal region, activation of the anterior septal region
mal His bundle catheter is the earliest recorded atrial activity, (His bundle atrial potential) and the posterior septal region
it times surprisingly close to that noted on the proximal CS (proximal coronary sinus atrial potential) occur nearly simul-
catheter. taneously. For the rare midseptal pathway, a similar phenom-
enon occurs; however, in that scenario, atrial activation of
Which is the least likely cause of simultaneous atrial acti-
the His bundle region is simultaneous with the mid coronary
vation of the proximal coronary sinus and the His bundle
sinus atrial potential (left midseptal pathway, His-atrial, and
region?
mid coronary sinus–atrial simultaneous).
A. The true earliest site is in the right midseptal region
If an anteroseptal accessory pathway and AV node con-
B. There are 2 methods of atrial activation: slow pathway
duction via the slow pathway are both present, simultane-
and anterior septal accessory pathway
ous activation of the anterior and posterior septal regions
C. The true earliest site is in the tricuspid annular region.
may occur. It would be unusual to see this during tachycar-
D. The true earliest site is in the anterior mitral annular
dia, however, because either atypical AV node reentry with
region
a bystander accessory pathway or ORT with a bystander
E. There are 2 methods of atrial activation: AV node and a
slow pathway conduction would have to be present, and
posteroseptal pathway
those situations are quite rare. As already described, ven-
Answer: D—The true earliest site is in the anterior mitral tricular pacing at a cycle length different from tachycardia
annular region. produced the same activation sequence, making this pos-
Whenever there are 2 simultaneous but anatomically sibility highly unlikely. Nevertheless, it is important to
separate sites of simultaneous electrical activation, recall that consider whether 2 different atrial sites are simultaneously
there are 2 methods of activating the atrium. Furthermore, early during ventricular pacing (one from a pathway and
there must be a site of activation earlier than either of the 2 one via the AV node).
recognized sites, but a recording electrode is not present at The true earliest site of activation may be spatially and
that location. temporally equidistant from the anterior and posterior septal
When the atrium near the His bundle and the proximal region (eg, location on the tricuspid annulus laterally, poste-
coronary sinus are activated at the same time, the true ear- rolaterally, or anterolaterally). In a true lateral origin of tachy-
liest site of activation is the right midseptal region. This is cardia, the anterior and posterior septum may be exactly
often important for recognizing the presence of a right mid- simultaneous. In contrast, if an anterolateral site is the true
septal accessory pathway. During ventricular pacing or ORT, site of origin, the anteroseptal region should be slightly ear-
because we do not usually have a recording electrode in the lier than the posteroseptal region.
Among the answer choices in the question above, the least Because mapping of the anatomic site of the fast pathway
likely cause is an anterior mitral annular tachycardia. The did not show early activation (Figure C20.7), other atrial loca-
fast-pathway region should be activated considerably earlier tions were mapped, including the midseptal region, the roof
than the posteriorly and inferiorly located proximal coronary of the coronary sinus, and the tricuspid annulus.
sinus because of conduction either via the Bachmann bundle
or the fossa ovalis.
Figure C20.8
With the mapping catheter on the lateral tricuspid annu- potential. The midseptal region was subsequently activated,
lar region, the electrogram obtained is shown in Figure and because the midseptum was late, no further mapping of
C20.8. Here, atrial activation clearly precedes the proximal the septal region was undertaken. Point-to-point mapping of
His bundle atrial potential and the proximal coronary sinus the right atrium continued.
Case 20 625
Figure C20.9
In Figure C20.9, note the timing of atrial activation near would entrain the tachycardia. Upon cessation of pacing, the
the orifice of the right atrial appendage, close to the annulus last ventricular paced beat was followed by an atrial potential
(ABL d), which was 62 milliseconds ahead of the His bundle and then a return ventricular potential (V-A-V pattern; see
atrial potential. If sites away from the atrial septum are found Chapter 4).
that show earlier activation than either anatomic locations of Altogether, these features were virtually diagnostic of AV
the fast and slow pathways, should the diagnosis of AV node node reentry. Against this body of evidence was the fi nding of
reentry be reconsidered? Often, in the midst of a difficult case, early sites of atrial activation preceding septal activation. To
conflicting data from the diagnostic electrophysiology study reconcile this conflict, consider anatomic variants in the con-
must be reconciled. duction system, both with and without other congenital heart
At this point, several characteristics of the easily induced disease (see Chapter 9). Although many rare variants have
arrhythmia were known. First, changes in the retrograde been described, in one scenario, the AV node may be located
H-A interval caused subsequent changes in the A-H inter- more anteriorly (sometimes seen with corrected congenital
val and the tachycardia cycle length. Second, changes in the transposition of the great vessels). Also, extensions of the AV
A-H interval caused subsequent changes in the A-A inter- node may occur along the tricuspid annulus. As with most
val (delay in A-H caused delay of the next A-A). Th ird, the congenital anomalies, a spectrum of variants likely exists. At
ventricle could be easily dissociated from the tachycardia. times, there is an extension similar to the posterior extension
Fourth, the tachycardia could be reset from the ventricle with or left ward extension of the AV node that occurs anteriorly on
premature ventricular contractions (PVCs) placed relatively the tricuspid annulus; in extreme forms, isolated portions of
early. The atrial potential could be advanced by advancing conduction tissue can be found along the tricuspid annulus,
the retrograde His bundle potential, without changing the with or without ventricular connection or atrial myocardial
atrial activation sequence and resetting the tachycardia. connections.
Fift h, ventricular pacing resulted in an atrial activation The catheter was then withdrawn to just outside the atrial
identical to that seen during tachycardia. Sixth, ventricular appendage and in an anterior-anterolateral location along the
pacing at a cycle length slightly faster than the tachycardia tricuspid annulus.
Figure C20.10
The white arrow in Figure C20.10 points to the site of bundle catheter.
the ablation catheter. The yellow arrow points to the His
Figure C20.11
The electrogram obtained with the ABL d catheter posi- an anteriorly located compact AV node or a tricuspid annular
tioned on the anterior tricuspid annulus (Figure C20.10) is extension (exit) off the AV node was established.
seen in Figure C20.11. The atrial potential at this location Although lateral or anterolateral extensions of the AV
was the earliest recorded after detailed mapping of the entire node and anteriorly displaced AV nodal tissue are exceed-
right atrium, and it preceded the His bundle atrial recording ingly rare (especially without coexisting congenital heart dis-
by 87 milliseconds. Given the evidence for AV node reentry ease), developmentally AV node–like tissue occurs all along
described above, a diagnosis of AV node reentry with either the atrial ventricular annuli. The exact incidence of remnants
Case 20 627
of such tissue in adult life along either annulus is unknown.

Presumably, when remnants do occur in these locations, if
they are not associated with atrial or ventricular (myocar-
dial) connections, they do not cause abnormal electrocardio-
grams or arrhythmias that would prompt attention and their
recognition.
Some forms of these anomalies occur in a low but com-
mon enough frequency that the electrophysiologist must be
familiar with them and understand how they differ from the
usual AV accessory pathway. (Usual accessory pathways are
muscular connections that bridge the annulus connecting
atrial and ventricular myocardium.)
Figure C20.13
Mahaim fibers occur almost exclusively along the tri-

cuspid annulus and are rarely seen in relation to the mitral
annulus. An exceptional circumstance may occur in which
an antegrade, decrementally conducting pathway sometimes
does not insert close to the annulus; this may be seen with
corrected congenital transposition of the great vessels, or the
pathway may be located in the vicinity of the anterior fibrous
trigone of the heart (atrial left anterior pathways, aortic mitral
continuity–related pathways) (Figure C20.13; arrows show
pathway activation).
Although displacement of the AV node anteriorly or pos-
Figure C20.12 teriorly and Mahaim-like fibers are rare, an even rarer condi-
tion is true duplication of the AV node or accessory AV nodal
structures. These structures almost exclusively occur in the
Mahaim fibers (various forms are discussed in Chapters setting of other congenital heart disease and can be distin-
4 and 6) are similar to AV nodal and infrahisian conduction guished from Mahaim fibers in that duplicate AV nodes may
tissue remnants. These structures are located on the annu- conduct both antegrade and retrograde and may demonstrate
lus, where they demonstrate antegrade decremental proper- dual AV nodal physiology. Accessory AV nodes, when they do
ties, and the ventricular insertion is typically not close to the occur, tend to do so in the anterior mitral annular region.
annulus. This is the primary distinguishing feature between In some electrophysiologic studies, mapping along the
such pathways and the usual AV muscular accessory path- annulus will reveal sharp His bundle–like or accessory path-
ways. As pictured in Figure C20.12, they may insert at variable way–like potentials; this can occur in patients with supraven-
distances closer to the apex into the ventricular myocardium tricular tachycardia and a suspected right free-wall accessory
or, more commonly, will connect directly to the infrahisian pathway. Such potentials are critical for identifying Mahaim
conduction system of the AV node (see Chapter 6). Unlike the fibers and represent the ideal ablation target for these struc-
AV node, however, Mahaim fibers (atrial Hisian/atrial fascic- tures. However, such potentials can be misleading, and the
ular fibers) do not conduct retrograde and do not have dual ablationist may target these potentials for ablation because
AV nodal physiology in the antegrade direction. they are recognized as abnormal and are assumed to be asso-
ciated with the arrhythmia being treated. Several examples in
this textbook (including Chapter 4) address this issue of rec-
ognizing bystander potentials along the tricuspid annulus.
No connection with atrium
Conduction via rapidly

conducting tissue to point of exit
Figure C20.14
If the electrophysiologist is aware of this phenomenon, the physiologic significance. Very rarely, PVCs or ventricular
usual maneuver is to diagnose the origin and significance of tachycardia may be mapped to the annulus and a spike-like
an unexplained potential (eg, a bystander Mahaim-like poten- (His-like) potential will precede ventricular myocardial acti-
tial would occur after the earliest ventricular potential dur- vation, often with the earliest ventricular activation being
ing antidromic tachycardia). These AV node remnants, with 1 or 2 cm apical to the annulus (Figure C20.14). Thus, the
or without His bundle–like tissue, are not connected to the annular AV node–like structures found in fetal development
atrium and therefore show no evidence of antegrade preexci- are normally replaced by the fibrous annulus, an insulating
tation or retrograde eccentric conduction to the atrium with structure that stops direct conduction between the atrial and
ventricular pacing. Although they are known to give rise to ventricular myocardium. Exceptions to this normal situation
misleading potentials, AV node remnants have no established are summarized in Table C20.2.
Table C20.2
Characteristics of AV Annular Electrical Abnormalities
AV Annular Electrical Description Salient Features Frequency of Occurrence Electrophysiologic Significance
Abnormality
Accessory bypass tract Myocardium that bridges the May conduct antegrade only, Most common Ablation must be targeted at the annulus, at
annulus, connecting the atrium retrograde only, or bidirectionally abnormality in this the site of the accessory pathway potential
and ventricle Typically no decremental properties group Ventricular and atrial insertions are generally
Insertions are very close to the close to the pathway location on the annulus
annulus and are secondary targets for ablation
Mahaim fibers (atrial-Hisian AV node-like structure with Antegrade-only conduction Rare Targeting the earliest site of ventricular
and atrial-fascicular attached His bundle and Decremental antegrade conduction activation is largely meaningless because it
pathways) right bundle–like structures property may be identical to the ventricular exit of
that insert variably into Earliest site of ventricular activation the normal right bundle
myocardium, the true His is 1-4 cm apical to the annulus Mapping an ablation that targets the His
bundle, or right bundle bundle–like potential close to the annulus
associated with the centrally is ideal
located “normal” AV node These pathways may be easily “bumped”
(mechanically traumatized)
Because of decremental properties and slow
conduction, preexcitation is often subtle
Accessory (duplicate) AV True remnants of AV nodal Antegrade or retrograde conduction Extremely rare, even Although rare, this should be distinguished
node tissue along the annulus, with (or both) are possible when associated with from other more common accessory
infranodal His bundle and Dual AV nodal physiology possible other congenital pathways
bundle branch system Earliest ventricular activation closer anomalies Should be suspected when annular activation
to the apex than the base, similar is decremental retrograde and early
to the usual right bundle or left ventricular activation is decremental
bundle exit antegrade, in a patient with congenital heart
disease
AV nodal remnant is AV node and His bundle–like Incidental findings of His bundle–like Unknown Sometimes, spike-like potentials are mistaken
isolated (no atrial structure located on the potentials during annular mapping for a Mahaim fiber or accessory pathway
connection) annulus, presumably from Usually a bystander potential with no potential when they actually are incidental
failure to degenerate during relationship to the arrhythmia or bystander potentials
fetal development
Figure C20.15
Returning to the case discussion, decisions must be made C. In the posteroseptal region, near the coronary sinus
about how to treat the arrhythmia in the electrophysiology ostium
laboratory. To recap, an unusual variant of AV node reentry D. The usual anatomic location of the fast pathway
was diagnosed; either the AV node was anteriorly displaced E. None of the above
or a rightward, anterior lateral extension of the AV node (exit) Answer: C—In the posteroseptal region, near the coronary
was present, giving rise to the site of earliest atrial activation sinus ostium.
(Figure C20.15) in this location 87 milliseconds ahead of the
His bundle region.
Where should ablation be performed to rid the patient of
this tachycardia?
A. At the site of earliest atrial activation
B. Attempt to record a pathway potential and ablate at that
site
Case 20 631
Table C20.3
Conditions in Which the Earliest Site of Activation Is Not Targeted for Ablation
Condition Reasons for Not Targeting the Earliest Site
Typical AV node reentry Earliest site of activation is the fast pathway, generally closer to the compact AV node, and associated
with a higher risk of AV block than ablation of the slow pathway
Note that the earliest activation can be targeted with atypical AV node reentry
Mahaim fiber–related antidromic Mahaim fibers may insert into the right bundle, and the earliest ventricular activation site is via the
tachycardia right bundle
Ablation should instead be performed close to the annulus at the site of the Mahaim potential
Reentrant tachycardia The site of earliest activation with reentrant arrhythmias represents the exit from the protected zone
to the rest of the myocardium
Ablation should instead target the slow zone responsible for maintenance of the tachycardia
(see Chapter 5, Cases 16 and 17)
Junctional tachycardia Sometimes, tachycardias arising from the slow-pathway region may exit via the compact AV node to
the fast pathway; ablation at the earliest site of activation or the compact AV node would more likely
result in AV block, whereas ablation of the slow pathway region may be successful without AV block
Fascicular tachycardia With fascicular ventricular tachycardia, the earliest ventricular site of activation may be very similar
to the earliest ventricular site of activation in sinus rhythm via the bundle
The Purkinje potential that is earliest or meets specific pacing-related criteria (ie, pacing stimulus to
earliest ventricular potential has a similar interval to the local His-Purkinje potential to the earliest
ventricular potential during spontaneous tachycardia)
Pulmonary vein tachycardia Circumferential isolation at the venoatrial junction or in the atrium is preferred because ablation at
the earliest site of tachycardia may result in pulmonary vein stenosis
Supravalvar aortic (or pulmonary The true origin may be close to the arterial system, and circumferential isolation at the
arterial) tachycardia ventricular-arterial junction or in the ventricular myocardium may be preferred
As described above with Mahaim fibers, in certain elec- pathway and should not be targeted initially for ablation. In
trophysiologic situations, the site of earliest activation specifi- this patient, the slow pathway was ablated in its usual ana-
cally is not targeted (Table C20.3). tomic location. The approach was linear ablation along the
The decision of whether ablation should be targeted to the posteroseptal annulus, up to and including the coronary
site of earliest activation depends on whether the extension sinus ostium at its floor. Junctional beats were seen during
of the AV node and its location is interpreted to be the fast ablation (with a similar retrograde atrial activation sequence).
pathway or slow pathway. Considering the AV nodal variants In addition, tachycardia was no longer inducible, including
described above, the AV node may be anteriorly displaced, with repeat testing using isoproterenol. The patient has been
and when an anterior exit is seen, it is analogous to the fast symptom free for 2 years after ablation.
His bundle (C) Mitral valve
Tricuspid valve Scar

VT focus (D)
Endocardial exit
Right bundle Left bundle
Fascicular
tachycardia (E) Epicardial focus (F)
RV
LV Scar
Mahaim fiber (A)
Moderator band (B)
Figure C20.16
Figure C20.16 illustrates further the concept of when the bundle potential; in addition, retrograde block to the atrium
earliest site of activation is not always the best site to target and atypical bundle branch aberrancy will give the mistaken
for ablation. Although the figure shows issues relevant to the impression of a primary ventricular tachycardia. In this
ventricle, as mentioned above, analogous situations may also instance, the earliest ventricular site of activation will be the
arise in the atrium and pulmonary veins. usual exit site of the infrahisian conduction system (bundle
In Figure C20.16 example A, a Mahaim fiber is shown tra- branch that conducts).
versing the moderator band and inserting close to the dis- In Figure C20.16 example D, a ventricular tachycardia
tal right bundle branch (its usual course). During maximal focus that arises within the interventricular septum may
preexcitation, the earliest ventricular site of activation would sometimes propagate into the conduction system and exit
be about two-thirds the distance from the base to the apex, into the ventricular myocardium fairly distant from the orig-
essentially identical to the usual exit site of the right bundle inal focus, especially if the myocardium near the ventricular
branch. Clearly, targeting ablation at its normal exit site to tachycardia focus has a scar or regions of slow conduction.
the ventricle would not be effective in eliminating conduction This can mistakenly suggest that the true site of origin is at
via the Mahaim fiber. The Mahaim fiber–related potential, as the exit site of the heart’s normal conduction system.
described above, is the ideal target for ablation close to the In Figure C20.16 example E, the true site of origin is noto-
tricuspid annulus. riously difficult to find in fascicular tachycardias (see Chapter
In Figure C20.16 example B, the moderator band may 6). Here again, the exit to the ventricular myocardium can
itself be the source of ventricular tachycardia. This would be a considerable distance from the true origin and is simi-
be an inappropriate target for ablation because branches of lar to the exit of the usual conduction system. Specific pacing
the right bundle traverse in this structure, and normally, the maneuvers are required to clarify the situation (see Chapter 6
earliest exit sites for a ventricular tachycardia originating in and several case examples presented).
the moderator band may be via this conduction system at the In Figure C20.16 example F, even without nearby con-
lateral wall or on the septum. duction tissue, the epicardial arrhythmogenic substrate for
In Figure C20.16 example C, tachycardia may originate in ventricular tachycardia may exit to the endocardium a con-
the insulated portion of the His bundle itself. The mechanism siderable distance away from the ideal site to target ablation.
of this tachycardia usually is clear because the His bundle Sometimes, the endocardial region may have multiple exits.
deflection will significantly precede the QRS complex and is Because the usual ablation techniques involve endocardial
usually associated with retrograde conduction to the atrium. mapping, multiple early sites or multiple sites of similar but
Sometimes, the His bundle catheter fails to record a clear His not identical concealed entrainment may be found during
Case 20 633
an electrophysiology study. Generally, whenever the earliest pathologic structure (eg, aneurysm, pouch, etc), or the epi-
site of an arrhythmia occurs at the known exit of a normally cardial surface.
conducting structure (eg, bundle branches, fast pathway) Now consider 2 other instructive examples of uncommon
or multiple early sites are found, the electrophysiologist manifestations causing a common arrhythmia to masquer-
should consider whether the true origin is located in the ade as an unusual or difficult case.
conduction system, a contralateral chamber, an unmapped
Figure C20.17
A 35-year-old patient presented with paroxysmal palpi- tachycardias. Occasionally, tachycardias arise just posterior
tation. In Figure C20.17, observe the initiation of a narrow to the eustachian ridge or on the mitral annulus anteriorly,
complex tachycardia with a long V-A interval. The induced where the earliest site of activation of the available catheters
tachycardia appeared identical (on a 12-lead electrocar- would be the proximal His bundle region. Nevertheless,
diogram) to that obtained clinically. The atrial activation whenever the fast-pathway region is the earliest site of activa-
sequence was stable from beat to beat, with the earliest atrial tion (or the slow pathway), AVNRT or junctional tachycardia
activation recorded by the proximal His bundle catheter. should also be considered.
After tachycardia was induced, the A-H and V-A intervals What about the initiation of tachycardia? Although the
were stable. Induction was with atrial extrastimuli at a cou- A-H interval is prolonged with the atrial extrastimulus and
pling interval of 270 milliseconds after a 500-millisecond the initiation of tachycardia, these characteristics are not
cycle length atrial drive train. The long R-P (V-A) interval uncommon for atrial tachycardias. The atrial extrastimulus
generally suggests a diagnosis of atrial tachycardia; other may be starting a reentrant atrial tachycardia, and by virtue
possibilities are atypical AV node reentry, a retrograde dec- of its early coupling interval, it will also result in a prolonged
rementally conducting accessory pathway, and AVRT. Before A-H interval. However, if a prolonged A-H interval is needed
narrowing down the diagnosis, however, it is worthwhile to consistently to initiate tachycardia, AV node–dependent
consider what is known about the method of initiation and tachycardias (eg, AVNRT, AVRT) are more likely.
atrial activation sequence. Is the tracing in Figure C20.17 consistent with AVRT? A
Is the tracing in Figure C20.17 consistent with atrial tachy- long V-A interval may be seen in some forms of orthodro-
cardia? Certainly the long V-A interval is consistent with mic AVRT. If the retrograde limb of the circuit (accessory
atrial tachycardia, but the site of earliest activation (proximal pathway) was long, previously damaged, or demonstrated
His bundle region) is not a common site for automatic atrial decremental conduction properties (persistent junctional
reciprocating tachycardia), then long R-P (V-A) tachycar- node reentry is a pseudointerval, with no real conduction
dia occurs. The method of induction is consistent with this occurring from the ventricle toward the atrium. In typi-
diagnosis, with A-H prolongation sometimes required for cal (and also atypical) AVNRT, the V-A interval represents
initiation of the arrhythmia; this allows differential timing a race between conduction to the atrium and to the His
of activation of the atrial tissue near the atrial insertion of bundle and ventricle from a common turnaround point
the pathway (from atrial pacing and from retrograde conduc- of the circuit. Thus, an atrial potential may occur before
tion). Decrementally conducting accessory pathways, how- or considerably after the ventricular potential, depending
ever, are extremely rare in the anteroseptal region (near the on who “wins” the race. There are 2 mechanisms that may
proximal His bundle catheter); more common locations are cause a long R-P (V-A) interval. First, the retrograde fast
the posteroseptal region and the left posterior region. pathway is considerably earlier than antegrade conduction
Is the tracing in Figure C20.17 consistent with atypical to the His bundle, creating an atrial potential and P wave
AVNRT? In this tracing, the ABL catheter is in the region of before the ventricular potential and QRS complex (long R-P
the slow pathway (right posteroseptal region), and electrodes tachycardia). Second, if the fast pathway is damaged (eg, by
CS 17,18 are at the ostium of the coronary sinus. The slow path- mechanical trauma), then very long conduction times can
way is a posteroseptal structure (exit site), and a diagnosis of result, making fast-pathway activation and the atrial poten-
atypical AVNRT would be inconsistent with early activation tials considerably later than the ventricular potentials. Note,
of the proximal His bundle region. In other words, it is not the however, that if this is typical AV node reentry from the fi rst
V-A interval that determines whether a patient with AVNRT mechanism (fast pathway quicker than antegrade conduc-
has the typical variant (retrograde fast pathway) or the atypi- tion), then the initiation must have been a 2:1 phenomenon,
cal variant (retrograde slow pathway), it is the location of ear- in which an antegrade fast pathway with decrement and
liest atrial activation that determines the variant. In this case, antegrade slow pathway with the fi rst echo beat (start of
earliest atrial activation is in the fast-pathway region, with the tachycardia) show the fi rst set of atrial potentials occurring
proximal His bundle catheter showing an earlier atrial poten- before the His bundle. If there is damage or slow conduction
tial than a catheter placed in the region of the slow pathway. up the anatomic fast pathway, then the initiation of tachy-
Thus, despite the long V-A interval, the diagnosis that most cardia is via the usual mechanism (not 2:1).
likely can be excluded on the basis of this tracing is atypical Also remember that whenever AV node reentry remains in
AV node reentry. Caution, however, should be exercised: if the the diagnosis, so does junctional tachycardia, although this
CS catheter is not mapping the ostium of the coronary sinus arrhythmia is rare. Junctional tachycardia with rapid, retro-
and no catheter is mapping the right posteroseptal region, grade, fast-pathway conduction will present with exactly the
the true earliest site of activation of the slow pathway may same atrial activation sequence as typical AV node reentry
be missed (resulting in mistaken exclusion of this diagnosis). with rapid retrograde fast-pathway conduction. Thus, with
However, in this case, both the right and left portions of the this tracing alone, even with analyzing the initiation of the
slow-pathway exit were mapped, and the potentials were later tachycardia, the differential diagnosis remains fairly broad.
than that expected in fast-pathway activation. Further analysis of termination of tachycardia, wobble in
Is the tracing in Figure C20.17 consistent with typical AV the circuit, and specific maneuvers (see Chapter 4) will be
node reentry? Remember that the R-P (V-A) interval in AV required to clarify the situation.
Case 20 635
Figure C20.18
What do we learn from the termination of this arrhyth- interpretation is valid, consistent observation of abrupt slow-
mia? The repeatedly observed phenomenon was just before ing of an atrial tachycardia focus before termination in an
spontaneous arrhythmia termination (Figure C20.18). The otherwise stable tachycardia (fi xed cycle length) would be
tachycardia slowed abruptly. One interpretation of this is unusual.
H-A prolongation before termination of tachycardia. The Another interpretation of the tracing in Figure C20.18
interval between the His bundle potential of the penulti- could be that a decremental retrograde-conducting pathway
mate beat (yellow arrow) to the earliest atrial potential of decrements further before block. If this mechanism is cor-
the last beat (white arrow) is longer than the relatively stable rect, the H-A interval should be prolonged before termina-
equivalent intervals of the prior beats of tachycardia. Of the tion of tachycardia; decrementally conducting pathways
various possible causes of a narrow complex tachycardia, in the anteroseptal region, however, are exceedingly rare.
if it is established that changes in the H-A interval occur Clearly, certain specific changes in an intracardiac interval,
before tachycardia termination or determine the subsequent when meticulously correlated with subsequent changes in
cycle length of tachycardia (resets the tachycardia), then AV the tachycardia, can be diagnostic of a particular arrhythmia
node reentry can be diagnosed because retrograde conduc- mechanism, but multiple mechanisms can explain changes
tion via the fast pathway would be critical only for AV node in intracardiac intervals before termination of tachycardia.
reentry. If for example, in Figure C20.18, the penultimate beat of
Nevertheless, many alternate mechanisms can explain the tachycardia showed His-ventricular prolongation without a
phenomenon shown in Figure C20.18. For example, this ter- marked change in the V-A interval before block, then the H-A
mination could be interpreted as a spontaneous atrial tachy- interval is the likely driver of the tachycardia, and it is reason-
cardia slowing just before termination. Naturally, because the able to exclude the permanent form of junctional reciprocat-
last atrial potential occurs late, the H-A interval will appear ing tachycardia (His-ventricle conduction is not part of the
longer just before restoration of sinus rhythm. Although this circuit).
Tachycardia was reinduced with atrial extrastimula-

tion and with isoproterenol infusion, and a short R-P (V-A)
tachycardia was observed with an identical atrial activation
sequence (Figure C20.19). Ventricular pacing maneuvers
confirmed the diagnosis of typical AV node reentry. When
uncommon manifestations of an arrhythmia such as AV
node reentry initially lead to confl icting conclusions, simply
re-inducing tachycardia with a slightly different circumstance
(eg, mode of induction, low-dose isoproterenol, forced hyper-
ventilation, or changing the level of anesthesia) often yields a
more recognizable manifestation of the common arrhythmia
that had been present throughout.
In this case, the electrophysiologist should be alert to the
possibility of this unusual arrhythmia being typical AV node
reentry for several reasons. First, the site of earliest activation
was the fast-pathway region. Second, the His bundle and ven-
tricle are not necessary components for the AV node reentry
circuit (V-A interval was not a true interval and not reflecting
conduction via a limb of the circuit).
It is equally important to recognize the typical P waves
associated with retrograde fast-pathway activation. P waves
are narrow (reflecting septal activation) and negative in leads
II, III, and aVF, often with a narrow positive P wave in lead
Figure C20.19 aVL, leads I and V1, or all 3.
Figure C20.20
Case 20 637
Figure C20.20 shows the surface 12-lead electrocardio- the PR and R-P intervals are identical. Phrased differently, P
gram recorded during narrow complex tachycardia. The waves are seen at the same rate as R-R intervals.
typical fast-pathway exit to P waves is seen, and importantly,
Figure C20.21
Figure C20.21 shows the intracardiac electrograms dur-

ing the same tachycardia. Now, the reason for this unusual
interval sequence is clear. The atrial cycle length is fi xed,
with the earliest atrial activation occurring in the region of A>V, no His
the proximal His bundle, as suggested by the surface elec- AV node
Coronary
trocardiogram. However, every other beat lacks an associ- sinus
ated His bundle or ventricular potentials (suprahisian block). FP
Considering only the beats marked by the arrows, typical AV Upper
node reentry would have been a likely mechanism. With the common Infrahisian
foreknowledge that the AV node itself, the His bundle, ventri- pathway
A>V, His+
cle, and others are not essential to the circuit of AVNRT, the V>A
observed arrhythmia is typical AVNRT but with an atypical Lower
manifestation, namely 2:1 suprahisian block. common pathway
A>V, no His
Figure C20.22
Figure C20.22 shows diagrammatically the multiple

mechanisms of A-V or atrial-Hisian dissociation during AV
node reentry. (In the Figure, “no His” and “His+” refer to
the absence or presence, respectively, of His bundle electro-
grams recorded during tachycardia.) Clearly, there can be His
bundle or infrahisian block with continuation of AV node bystander). If the upper common pathway was to have a block,
reentry (more atrial than ventricular potentials). Because the more ventricular than atrial potentials would be observed.
slow pathway and fast pathway (or in atypical AVNRT, 2 slow The important clues are an understanding of the typical
pathways) may have an associated lower common pathway P-wave morphology associated with retrograde fast pathway
before insertion into the compact AV node, block at the lower (and retrograde slow pathway) exits, the finding of earli-
common pathway would also result in more atrial potentials est activation in the intracardiac electrograms either at the
than ventricular but without an antegrade His bundle poten- fast- or slow-pathway exit sites, and the unusual occurrence
tial. Rarely, the fast pathway and slow pathway (or 2 slow of the PR (A-V) interval being exactly half the tachycardia
pathways) may have an upper common pathway before exit cycle length.
to the rest of the atrium (the rest of the atrium serving as a
Figure C20.23
The tracing shown in Figure C20.23 is an even more AVNRT shows an atrial potential without a His or a ven-
unusual variation of the phenomena described above. tricular potential (suprahisian block), and the next beat of
Here again, some telltale signs suggest that the patient has AVNRT shows the His bundle potential and ventricular
uncommon manifestations of a common arrhythmia (ie, potential without an associated atrial potential (upper com-
AV node reentry). First, the fast-pathway location (proximal mon pathway block).
His bundle catheter) is the site of earliest activation in the If the tracing in Figure C20.23 was the only one available
atrium during tachycardia. In this case, a mapping cath- to the electrophysiologist, certainly a diagnosis of an atrial
eter was placed at the anatomic fast-pathway location (not tachycardia originating near the fast-pathway site and a pro-
shown) and was the earliest site of activation. Second, the longed A-H interval during tachycardia can be diagnosed.
A-V interval was exactly half the A-A interval, and the A-A However, with the clues of the fast pathway site being early
interval was exactly the same as the ventricular-ventricular and the unusual relationship of the A-V interval to the tachy-
(V-V) interval. However, unlike the situation shown in cardia cycle length, the ablationist should be alert to the pos-
Figures C20.20 and C20.21, there is no atrial potential asso- sibility of an unusual variant of AV node reentry. At other
ciated with the alternate beats showing a His bundle deflec- portions during this patient’s electrophysiology study and
tion and ventricular potentials. Th is represents an unusual ablation, typical AVNRT with 1:1 A-V:V-A conduction were
situation—in addition to the 2:1 suprahisian block (Figures obtained with pacing maneuvers consistent with AV node
C20.20 and C20.21), there is 2:1 upper common pathway reentry. A slow-pathway ablation was performed, and neither
block resulting in dissociation of the His bundle and ven- the typical AVNRT nor the variants of typical AVNRT could
tricular potential with the atrium. Thus, one beat of typical be induced.
Case 20 639
Figure C20.24
Linear ablation of the slow pathway was performed for or typical AVNRT because the fast-pathway site is equidis-
this patient, with radiofrequency ablation energy delivered tant to the Bachmann bundle and the ostium of the coronary
along the posteroseptal tricuspid annulus at the level of the sinus. This pattern of activation is quite different from that
floor of the coronary sinus ostium. Figure C20.24 shows the seen during retrograde slow-pathway conduction because
tracing obtained during completion of this line, just as the the proximal coronary sinus is early, and subsequent linear
ablation catheter turned into the floor of the coronary sinus activation of the remainder of the coronary sinus is seen (no
at the ostium. Relatively regular junctional rhythm was seen, bowing).
with good retrograde conduction to the atrium. Note that the Sometimes, it can be very difficult to distinguish between
third beat on the tracing (white arrow) shows shortening of junctional tachycardia, either during ablation or after abla-
the A-H (P-R) interval. This is a fusion beat between sinus tion of the slow pathway and with the use of isoproterenol
rhythm and the first junctional beat from ablation. There is with reinduced AV node reentry (see Chapter 4). In Figure
no retrograde conduction to the atrium, likely because of the C20.24, however, several clues strongly suggest the diagnosis
immediately preceding sinus beat that prevents exit through of junctional tachycardia beyond the fact that this occurred
the fast pathway. during ablation of the slow-pathway region. The fused junc-
The retrograde atrial activation sequence during junctional beat and sinus rhythm initiating the run of tachycardia
tional rhythm is identical to that seen during AV node reen- is strongly suggestive of junctional tachycardia.
try, as shown above. Note the similarity in the coronary sinus In the beat shown by the yellow arrow, the H-A inter-
atrial activation sequence between that observed during sinus val is considerably longer than the preceding beat. Despite
rhythm and junctional tachycardia. In both instances, there this, the next His bundle potential (ie, the beat after the
is a bowing, with the mid coronary sinus activated later than yellow arrow) is earlier. If this was AV node reentry, pro-
the proximal and distal portions of the vein. In sinus rhythm, longation of the H-A interval would likely result in pro-
this is because of fused activation of the coronary sinus, with longation of the next His bundle potential and reset the
the distal portion being activated via the Bachmann bundle tachycardia. Here, regardless of H-A interval, the His-His
and the proximal portion via the ostium of the coronary sinus. interval is either constant or “out of sync” with changes in
A similar situation also occurs during junctional tachycardia the H-A interval.
Figure C20.25
After radiofrequency ablation of the slow pathway, double AV node reentrant echo with antegrade, long, slow-pathway
atrial extrastimulus testing was performed. The tracing in conduction and retrograde activation via the fast pathway.
Figure C20.25 was obtained. Note that the retrograde activation sequence for the last beat
Which conclusion can be drawn from the tracing in Figure (yellow arrow) is identical to that observed during tachycar-
C20.25? dia. Another possibility is that with the last atrial extrastimu-
A. Induced AV node reentrant echo beats continue; there- lus, there is now block in the compact AV node, resulting in
fore, further ablation is required a junctional escape beat. Note that the retrograde atrial acti-
B. Induced AV node reentrant echo beats continue; how- vation sequence of atypical AVNRT echo and a junctional
ever, no further ablation is required escape with retrograde conduction via the fast pathway would
C. Antegrade slow-pathway conduction is evident; there- be identical. In this instance, the distinction between a single
fore, further ablation is required typical echo or a junctional escape is not important because
D. Antegrade slow-pathway conduction is evident; how- no further ablation is indicated. More confusing situations
ever, no further ablation is required would be if 2 junctional escape beats occurred consecutively
E. None of the above or if the retrograde activation sequence suggested retrograde
slow-pathway conduction (proximal CS potential is early).
Further ablation would be recommended for an atypical echo
Although AVNRT typically has a straightforward, cura- but not for a junctional escape with retrograde slow-pathway
tive ablation technique (namely, anatomic ablation in the conduction.
slow-pathway region), it can be difficult to gauge when more One of the simplest methods to distinguish between
ablation is needed. Generally, single AV node reentrant echo typical AVNRT echo beats and junctional escape beats is
beats of the slow-fast variety (when the clinical tachycardia to decrease the coupling interval of the second atrial extra-
is slow-fast AVNRT) are considered acceptable after ablation, stimulus. If the atrial refractory period is reached and the
and the risk of recurrent tachycardia is low. With atypical questioned beat is still present (arrow), then clearly this rep-
AVNRT (retrograde slow pathway), even one atypical echo resents a junctional escape. If the subsequent A-H interval is
beat after ablation portends a relatively high risk of recurrence prolonged with a further decrease in the coupling interval of
(5%-10%), and further ablation of the slow pathway is recom- the second atrial extrastimulus, then the beat likely is in fact
mended. The presence of antegrade slow-pathway conduction an echo beat and not a junctional escape. Other maneuvers
(dual AV node physiology) is common after successful curative (detailed in Chapter 4) can be applied, including placing a
ablation of AVNRT and should not prompt further ablation. third atrial extrastimulus at varying coupling intervals to see
In this particular tracing (Figure C20.25), the beat after the whether the questioned beat can be easily “reset” from the
second atrial extrastimulus (arrow) may represent a typical atrium.
Case 20 641
Figure C20.26
Regardless of the maneuver used to distinguish between beat on the tracing is a junctional escape beat. In all 3 situ-
these similar tachycardias (AVNRT vs junctional tachycar- ations, the atrial activation sequence on the His bundle and
dia), remember that the distinction cannot be made on the coronary sinus catheters are identical.
basis of the retrograde atrial activation sequence. Figure Why is the His bundle potential earlier than the ventricu-
C20.26 was obtained during ventricular extrastimulus test- lar potential in the first beat and later than the ventricular
ing (arrows indicate His bundle potentials). Note that in the potential (with a significant ventricular-His [V-H] interval)
first beat (a ventricular-paced beat and the last of the drive on the second beat? The ventricular pacing site and rate
train), the His bundle potential precedes the ventricular (coupling interval) can influence whether the retrograde
potential on the HBE 1 catheter, whereas on the ventricular His bundle potential can be clearly seen and may affect its
extrastimulus beat, the His bundle potential comes after the timing relative to the ventricular potential on the His bundle
ventricular potential on this electrode, and then the third catheter.
Ventricular pacing Ventricular pacing

at midseptum at base
HV A V H A
VA 70 ms VA 110 ms
Ventricular pacing Ventricular pacing

at apex with RBBB at apex
V H A VH A
VA 110 ms VA 90 ms
Figure C20.27 illustrates this concept diagrammatically. In The top panel of Figure C20.28 shows another useful
the top panel, note that if the ventricular pacing site (“B”) is method to delineate the retrograde His bundle deflection.
close to the exit/entrance site of the right bundle branch, then Here, the pacing site is close to the tricuspid annulus (ven-
retrograde conduction to the His bundle via the right bundle tricular pacing at base). The ventricular myocardium near the
branch is faster than intraventricular conduction to the ven- His bundle catheter is immediately activated, but for the His
tricular myocardium near the His bundle. This results in a bundle itself to get activated, the wave front must propagate
His inflection that slightly precedes the ventricular potential about two-thirds of the distance to the apex, enter the right
on the His bundle recording catheter. The bottom panel illus- bundle branch, and travel retrograde to activate the His bun-
trates pacing at a shorter coupling interval. Retrograde block dle itself. This pacing site is useful not only during ventricular
may occur in the right bundle branch, and although there is pacing to define the retrograde His and analyze the resulting
little difference in the intraventricular conduction to the His atrial activation but also when placing PVCs during narrow
bundle region, the His bundle itself gets activated late (the complex tachycardia. To distinguish retrograde conduction
wave front must propagate transseptally to the left ventricle via the AV node from a retrograde accessory pathway during
and then up the left bundle branch to reach the His bundle, narrow complex tachycardia, if the retrograde His bundle can
creating a long V-H interval). When it becomes critical to be clearly seen, then one can determine whether it was nec-
assess the effects on atrial conduction (activation sequence essary to preexcite the retrograde His to preexcite the retro-
and timing) relative to the His bundle recording, purpose- grade atrium (suggestive of retrograde AV node conduction).
ful induction of retrograde right bundle branch block can be If retrograde atrial activation can be advanced without preex-
useful. citing the retrograde His or by preexciting the retrograde His
by a lesser amount than the atrial activation is advanced, then
a retrograde accessory pathway is present.
In the bottom panel of Figure C20.28, pacing from the
ventricular apex results in a fusion of the ventricular and His
bundle potentials on the His bundle recording catheter, mak-
ing it difficult to comment on relative retrograde His bundle
activation.
Case 20 643
Ectopic atrial rhythm followed by sinus bradycardia
Sinus rhythm into ectopic atrial tachycardia
Figure C20.29
A 26-year-old female athlete had recurrent palpitations. superficially similar to the P wave during tachycardia. When
Tracings during ambulatory monitoring were obtained a 12-lead electrocardiogram was obtained, the tachycar-
(Figure C20.29) and showed numerous spontaneous initia- dia P waves were negative in leads II, III, and aVF, as were
tions and terminations of a narrow complex tachycardia with the P waves of the occasional ectopic beats. However, the
a long R-P interval. The P-wave morphology during tachycar- P-wave duration is distinctly narrow with a single ectopic
dia was always similar to sinus rhythm. The clinical diagnosis beat (arrow). Narrower P waves are seen when the exit is
was atrial tachycardia. In the top panel of Figure C20.29, an on the true interatrial septum such as in the fast-pathway
ectopic beat (arrow) after termination of tachycardia shows region. An exit or origin of an atrial focus near the coro-
an inverted P wave suggestive of a single ectopic atrial beat. nary sinus ostium (slow pathway, coronary sinus muscu-
Because this P wave resembled the P wave during tachycardia, lature) show wider negative P waves in the inferior leads
the long R-P interval, the spontaneous initiations, and other because this region (pyramidal space) is not truly part of
features all strongly suggested ectopic atrial tachycardia. the interatrial septum; exit typically occurs to one atrium,
Upon closer scrutiny of these tracings, the possibility of an with interatrial conduction required to depolarize the other
alternate diagnosis should be apparent. Examine the initia- atrium (longer P-wave duration). Thus, atypical AVNRT,
tion of tachycardia in the lower panel and note that the initi- posteroseptal accessory pathways, and proximal coronary
ating beat (arrow) has a P-wave morphology that differs from sinus musculature–related tachycardias have wider P waves
the ensuing tachycardia. In an automatic atrial tachycardia, than typical AVNRT, anteroseptal accessory pathways, and
the initial beat is from the focus of the tachycardia itself and anteroseptum-related tachycardias.
is thus of similar morphology. With reentrant arrhythmias, When attempting to perform ablation in a patient with
including AV node reentry and AV reentry, any premature the working diagnosis of atrial tachycardia but also with the
atrial contraction may start tachycardia if critically timed tracings like that shown in Figure C20.29, be prepared to
and will have likely a different P-wave morphology than the perform the various maneuvers to exclude AVNRT or ORT
reentrant tachycardia’s retrograde P wave. using a slowly conducting retrograde pathway (see Chapter
With closer inspection of the top panel, note that the 4). Sometimes, however, only fairly simple observations, cor-
ectopic beat after termination of tachycardia (arrow) is only rectly interpreted, will yield the correct diagnosis.
Figure C20.30
While catheters were being placed, the tracing in Figure The termination of tachycardia is shown in Figure C20.30.
C20.30 was obtained. The CS catheter was placed in a fairly A very late coupled PVC (arrow) occurred just before ter-
large coronary sinus with poor contact close to the ostium, mination. On numerous occasions (with or without PVCs),
and the ABL catheter was placed on the posterior tricus- tachycardia repeatedly terminated with the last recorded
pid annulus. Which diagnosis can likely be excluded, given potential being that of atrial activation. For atrial tachycar-
that the phenomenon shown in Figure C20.30 was repeat- dia to terminate with atrial activation, there must be seren-
edly observed? dipitous block in the AV node and cessation of firing from
A. Atrial tachycardia the ectopic focus. Although this may happen occasionally, a
B. AVNRT repeated occurrence strongly argues against the diagnosis of
C. ORT using an endocardial accessory pathway atrial tachycardia. Note in Figure C20.30 that the site of earli-
D. ORT using an epicardial accessory pathway est activation appears to be in the proximal coronary sinus, a
E. None of the above finding consistent with the relatively wider negative P waves
Answer: A—Atrial tachycardia. seen in leads II, III, and aVF on ambulatory monitoring and
the 12-lead electrocardiogram.
Case 20 645
Figure C20.31
During ventricular pacing (Figure C20.31), the retrograde sequence during tachycardia and ventricular pacing usually
atrial activation sequence was identical to that observed dur- excludes the diagnosis of atrial tachycardia.
ing tachycardia. Note that upon cessation of pacing, a single The findings in Figures C20.30 and C20.31 make atrial
echo beat again occurred, with an atrial activation sequence tachycardia unlikely, but the ablationist must still distinguish
identical to that of tachycardia (and ventricular pacing). When between atypical AVNRT (proximal coronary sinus early,
retrograde conduction to the atrium from ventricular pacing slow pathway exit site) and ORT using a slowly conducting
shows a similar P wave and intra-atrial activation sequence as or decremental posteroseptal accessory pathway (persistent
tachycardia, atrial tachycardia becomes highly unlikely. Th is junctional reciprocating tachycardia).
is because, for atrial tachycardia to be the diagnosis with the Here again, the various maneuvers explained in Chapter 4
above-mentioned phenomena, the focus must by chance be can be used to distinguish between these 2 entities. If, how-
located very close to or exactly at the site of the structure that ever, it can be convincingly demonstrated that ventricular
conducts from ventricle to atrium during ventricular pacing atrial conduction that produces the atrial activation sequence
(retrograde fast pathway, retrograde slow pathway, accessory of the tachycardia is via the AV node, then atypical AVNRT
pathway). The simple observation of identical atrial activation would overwhelmingly be the likely diagnosis.
Figure C20.32
Figure C20.32 shows parahisian pacing with a gradual output captures only ventricular myocardium and “releases”
decrease in the pacing output; the pacing site is close to the the His bundle potential. The atrial activation sequence is
distal His bundle. Note that the first beat is a relatively nar- identical for both beats, but the conduction time from the
row complex, whereas the second is wider. The retrograde His stimulus to the atrial potentials is delayed with the second
bundle deflection (arrow) is seen with the second paced beat beat. Thus, when conduction is delayed to the His, it is also
(wider QRS, decreased pacing output). The first paced beat delayed to the atrium without a change in the atrial activa-
(at higher output) captures both the local His bundle and tion sequence, a finding that is diagnostic of retrograde AV
ventricular myocardium, whereas the second beat at lower node conduction.
Case 20 647
Figure C20.33
Figure C20.33 shows ventricular pacing with spontane- pacing is performed and the retrograde activation sequence
ously occurring PVCs. On the beat indicated by the arrow, is AV node dependent but different from that observed dur-
note the long V-H interval from retrograde right bundle ing tachycardia, then the tachycardia could still be an ORT,
branch block, as explained above. Again, the conduction time and pathway conduction is just not apparent or present when
to the His bundle is prolonged, which delays conduction to parahisian pacing is performed (see Chapter 4).
the atrium without changing the atrial activation sequence. Thus, with the fairly straightforward findings that help
It cannot be overemphasized that the activation sequence exclude atrial tachycardia (Figures C20.30 and C20.31) and
must be closely examined, whether analysis is for the effects ventricular pacing maneuvers that exclude retrograde conduc-
of parahisian pacing or induction of a retrograde right bundle tion via an accessory pathway (Figures C20.32 and C20.33),
branch block. Not only should the atrial activation sequence the diagnosis of atypical AV node reentry can be made fairly
not change with the maneuver, it must be identical to that quickly, despite the unusual R-P interval during tachycardia
observed during tachycardia. In other words, if parahisian and the somewhat unusual atrial activation sequence.
Figure C20.34
Having established the diagnosis, the slow pathway was activation is advanced, and sinus rhythm is seen. The ability
ablated. Figure C20.34 shows a slow junctional rhythm that of sinus rhythm or atrial pacing that is slightly faster than
was observed during linear slow-pathway ablation. Note that the junctional tachycardia (rhythm) rate to easily advance the
in the tracing, the high right atrial potential gradually comes His bundle potential with a normal A-H interval is typical of
earlier than the His bundle potential. In the third beat, the junctional rhythm; it is almost never seen with atrial pacing
high right atrial potential is sufficiently early, the His bundle during AV node reentry.
Case 20 649
Figure C20.35
The rhythm strip and intracardiac electrograms shown the atrial myocardium is not part of the circuit. Successful
in Figure C20.35 were obtained in a young patient with par- ablation was in the region of the slow pathway, with no induc-
oxysmal narrow complex tachycardia. Th is was another ible tachycardia at the end of the procedure.
uncommon manifestation of a very common cause for The tachycardia, once induced, had all the established
supraventricular tachycardia: beats of sinus rhythm alter- characteristics of AV node reentry. Knowing that the
nated with what appeared to be junctional ectopic beats patient’s arrhythmia was AV node reentry, how can the
(junctional bigeminy) throughout the procedure. When beats in Figure C20.35 be explained? Consider concurrent
tachycardia was induced, however, it was induced in an iden- antegrade conduction via the fast pathway and the slow
tical pattern (a sinus beat and then an apparent junctional pathway to the AV node. Th is phenomenon is sometimes
beat), except that the second beat showed retrograde atrial termed antegrade 2:1 conduction. When it occurs, the sec-
activation and then subsequent initiation of tachycardia (not ond beat may be mistaken for junctional ectopy, and an
seen during the tracing shown in Figure C20.35). Tachycardia unusual method of initiating tachycardia without appar-
requiring conduction to the atrium strongly favors a diagno- ent antegrade conduction via the slow pathway may be
sis of AVNRT rather than junctional tachycardia, for which observed.
RAO LAO
Eustachian valve
or ridge
Figure C20.36
Figure C20.36 shows diagrammatically the mechanism not uncommon phenomenon occurred consistently for more
of antegrade 2:1 conduction to the His bundle. In patients than 1 hour. The mechanism involved concealed penetra-
with both fast- and slow-pathway inputs to the AV node dur- tions retrograde into the nonconducting bundle from the
ing sinus rhythm, the fast-pathway route typically reaches conducting bundle, altering the pattern of long-short inter-
the AV node earlier than the slow-pathway mechanism, and vals required to create aberrancy. Thus, in the first aberrantly
there is retrograde penetration of the atrial myocardium conducted beat (second beat on the tracing), the right bundle
from the slow pathway. Th is results in the absence of mani- branch block antegrade conduction occurs through the left
fest slow-pathway conduction on the 12-lead electrocardio- bundle and retrograde into the right bundle. The right bundle
gram or intracardiac electrograms. Presumably in some conduction time, therefore, is relatively late with that beat. If
patients, retrograde penetration of the slow pathway (after we examine the interval from the right bundle activation for
fast-pathway conduction) is absent. If the conduction time the second beat to right bundle activation for the third beat
between antegrade fast and antegrade slow pathways are (normal beat), note the absence of a distinctly long-then-short
sufficiently different, then the initial wave front via the fast interval for right bundle conduction; thus, the right bundle
pathway reaches the AV node and then the His bundle and does not block. In contrast, in the second beat on the tracing,
activates the ventricle. Th is is then followed by conduction, the left bundle had conducted fairly early. Thus, the interval
again via the AV node (slow pathway), which reactivates the from the left bundle activation for the second beat to the left
His and the ventricle. bundle activation for the third beat is long, but for the ante-
An interesting phenomenon is noted in Figure C20.35, grade slow-pathway conducted beat, the left bundle to left
in addition to 2-for-1 antegrade conduction. Note these bundle activation time is short, and the left bundle branch
clock-like alternations of the QRS morphology in every other block now blocks. Now, the right bundle conducts antegrade
beat (antegrade slow-pathway conducting beat). The sinus and penetrates late into the left bundle, creating a uniform
beat is followed by the 2-for-1 conducted beat with right interval for left bundle conduction for the next 3 beats, with a
bundle branch aberrancy, then the next sinus beat is followed long-short interval for the right bundle conduction, making
by the 2-for-1 conducting beat with left bundle branch aber- the sixth beat in the tracing show conduction with the right
rancy, and then the cycle repeats itself. This interesting but bundle branch block aberrancy, and so on.
Case 20 651
Figure C20.37
Considering the surface electrocardiogram and intra- this tracing and the phenomenon seen in Figure C20.35 (and
cardiac electrograms in Figure C20.37, which diagnosis is diagrammed in Figure C20.36) is that the second His bun-
likely? dle potential does not conduct to the ventricle. If this were
A. Antegrade 2:1 conduction with infrahisian block the diagnosis, it could be described as 2:1 conduction with
B. Intermittent antegrade 2:1 conduction with infrahisian infrahisian block after the second His bundle activation.
block Since this “extra” potential is not seen after the third beat,
C. Antegrade 2:1 conduction with suprahisian block the phenomenon of 2:1 conduction and infrahisian block, if
D. Retrograde His bundle activation via an accessory present, is intermittent. However, upon closer inspection of
pathway the third beat without the extra potential, notice also that the
E. Cannot be determined from this tracing QRS morphology has changed, with a left bundle–like pat-
tern, rather than the right bundle branch block pattern seen
Answer: E—Cannot be determined from this tracing.
on the other beats.
At first glance, Figure C20.37 appears to have complex The ABL p electrode was placed just anterior and distal
electrograms, particularly on the HBE catheter, that may to the His bundle recording catheter and the hRA cath-
be difficult to interpret. This particular tracing, however, is eter was placed on the floor of the atrial appendage, just
even more complex than it first appears. The critical poten- above the tricuspid annulus. Note that each of these elec-
tials are on the HBE 1 (distal) electrode. Note the usual atrial trodes also recorded the extra potentials, and the poten-
potentials followed by a His potential and then a local ven- tials vanished on the third beat when the QRS morphology
tricular potential. Following this is another potential that is changed.
seen consistently (on the first, second, and fourth beats [white If the phenomenon was simply antegrade 2:1 conduction,
arrows]). One possibility is antegrade 2:1 conduction via the there would be no reason to observe the change in the QRS
fast pathway and the slow pathway. The difference between morphology or axis.
Figure C20.38
In Figure C20.38, again notice that when the extra poten- identified as exhibiting occasional ectopy (the patient’s
tial after the QRS complex is absent, the QRS morphology clinical arrhythmia). Th is and similar cases are detailed
changes. In fact, in the second beat, note that this “extra” elsewhere (see Case 19 and Chapter 6). Note that the second
potential now is early and appears close to the antegrade beat of the tracing appears to have a split His potential. In
His bundle deflection. In this case, the repeated observa- this case, the potentials near the His are not indicative of
tion was that whenever this extra deflection came early intrahisian conduction because the phenomenon is inter-
(sometimes earlier than the atrial potential), a “PVC” with a mittent. The 2 His potentials are not arising from the same
bundle branch block morphology would occur. Eventually, structure but are superimposed on this catheter. The extra
a relatively isolated fiber near the annulus (similar to an potential was targeted for ablation, and the ectopic rhythm
accessory His bundle without an atrial connection) was was eliminated.
Case 20 653
LB
RB
AV node
H H´
Figure C20.39
A true double His recording is unusual and is indicative of abnormality (rare). Figure C20.39 diagramatically shows the
slow conduction through the normally rapidly conducting His concept of slow conduction through the His bundle, with the
bundle. It may occur after inadvertent ablation, may be seen consequent delayed or isoelectric period between conduction
in elderly patients, or may be a congenital conduction tissue of the proximal and distal portions of the His bundle.
Split His
Figure C20.40
Figure C20.40 was obtained from a patient with intra- recording on the His dist catheter.
hisian conduction disease. Note the fragmented (split) His
Case 20 655
After procainimide
Figure C20.41
After administration of procainamide, a drug that affects no QRS complex (Figure C20.41). This is a rare example of AV
Hisian and infrahisian conduction, the second component of conduction block resulting from block within the His bundle
the split His bundle recording is no longer seen and there is itself.
RBBB
Figure C20.42
Figure C20.42 is a diagrammatic representation of another first His-like deflection is seen. After activation at this site,
occasionally seen cause of 2 His-like potentials on the His conduction proceeds via the left bundle and to the ventricular
bundle recording catheter. In patients who have both ante- myocardium, thus generating the QRS complex. After trans-
grade and retrograde right bundle branch block, if the His septal conduction back to the right ventricle, retrograde con-
bundle catheter is placed such that the recording electrode duction to the right bundle occurs, up to the tissue just distal
straddles the exact site of block, 2 potentials separated by a to the site of block at the junction of the His bundle and right
fairly long isoelectric interval may be recorded. Here, con- bundle branch. This activation is also recorded on the map-
duction occurs antegrade down the AV node to the portion of ping catheter that straddles the level of block and produces
the His bundle that is just proximal to the level of block at the the second His bundle-like deflection that occurs after the
junction of the His bundle and right bundle branch. Thus, the QRS complex.
Case 20 657
RBBB
Figure C20.43
A similar mechanism for recording 2 His bundle–like myocardium. Again, if the catheter is located at the block in
potentials on a recording catheter placed at the junction the right bundle branch, then antegrade and retrograde acti-
of the His bundle and right bundle branch is illustrated in vation would be recorded as 2 His bundle–like potentials on
Figure C20.43. An antegrade conducting accessory pathway this catheter.
is present, as is antegrade and retrograde right bundle branch The His-like potentials will have an interesting response to
block. Conduction occurs via the AV node and the accessory incremental atrial pacing. As the pacing rate increases, the His
pathway. If the accessory pathway shows decremental con- potentials will exhibit decrement via the AV node so the first
duction properties, then the most proximal portion of the His bundle deflection (resulting from antegrade conduction
right bundle branch (proximal to the site of block) is acti- via the AV node) will occur later. In contrast, the His bundle–
vated antegrade via the AV node; in contrast, the distal por- like potential found more distally (occurring via activation
tion of the right bundle is activated retrograde via conduction through the accessory pathway) showed little or no decremen-
through the accessory pathway and intervening ventricular tal conduction (the exception is a Mahaim-type fiber).
Figure C20.44
The patient, during whose ablation procedure Figure strongly suggests that the catheters are mechanically bump-
C20.43 was obtained, had a long history of narrow complex ing into each other. Note with relation to the first beat in
tachycardia that started and stopped abruptly. An apparently Figure C20.44 and just before the atrial potentials in the last 2
spontaneous termination of tachycardia is shown in Figure beats (sinus beats), the same phenomenon is seen. Again, this
C20.44. A sharp near-field potential is seen on the proximal strongly suggests an artifact.
CS 15,16 catheter (yellow arrow) and also seen simultaneously The next main clue is that the CS 19,20 catheter clearly
on the proximal HBE 4 catheter (white arrow). is not in the coronary sinus (far-field potentials) because the
What is the likely cause of these simultaneous sharp catheter enters from an internal jugular route. If the proxi-
deflections? mal electrodes are not beyond the ostium of the coronary
A. Pathway potential associated with an epicardial coro- sinus, then the proximal HBE catheter can make mechani-
nary pathway cal contact with the proximal electrodes of the CS catheter.
B. Pathway potential associated with an endocardial pos- Sometimes, exclusion of artifacts can be exceedingly difficult.
teroseptal pathway Several of the cases discussed in this textbook have attempted
C. They are artifacts to illustrate the principles of association and dissociation. If
D. Slow pathway potential with decrement before termi- a potential, however unusual looking or unexpected, can be
nation of tachycardia clearly associated with some other physiologic signal (eg, atrial
E. Fast pathway potential with decrement just before ter- potential, pathway potential activation, presence of PVCs,
mination of tachycardia etc), then it is highly unlikely to be an artifact (ie, it is likely
associated with the primary diagnosis being investigated).
Answer: C—They are artifacts.
Sometimes, however, artifacts themselves can be physi-
The preceding description of the unusual cases has empha- ologic, that is, associated with certain regions of the heart (eg,
sized the importance of pacing maneuvers and character- supravalvular great arterial potential, coronary sinus muscu-
istics to identify the true source of an unusual potential. In lature potential, etc). Such artifacts may lead the ablationist
doing these maneuvers, it is important to exclude artifacts. to believe that they are arrhythmogenic signals. Elsewhere in
In the tracings in Figure C20.44, this distinction is relatively this textbook (see Cases 14 and 19) are descriptions of cases in
straightforward, especially if the exact catheter positions are which an unusual potential was found beyond the pulmonic
known through real-time fluoroscopy. The first main clue is valve that was in fact a bystander and the true source of tachy-
that the potential occurs simultaneously on 2 catheters, which cardia was in the ventricular myocardium.
Case 20 659
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II
Figure C20.45
Figure C20.45 is an electrocardiogram obtained from a transition from a negative delta wave in V1 to a positive
patient with documented narrow complex tachycardia and delta wave in V2 signifies a septal location for the pathway.
preexcited atrial fibrillation. Analysis of this electrocardio- The delta wave is negative in leads II, III, and aVF, signi-
gram should warn the electrophysiologist of the possibility fying a posterior location for the accessory pathway, and
of an unusual potential; in this case, physiologic artifacts thus, a likely right posteroseptal accessory pathway can be
(bystanders) will have to be delineated and their nature diagnosed. However, the delta wave in lead II is immedi-
exactly defined. ately negative (fi rst 40–80 milliseconds). Th is is a specific
What is the most likely location of the accessory pathway sign that the pathway may be epicardially located related to
in the patient whose electrocardiogram is shown in Figure the middle cardiac vein. In a sense, all pathways are epicar-
C20.45? dial, in that the myocardium of the accessory pathway con-
A. Right posteroseptal region nects the ventricular and atrial myocardium just outside
B. Right anteroseptal region the annulus. However, true epicardial pathways are those
C. Left posterior region that insert fi rst into the musculature of the cardiac venous
D. Related to the middle cardiac vein system and travel from there to the atrial myocardium. The
E. Related to the small cardiac vein most common location for difficult-to-ablate epicardial
pathways is in relation to the middle cardiac vein. Thus,
Answer: D—Related to the middle cardiac vein.
leading into the procedure, the electrophysiologist should
The left bundle branch block pattern in lead V1 (no R be looking specifically for unusual potentials consistent
wave) and positive delta wave in leads I and aVL strongly with a pathway potential in the region of the middle car-
suggest that the pathway is not on the left free wall. The diac vein.
Figure C20.46
The intracardiac electrogram shown in Figure C20.46 Exact delineation of potential in this region, however,
shows an unusual but consistently seen potential. The ABL d is important for several reasons. First, bystander coronary
catheter was located at the floor of the coronary sinus, close sinus muscular potentials are rampant in this location, and
to the ostium of the middle cardiac vein. The first beat in the nearly every patient will have even sharper near-field poten-
tracing was the last beat of a ventricular-paced drive train. tials that either just precede the atrial potential or appear
The second beat is the ventricular extrastimulus, and tachy- to succeed the ventricular potential. Second, because of
cardia follows. The arrow points to a potential that occurred potential damage to the coronary arterial vasculature, abla-
between the ventricular and atrial potentials, suggestive of tion should not be targeted at sites without certainty of their
a pathway potential. Knowing that the surface 12-lead elec- arrhythmogenic nature. Considering these important cave-
trocardiogram was suggestive of an epicardial pathway, the ats, if a pathway is truly epicardial, ablation often must be
electrophysiologist might consider this an excellent site for performed within the venous system (or via an epicardial
ablation. approach, etc).
Accessory pathway Epicardial accessory pathway
Coronary
sinus
Sinus
node
AV node
Figure C20.47
Case 20 661
Figure C20.47 shows diagrammatically the difference septum. Second, inadvertent ablation in the middle cardiac
between so-called endocardial and epicardial accessory path- vein can injure the arterial vasculature. Third, potentials
ways. Note in the left panel, the “endocardial” pathway is in from the musculature within the vein may be bystanders to
fact epicardial to the fibrous tissue that makes up the mitral a circuit of ORT and may be mistaken for pathway-related
valve. In the right panel, a true epicardial pathway is shown; potentials in the posteroseptal region on the septum.
the main difference is the relation to the coronary sinus.
Ventricular myocardial musculature may either traverse
with the musculature of the coronary sinus, or the body of
the pathway may traverse epicardial to the vein itself. Thus, a
catheter placed in the coronary sinus, in addition to recording
the atrial and ventricular signals, may record potentials from
the coronary sinus musculature and the accessory pathway.
PCV
Figure C20.49
MCV
In Figure C20.49, a right anterior oblique projection is
shown. The arrow points to the ablation catheter.
Where is the ablation catheter (Figure C20.49, arrow)
located?
A. Middle cardiac vein
B. Posterior cardiac vein
C. Right posteroseptal region
Figure C20.48 D. An LAO projection is required to be certain of the loca-
tion of this catheter
E. The location cannot be determined by fluoroscopy
Figure C20.48 shows a posterior view of the heart and the alone
location of the middle cardiac vein and the posterior cardiac
Answer: E—The location cannot be determined by fluoros-
vein, 2 veins relevant in electrophysiology and left ventricu-
copy alone.
lar pacing. These veins are often confused with each other,
and epicardial accessory pathways may be associated with the Figure C20.49 is a typical right anterior oblique (RAO)
musculature of either vein. Note the course of the middle car- view of a catheter in the middle cardiac vein. It is also a typi-
diac vein in the posterior intraventricular groove. The vein, cal RAO view of a catheter on the intraventricular postero-
therefore, runs parallel to the interatrial and interventricu- septal region with good contact. The LAO view can indicate
lar septum. This makes it difficult for an operator to know whether the catheter is deep, but it cannot show how deep it is
whether a catheter is actually located within this vein or out- in the coronary sinus. The LAO projection also will not help
side the vein but with good contact against the intraventricu- distinguish between catheters located in the middle cardiac
lar septum. vein or the right posteroseptal region. The ideal maneuver
The distinction between a catheter within the vein or on that can be performed is counterclockwise torque applied to
the interventricular septum is critical for several reasons. the catheter during continuous fluoroscopy in the LAO pro-
First, if a middle cardiac vein pathway is to be ablated, it jection. If the catheter is making good contact only on the
is rarely successful when ablating on the interventricular septum, counterclockwise torque will immediately move
the catheter away from the septum. In contrast, if the cath- Usually, the posterior descending artery (a branch of the
eter is located within the middle cardiac vein, even vigorous right coronary artery) travels in the posterior intraventric-
counterclockwise torque will show lateral movement of the ular groove along with the middle cardiac vein. Ablating
proximal portions of the catheter (LAO projection), but the at the ostium of the middle cardiac vein generally does not
tip of the catheter will remain within the vein and the entire risk damaging the posterior descending artery, but another
catheter suddenly will torque off the septum. This is a very branch of the right coronary artery (rarely a branch of the
typical response, and all operators should be familiar with circumflex) loops upward toward the atria and then comes
this maneuver. to the ventricle again (arrow). Th is is a constant branch and
Whenever ablating in the posteroseptal region, be it for an can be injured during ablation of accessory pathways at
accessory pathway, slow-pathway ablation, or a septal cavotri- the middle cardiac vein ostium. Sometimes, an even more
cuspid isthmus–dependent flutter line, be wary of inadver- superior branch to the AV node may occur in this area, but
tent ablation within the middle cardiac vein if the electrode injuries during ablation of epicardial accessory pathways
location has not been determined exactly. Several clues may are rare.
indicate that the catheter is wedged in a venous structure: 1)
if the patient is awake, chest pain may occur when ablating in
the coronary vasculature; or 2) if the patient is deeply sedated
or under general anesthesia, relatively high temperatures at
low power and high impedances (typically >140 ohms) may
be observed.
Figure C20.51
Further complicating the issue are the multiple variations

in the architecture of the coronary sinus musculature. Rarely
will there be a single “accessory pathway” that is a discrete
musculature connection between atria and ventricles, in the
Figure C20.50
case of epicardial pathways. More commonly, the coronary
sinus and middle cardiac vein musculature may insert into
several locations, sometimes relatively distally into the ven-
Figure C20.50 shows one of the main problems of ablat- tricular myocardium, and the connections between the coro-
ing within the coronary sinus, specifically near the ven- nary sinus musculature to the left and right atria are multiple
tricular veins. Branches of the right coronary artery and as well (Figure C20.51). Often, relatively extensive ablation or
the left circumflex artery may be associated with the middle attempts to isolate one of these veins by ablating at the ostium
cardiac vein, posterior vein, and the coronary sinus itself. is required for a successful result.
Case 20 663
Figure C20.52
Having established the difficulty in knowing whether the tachycardia). These maneuvers are regularly performed by the
catheter is in the middle cardiac vein and the importance of electrophysiologist and can be accomplished quickly (10–15
exactly knowing whether ablation is required within or out- minutes after catheter insertion). During further investiga-
side of the vein, now return to the tracing in the patient with tion, junctional tachycardia can be excluded by placing PACs
a possible middle cardiac vein accessory pathway (Figure during tachycardia (see Chapter 4) in another few minutes,
C20.52). Is the potential between the ventricular and atrial which could exclude other conceivable differential diagnoses.
signals (arrow) a pathway potential or not? How should the The most important reason, however, for a complete study is
electrophysiologic study and ablation be approached in a for the developing electrophysiologist to become intimately
patient with a classical history of paroxysmal supraventricu- familiar with the idiosyncrasies and hostilities of these vari-
lar tachycardia and an electrocardiogram highly suggestive ous maneuvers and measurements, so that in the unusual or
of typical AVNRT? difficult case, appropriate changes in technique can be made
Given the typical practitioner’s busy schedule, one could to achieve the desired results.
consider anatomic ablation of the slow-pathway region with- The following questions are useful in determining the
out extensive electrophysiologic study or stimulation; how- nature of a potential, particularly with relevance to accessory
ever, because of coexisting diagnoses and the occasional pathway conduction. Is the potential originating in the ven-
anatomic variation in the atrial septal region and conduction tricle? Is the potential originating in the atrium? Is the poten-
tissue, an accurate diagnosis is preferred. Knowing the func- tial an artifact? Is the potential a His bundle deflection? Is the
tional characteristics of the conduction system before and potential a bystander coronary vein musculature potential?
after ablation is also important, particularly if the patient has The maneuvers that are useful when answering the above
development of unexplained syncope or other symptoms. A questions are reviewed in detail in Chapter 4; they are dis-
concern about damage during ablation to the conduction tis- cussed only briefly here in the context of their role in facilitat-
sue may arise subsequently. A complete study would involve ing ablation for the difficult case. Of the questions, whether
exclusion of an accessory pathway (atrial and ventricular pac- the potential is a His bundle deflection is relevant primarily
ing and parahisian pacing) and induction of tachycardia; it for anteroseptal accessory pathway ablations. For cases such
would also confirm a diagnosis of typical AV node reentry as the one discussed above (Figure C20.52), the main issue
(ie, PVCs during tachycardia preexcite the atrium without would be distinguishing the potential from the ventricular
changing the retrograde atrial activation, only by preexciting and atrial signals. After this is done, ensure that it also is not
the retrograde His by about 10 milliseconds and resetting the a bystander coronary muscle–related signal.

Surface ECG
Stim 440 Stim 430 Stim 420 Stim
A V A V A V A
Annular EGM
Ap Ap

Conduction

Recording Recording
catheter catheter
AP AP AP
AP AVN-only Block in
Figure C20.53
Figure C20.53 diagrammatically shows the primary potential certainly does not have an atrial origin. It is reason-
maneuver used to help define the nature of an unknown able to surmise that it is unlikely to have a ventricular origin
potential (labeled “Ap”). In patients with antegrade accessory because the unknown potential is not associated with the ven-
pathway conduction, start by pacing the atrium at relatively tricular potential when the pathway is blocked. If it is neither
short cycle lengths. On the third beat in the figure, accessory atrial nor ventricular and the catheter is nowhere near the His
pathway conduction is no longer seen. Conduction to the ven- bundle region, the potential highly likely represents the path-
tricle for the third paced beat is only via the AV node, with way potential and should be targeted for ablation. The above
a relatively longer AV interval. On the fourth beat, there is maneuver is straightforward and simple to perform; however,
loss of conduction to the ventricle altogether (AV node and in some patients, the AV node will block before the acces-
accessory pathway). Note that the unknown potential is not sory pathway (making it difficult to distinguish the unknown
seen when the pathway is blocked or when there is no AV con- potential from the ventricular potential). At times, the atrial
duction. Because the atrial potential is present on the third refractory period will be reached before pathway block, and
and fourth beats but the unknown potential is absent, the thus the maneuver cannot be effectively implemented.
Case 20 665
Surface ECG
Stim Stim Stim Stim
A V AV V A
Annular EGM
Ap Ap Ap
Anterograde Ventricular potential Very early PVC

AP conduction advanced by PVC dissociates ventricular
potential from A and AP
Figure C20.54
Surface ECG
Stim Stim Stim
A V A V V A
Annular EGM
AP AP APR
Antegrade AP A single PVC advances the ventricular potential;

fixed-rate atrial with block to the atrium; atrial stimulation (Stim)
pacing is followed by the atrial potential alone
Figure C20.55
A more universally applicable maneuver is shown dia- potential). Eventually, with PVCs placed very early, the ven-
grammatically in Figure C20.54. Here again, antegrade acces- tricular potential is far ahead of the atrial potential. If retro-
sory pathway conduction produces a preexcited complex, as grade conduction does not occur through the pathway, then
shown in the first beat. During sinus rhythm or fi xed-rate the accessory pathway potential will occur after the atrial
atrial pacing, sensed PVCs are placed at relatively shorter potential (Figure C20.55).
coupling intervals and eventually are placed at negative cou- In contrast, if bidirectional conduction through an acces-
pling intervals (before the atrial paced event or sensed atrial sory pathway is present when the PVC is placed very early, the
activity during sinus rhythm). With PVCs placed progres- retrograde accessory pathway potential will now be seen after
sively earlier, the ventricular potential is advanced (second the ventricular and atrial potentials.
beat in Figure C20.54). Although the ventricular potential is Importantly, if the potential being analyzed was a coro-
advanced, the unknown potential (“Ap”) is not changed, and nary vein musculature–related bystander potential, there will
thus, it is effectively dissociated from the “V” (the ventricular be limited variation in the relationship of the coronary sinus
muscle potential to the atrial potential. This is because coro-

nary musculature is essentially atrial myocardium, typically
with multiple connections to the remainder of the atrium.
Thus, one will not see a clear reversal (eg, after and before
the atrial electrogram) in its activation relative to the atrial
potential. These distinctions can be difficult to define, and
even experienced ablationists may mistakenly target the cor-
onary vein potential as a pathway potential.
The context of the entire case always must be kept in mind,
and the essential questions of whether the potential is clearly
associated with pathway conduction (ie, as evidenced by cri-
teria such as overall atrial activation sequence or evidence of
preexcitation on the electrocardiogram) should be considered
continuously. If, for example, a particular potential is disso- Figure C20.56
ciated from the “V” (ventricular potential) yet consistently
occurs after the “A” (atrial potential) during antegrade con-
duction even without preexcitation or without varying the The situation can be particularly challenging when the
intervals from the atrial electrogram to the candidate poten- coronary sinus has an anatomic anomaly such as a diver-
tial at varying degrees of preexcitation, it is highly likely to be ticulum (Figure C20.56). The multiple interdigitating myo-
a bystander. cardial fibers (continuous in some parts and discontinuous
elsewhere), with variable ventricular and atrial connections,
make complete analysis of electrograms nearly impossible.
Most electrophysiologists would not try to identify true
accessory pathway potentials (conducting fibers responsible
for antegrade or retrograde atrial ventricular conduction);
rather, they would isolate the fibers within the diverticulum
by ablating nearly circumferentially at its neck. This concept
is discussed in detail in Case 19.
Figure C20.57
Case 20 667
The electrogram shown in Figure C20.57 was obtained patient with paroxysmal narrow complex tachycardia and a
from a 21-year-old woman with paroxysmal palpitations. She short R-P interval (ie, T wave occurring just after the QRS
was otherwise healthy and had no clinically significant con- complex seen in leads V1, II, and III) is AVNRT, likely the
genital cardiac or other developmental anomalies. typical variant. The electrophysiology study in ablation for
Which diagnosis is most likely, considering her clinical such cases is generally straightforward, with atrial stimula-
history and the electrogram obtained during tachycardia tion performed to look for dual AV nodal physiology and
(Figure C20.57)? induction of tachycardia, beginning with prolongation of
A. AVNRT the A-H interval. The site of earliest activation during tachy-
B. Fascicular tachycardia cardia is expected to be in the fast-pathway region near the
C. Orthodromic reentrant tachycardia proximal His bundle catheter. PVCs placed during tachy-
D. Antidromic reentrant tachycardia cardia preexcite and reset the tachycardia only by preexcit-
E. Atrial tachycardia ing the retrograde His bundle deflection (see Chapter 4).
Ablation may occur at discrete points in the anatomic region
Answer: A—AVNRT.
of the slow pathway or in a linear fashion at the level of the
Several possible diagnoses exist (eg, junctional tachycar- floor of the coronary sinus ostium. Recurrence is generally
dia, septal atrial tachycardia with a long P-R interval, etc). rare, and complications such as complete heart block are
The most common and likely diagnosis in a young, healthy uncommon (<1%).
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure C20.58
Figure C20.59
Yet even the “simple” cases occasionally can be exceed- C. Left-sided His bundle variant
ingly challenging (Figure C20.58). Despite an hour-long D. Aberrant AV nodal tissue on right anterior annular
effort of mapping with an octapolar catheter (Figure C20.59, position
arrow) at the anatomic location where the His bundle is usu- E. A and B are possible
ally recorded, a His bundle potential could not be identified F. C and D are possible
(Figure C20.59).
Answer: F—C and D (left-sided His bundle variant and
What is (are) the possible reason(s) why a His bundle poten- aberrant AV nodal tissue on right anterior annular posi-
tial cannot be recorded by an experienced electrophysiolo- tion) are possible.
gist mapping the anteroseptal region on the right side of
the intraventricular septum, close to the annulus? A thorough examination of the anteroseptal region close to
A. Congenital absence of the His bundle the membranous septum failed to reveal a His bundle record-
B. Complete suprahisian block ing (Figure C20.59). Although occasionally the His bundle
Case 20 669
recording cannot be readily obtained because of catheter associated with needing an unusual location to record the His
contact, an experienced electrophysiologist with appropriate bundle potential. In this case, however, the entire tricuspid
changes made to exact catheter location and contact should annulus was mapped and a catheter was placed retrograde on
be able to define this electrogram within 10 to 15 minutes, the septum, just below the aortic valve, yet no His bundle poten-
even in a difficult case. Knowing that there is AV conduction tial could be recorded. How should the operator proceed?
without obvious preexcitation, complete suprahisian block Considering the patient’s history and electrocardiogram
or congenital absence of the His bundle can be excluded as a (classical AVNRT), empiric slow-pathway ablation could be
cause of the problem. performed, particularly if tachycardia is easily inducible (as
The His bundle may rarely develop on the left side of the was the case in this patient). However, if the His bundle is not
membranous AV septum; this anatomic variation sometimes in its usual location, the AV node also may not be in its usual
is associated with correction of congenital transposition of location, and any form of empiric therapy then is fraught
the great vessels. Other AV nodal variants (eg, aberrant AV with the possibility of inadvertently producing AV block and
nodal tissue elsewhere on the tricuspid annulus) may also be causing the patient to require a pacemaker.
Figure C20.60
Figure C20.60 shows an electrogram from the same a small atrial potential and the proximal electrode show-
patient. Note the clearly recorded His bundle potential ing progressively larger atrial potentials. Where was the
on the His 1,2 catheter. The features of the recording are catheter located when it recorded the elusive His bundle
fairly classical, with the distal His bundle catheter showing potential?
RAO LAO
Figure C20.61
Figure C20.61 shows the RAO and LAO projections, taken to the thebesian vein in the right ventricle and wedged there.
when the His bundle tracing was eventually obtained. The With gentle catheter manipulation, it became clear that the
arrows denote the position of the His bundle catheter. As catheter was not in the coronary sinus and appeared wedged
detailed in the introductory chapter to fluoroscopic anatomy to some structure. With appropriate changes in the angle of
(Chapter 1), the RAO projection is essentially a “profi le” view the RAO projection, the “ostium” through which the catheter
of the heart, with the CS catheter defining the plane of the repeatedly could be inserted was just on the atrial side of the
annulus. The His bundle catheter in the RAO projection is annulus; by manipulating the catheter, the subselect various
ventricular relative to the annulus and curves back toward orientations of the catheter tip including superiorly. To define
the atrium. In the LAO projection, the His bundle catheter this structure, the octapolar His catheter first was removed
appears to be going right toward the left atrium and the tip is and a deflectable catheter advanced through a sheath to a posi-
directed inferiorly toward the coronary sinus. tion that could record the His bundle potential. The sheath
Where was this recording obtained? The His catheter could was then advanced over the catheter and careful angiography
be in the coronary sinus itself, or possibly it could be anterior was performed.
Case 20 671
RAO LAO
Figure C20.62
The RAO and LAO projections of the angiogram are procedure may get sidetracked by focusing on the unusual
shown in Figure C20.62 (arrows point to unusual atrial fi nding and not the primary arrhythmia. However, be
veins). Careful examination of this venous structure in the mindful that the primary objective of the electrophysiol-
LAO projection shows various sub-branches, some proceed- ogy study and ablation is to cure the patient of arrhyth-
ing low and others higher. What is this structure, and why is mia. The best option is to fi rst defi ne the arrhythmia and
the His bundle potential recorded there? then defi ne the anatomic variant only as it pertains to the
It could be an unusual anatomic variant or anomaly arrhythmia, either to facilitate ablation at an appropriate
of the coronary venous circulation. Sometimes, in the site or to avoid ablation at a risky site (eg, likely to house
course of a procedure, an unusual fi nding occurs, and the conduction tissue, etc).
Figure C20.63
Examine the other electrophysiologic findings (ie, from unusual situation, an accessory pathway in the venous loca-
mapping and maneuvers) before thinking about what the tion cannot be excluded as the mechanism of retrograde ven-
structure is and where the His bundle is located. Figure tricular atrial activation, nor can it be determined whether
C20.63 shows ventricular pacing when the His bundle cath- the His catheter is closer to the slow pathway input or to the
eter was placed into this venous structure. As expected with abnormally located AV node. Additional maneuvers, includ-
retrograde fast-pathway conduction, the HIS prox electrode ing during tachycardia, must be performed to define precisely
shows the site of earliest atrial activation. Of course, in this the mechanism of tachycardia.
Case 20 673
HIS catheter in the atrial vein (unusual);

ABL catheter at the fast pathway in the right intra-atrial septum (usual)
Figure C20.64
In Figure C20.64, the electrograms were obtained during HIS dist catheter markedly precedes the far-field atrial signal
easily induced tachycardia. Note that the atrial potential on the on the ABL dis catheter located on the usual fast-pathway site.
ABL dis catheter on roof of the coronary sinus, near the atrial vein
Figure C20.65
Figure C20.65 shows electrograms obtained during ven- earliest site during tachycardia. When the earliest site in the
tricular pacing with the ABL dis catheter located on the roof atrium to register a potential is the same during tachycardia
of the coronary sinus, very close to the atrial vein (where the and ventricular pacing, atrial tachycardia is unlikely; either
His bundle catheter was placed). This site showed the earliest AV node reentry or AV reentry is the probable mechanism of
atrial activation during ventricular pacing and was also the arrhythmia.
RAO LAO
Figure C20.66
Case 20 675
A similarly timed potential was obtained with the ABL the His bundle recording was obtained. The roof of the
catheter placed as shown in Figure C20.66 (arrow). Note coronary sinus and the floor of the atrial vein both register
that the catheter was oriented with the tip down into one the site of earliest activation during ventricular pacing and
of the inferior branches of this unusual atrial vein where tachycardia.
Figure C20.67
Two beats of tachycardia, termination of arrhythmia, catheter records the His bundle def lection in that loca-
and a sinus beat are shown in Figure C20.67. In the f luo- tion, but the branch with the ablation catheter shows only
roscopic portion of Figure C20.67, the His bundle catheter atrial and ventricular potentials (no His bundle def lec-
and the ablation catheter have been placed in 2 branches tion). The atrial potentials are about equally early during
of the unusual atrial vein. Note that the His bundle tachycardia.
The ablation catheter in Figure C20.67 is slightly ventricu-

Box C20.1 lar to the site that records the His bundle. Parahisian pacing
Characteristics of Arrhythmia Observed in This Case was performed from that location (note the large ventricular
Premature ventricular contractions inserted during tachy- potential) and using this maneuver, retrograde conduction
cardia could preexcite the atrium only by preexciting the was shown to be AV node dependent. Box C20.1 shows the
retrograde His bundle recording by at least 10 milliseconds,
characteristics of arrhythmia for this patient.
without changing the retrograde atrial activation sequence
and resetting the tachycardia Because exact delineation of the fast and slow pathways is
The His-atrial interval during ventricular pacing was 12 difficult when encountering anatomic variants, the fast path-
milliseconds shorter than the His-atrial interval during way was assumed to be the site of earliest activation, given
tachycardia its proximity to the site where the His bundle potential was
The ventricle could be easily disassociated from tachycardia
recorded. Ablation was undertaken on the floor of the coro-
during ventricular pacing
When ventricular pacing was performed slightly faster than nary sinus after coronary arteriography excluded the presence
the tachycardia, the tachycardia could be untrained; upon of a neighboring coronary artery. Slow junctional tachycar-
cessation of ventricular pacing, the return sequence of dia was seen during the ablation. After ablation, tachycardia
potentials was ventricular–atrial–His bundle–ventricular could no longer be induced, and the patient has remained
Parahisian pacing and induction of retrograde right bundle
symptom-free for 3 years after ablation.
branch block clearly showed that retrograde activation was
via the AV node only What was the structure where the His bundle potential
The characteristics and fi ndings shown in Figure 20.67 are was recorded? Just as thebesian ventricular veins drain into
diagnostic of typical atrioventricular nodal reentrant the right ventricle (drainage from mostly the right ventricular
tachycardia myocardium), there are similar veins, usually very small, that
drain into the right atrium. Sometimes, one of these veins can
be fairly prominent.
Case 20 677
Atrial vein orifice
Figure C20.68
Figure C20.68 shows a common site for one of the promi- needle and sheath are being “brought down” from the supe-
nent veins, located just behind the tricuspid annulus on the rior vena cava, and in the lateral or LAO projection, the char-
interatrial septum. Note the propatency demonstrated in the acteristic fall of the tip of the needle left ward/posteriorly into
images. The RAO fluoroscopic view shows the His bundle the fossa ovalis may actually be entering one of these veins
catheter located inside the vein. The larger veins are rem- if it is larger than normal. When contrast is injected, stain-
nants of the atrial cardinal veins. The dextral retro-atrial caring instead of the tenting of the fossa ovalis is sometimes
dinal veins usually seen more posteriorly may be a cause of noted. The anomalous presence of conduction tissue in the
minimal but unexplained shunting of the right- and left-sided veins (or the anecdotally reported tachycardias arising from
circulation and when epicardial, may even be visualized by such veins) is exceedingly rare. Catheters falling into such
transesophageal echocardiography. veins may, however, be more common than previously real-
Although these veins are present, they generally have little ized because a single fluoroscopic projection cannot always
or no role in cardiac pathology. They sometimes are encoun- indicate that the catheter is mapping or within an unusual
tered during transseptal puncture when the transseptal structure.
RAO LAO
Figure C20.69
RAO LAO
Figure C20.70
An example of this is illustrated in Figures C20.69 and which the marked leftward position and orientation of this vein
C20.70. In Figure C20.69, the appendage catheter (arrow) is can easily be distinguished from the right atrial appendage.
located in the right atrial appendage. Note the anterior orienta- The remnants of the cardinal venous system must not be
tion and position in the RAO view but also note that it is pointed confused with the much more common epicardial veins that
slightly away from the septum in the LAO view. If only the RAO drain the left atrium (and sometimes pulmonary veins) into
projection is considered and compared with the venogram the coronary sinus. Typically, several veins are present, but
shown in Figure C20.70, a catheter in this vein would appear to the largest is usually located about 2.5 to 3 cm from the coro-
be in the right atrial appendage. However, the situation is eas- nary sinus ostium and is a vestigial remnant of the left supe-
ily differentiated by looking at the orthogonal (LAO) view, in rior vena cava (vein of Marshall).
Case 20 679
RAO LAO
Figure C20.71
In Figure C20.71, the yellow arrows point to a mapping/ Ap, unknown potential (possible accessory pathway
ablation catheter placed at the ostium of the vein of Marshall. potential) [f]
Note that in the RAO projection, the catheter tip is oriented AP, accessory pathway [f]
posteriorly (atrially) to the coronary sinus catheter (white AV, atrioventricular
arrow). This vein sometimes needs to be specifically mapped AVN, atrioventricular node [f]
and even circumferentially isolated if it triggers arrhythmia, AVNRT, atrioventricular nodal reentrant tachycardia
particularly atrial fibrillation. AVRT, atrioventricular reentrant tachycardia
The cases in this series illustrate some highly unusual ECG, electrocardiogram [f]
situations and anatomic variants that an electrophysiologist EGM, electrogram [f]
may see only once in a career. Although the manifestations FP, fast pathway [f]
are extremely rare, the arrhythmias discussed above were H, His potential [f]
essentially very common diagnoses (eg, AVNRT, AVRT, etc) H-A, His-atrial
with uncommon manifestations attributable either to unique LAO, left anterior oblique
anatomy or unusual physiology. It is important that the elec- LB, left bundle [f]
trophysiologist remember that only a limited number of diag- LV, left ventricle [f]
noses are possible for narrow- and wide-complex tachycardia. MCV, middle cardiac vein [f]
Regardless of how unusual or difficult the situation may seem, ORT, orthodromic reciprocating tachycardia
by systematically applying knowledge of the characteristics of PCV, posterior cardiac vein [f]
common arrhythmias and appropriately using common pac- PVC, premature ventricular contraction
ing maneuvers, the true nature of the arrhythmia and a viable RAO, right anterior oblique
plan for treatment will become apparent. RB, right bundle [f]
RBBB, right bundle branch block [f]
RV, right ventricle [f]
Stim, stimulus [f]
Abbreviations V, ventricular potential [f]
V-A, ventriculoatrial
A, atrial potential [f] V-H, ventricular-His
A-A, atrial-atrial VT, ventricular tachycardia [f]
A-H, atrial-His V-V, ventricular-ventricular
Index
Note: Page numbers followed by b, f, or t indicate a box, figure, or table, respectively.

A-A interval ablation injury endocardial, 660–61, 660f
in paroxysmal palpitation, 398, to esophagus, prevention of, left-sided, 303, 303f
398f 256–58, 256f, 257f, 258f epicardial, 660–61, 660f
prolongation of, 620, 620f with rapid narrow QRS complex ablation of, 305–7, 305f, 306f
V-V interval and, 638, 638f tachycardia ablation, 10–11, His bundle potential and, 544–47,
in wide QRS complex tachycardia, 10f, 11f, 12t 545f, 546f, 549
146 ABL dis. See distal ablation catheter isolation procedure for, 608t
wobble in, 108, 108f, 109t ABL prox. See proximal ablation LV activation and, 137, 138f
A-A-V sequence, 112–13, 113f catheter in middle cardiac vein, 659, 659f,
ablation catheter accessory pathway ablation, 219–20, 219f 663, 663f
in atrial myocardium, 39, 39f after AV node ablation, 21–22, 22f parahisian pacing and, 91–92, 96f,
in CHD, 374, 374f on left free wall, 269–70 277–78, 277f
dissociating potentials with, left-sided, 11, 12t preexcitation and, 392
224–25, 224f right-sided free wall, 22 QRS complex of, 296, 296f
distal, in typical intracardiac elec- accessory pathway conduction retrograde, decremental pacing for,
trogram, 8, 8f antegrade, tachycardia with, 103–4, 105f
at fast pathway region, 319, 319f 154–55, 154f retrograde His bundle activation
fluoroscopy of, 44, 45f, 661–62, 661f intermittent, with antegrade 2-for-1 and, 400, 400f
infradiaphragmatic venous map- phenomenon, 228–29, 228f in retrograde right bundle branch
ping with, 273, 273f retrograde, in parahisian pacing, block induction, 95, 97, 99f, 100t
labeling for, 8, 8f 92, 96f, 97b in sinus tachycardia, 329, 329f
location of, 24, 26f accessory pathways (AP). See also slant of, 293, 293f
pathway potentials on, 224, 224f left-sided accessory pathway; two, 596, 596t
near-field, 224f, 225 right-sided accessory pathway types of, 116–17, 118f
prosthetic valves and, 276, 276f AV nodal conduction anomalies VA conduction through, 403, 403f
proximal, in typical intracardiac and, 550f, 550t, 551 V-A interval of, 411, 411f, 414
electrogram, 8, 8f coronary sinus activation and, 402, ventricular potential and, 220,
respiration and position of, 40, 40f 402f 220f, 294
signal loss on, 225, 225f diagnosis of, 89–90, 92f, 149–50, in wide QRS complex tachycardia,
for supraventricular tachycardia, 409b 109–10, 110f
location of, 11–13, 12f, diagnostic maneuvers for, 120–21 acquired cardiac channelopathies,
13f, 14f of pathway potentials, 121, 121b, 186, 187t
for ventricular potential, 224, 224f 122f, 123f, 124f, 125f, 125t atrial fibrillation, 186, 187t
ablation depth of pathway slant, 121–24 cardiac hypertrophy, 186–87, 187t
energy delivery and, 263, 263f in differential pacing, 106, 107f heart failure, 186, 187t
tip temperature and, 263, 263f with Ebstein anomaly, 204 myocardial infarction, 187, 187t
681
682 Index
action potential duration (APD), clockwise torque and, 20, 20f antegrade His bundle activation
drugs for, 194, 197f, 198f coronary sinus catheter location, associative and dissociative
action potentials 20, 21f maneuvers for, 228b
antiarrhythmic agents and, 201, 201f coronary sinus catheter place- distal-to-proximal, 143, 144f, 302f,
ion channels and, 176–77, 177f, 178f ment for, 13–15, 14f, 15f 303
activation mapping, for VT ablation, counterclockwise torque and, with PAC placement during wide
459, 459f 18–20, 19f QRS complex tachycardia,
activation time, in electroanatomic diverticulum, 20, 21f 110–11
mapping, 30, 32f, 75 with dual-chamber pacemaker, in paroxysmal palpitation, 395,
adenosine 21–22, 22f 395f, 395t, 398, 398f
decremental atrial pacing with, rapid narrow QRS complex proximal-to-distal, 143, 144f, 302,
114, 117f tachycardia ablation, 10–11, 302f
differential atrial pacing and, 355, 10f, 11f, 12t retrograde compared with, 156, 158f
355f right bundle branch block, 17, wide QRS complex tachycardia
adenosine triphosphate–sensitive K+ 17f, 18t and, 150
(K ATP) channel, 171 tricuspid annulus multielectrode antegrade left bundle branch block,
β-Adrenergic receptor blockers, 192f, catheter placement, 22 during ORT, 161, 163f
193t ventricular pacing, 15–17, 16f antegrade preexcitation, wide QRS
automatic tachycardia and, 195 venous, 264, 264f complex tachycardia with, 109,
EAD and DAD suppression, 196, views for, 3 109b
198f angiography, with supraventricular antegrade right bundle branch block
AF. See atrial fibrillation tachycardia ablation, 20, 21f retrograde right bundle branch
A-H interval. See atrial-His interval anisotropic reentrant model, 130t block with, 656, 656f
air bubbles. See also microbubbles annular mapping catheter, 28, 28f antegrade conducting accessory
in transseptal puncture of aorta, annular tachycardia, imaging of, 22 pathway with, 657, 657f
363, 363f annulus sinus rhythm with, 230, 230f
in left atrium, 367, 367f ablation injuries with, 10–11, anterior interventricular vein
amiodarone 10f, 11f ablation of, 264
for atrial flutter, 468, 468t catheter localization on, 7–8, 7f, anatomy of, 264, 264f
capture latency and, 338 28, 28f anterior mitral annular tachycardia,
anatomic reentry, 130t coronary sinus and, 61f, 62 596t
anatomy electrical abnormalities of, 629t anteroposterior (AP) view
of aorta, 367f, 368 fossa ovalis and, 7, 7f for anatomic structure evaluation, 3
of aortic valve, 280, 280f Mahaim fibers on, 627 LAO projection and, 4, 5f
of atria, 33, 33f mapping along, 627 anteroseptal accessory pathway, 13
of fast pathway region, 13, 15f pathway potentials with, 121, 121b, ablation of, 394
heart position in open chest, 3, 4f 122f, 123f, 124f, 125f, 125t AV node conduction and, 623
of interatrial septum, 364, 364f pathway slant with, 121–24 paroxysmal narrow QRS complex
landmarks in RAO and LAO pro- in RAO projection, 5 tachycardia electrograms and,
jections, 5–7, 7f anodal stimulation, 435f, 436 13, 14f
of left atrium, 40, 41f antegrade 2-for-1 conduction anteroseptal (AS) region, preexcita-
of LSPV, 35 differential diagnosis for, 651, 651f tion index for, 88f
of parahisian pacing, 90–91, 93f His bundle and, 650, 650f antiarrhythmic drugs, 191
principles of, 3–10 intermittent accessory pathway for atrial flutter, 468, 468t
of RSPV, 35 conduction with, 228–29, 228f for Brugada syndrome, 340
of subeustachian pouch, 24, 26f antegrade AV nodal bystander, classification of, 191–92, 192f, 193t
for supraventricular tachycardia, pathway-to-pathway tachycar- EAD and, 181t
10, 25t dia with, 154–55, 154f electropharmacology, 192
angiography with, 20, 21f antegrade conducting accessory additional points, 194
atrial pacing with right-sided pathway channel state and, 192–93, 193f,
accessory pathway, 22–23, 23f with retrograde and antegrade 193t
cardiac vein catheter location, RBBB, 658, 658f use dependence, 193–94, 194f,
17, 19f tachycardia with, 154–55, 154f 195f, 196f, 196t
catheter position for ablation, unknown potential and, 664–66, for enhanced or abnormal automa-
11–13, 12f, 13f, 14f 664f, 665f ticity, 194–95, 197f
Index 683
monitoring of, 199 coronary arteries relationship with, ART. See antidromic reciprocating
class I, 199–201 368, 368t tachycardia
class III, 201, 201f aortic valve artifacts in signal, 592, 658, 658f
selection of, 194, 196t anatomy of, 280, 280f AS. See anteroseptal region
antidromic activation, bundle branch AV valve and, 52, 54f asplenia syndrome, 205
block and, 297, 297f ICE for localization of, 71, 72f associative maneuvers
antidromic reciprocating tachycardia RVOT and, 54, 55f, 429, 429f arrhythmia cause and, 239, 239f
(ART) aortocaval sinus, 251, 251f, 368 to determine potential source, 228b
characteristic features of, 167b ablation at, 251f, 252 for exercise-related VT, 233, 233f
initiation of, 163, 165f views of, 252, 252f atrial action potential, 176, 178f
with left-sided accessory path- AP. See accessory pathways on His bundle catheter, 623, 623f
way, 165, 165f, 166f APD. See action potential duration atrial activation sequence
with left bundle branch block, 141, AP view. See anteroposterior view in atrial arrhythmias, 378–79, 378f,
141b arrhythmias. See also specific 379f
with Mahaim fiber, 154f, 155 arrhythmias in atrial flutter, 491–94, 492f, 493f,
with right bundle branch block, associative and dissociative 494f
140, 140b maneuvers and cause of, 239, atrial tachycardia and, 644, 644f
wide QRS complex tachycardia 239f change in, 411f, 414–17, 414f, 415f,
and, 111–12, 112f, 113f, 139t atrial switch operation resulting 416f, 417f, 422
His bundle and, 143, 144f in, 210 conduction to ventricle, 294
antidromic reentrant tachycardia, with Brugada syndrome, 340 His bundle potential and, 403–4,
165, 167f with cc-TGA, 211–12 403f
antidromic tachycardia in CHD, 203, 204t mitral annulus and, 623
atrial cycle length and, 166–68, 168f after surgery, 468, 468t pathway slant of, 122–24
atriofascicular pathway with, 154f, diagnosis of, 675–76, 675f, 676b retrograde AVN activation of, 294
155 with Ebstein anomaly, 212 septal activation and, 625, 625f
diagnosis of, 149–50 electroanatomic mapping for, 75 during sinus rhythm, 9, 9f
distal coronary sinus PAC place- background on, 75–76 during tachycardia, 291, 291f
ment for, 153 enhanced or abnormal automatic- during ventricular pacing, 622, 622f
figure-of-8, 154f, 155 ity resulting in, 179, 180f atrial appendages. See also left atrial
Mahaim fiber in, 116 drugs for, 194–95, 197f appendage
preexcitation with, 142–43 epicardial ablation for, 260–61, accessory pathway ablation near,
with retrograde bystander acces- 260f 219–20, 219f
sory pathway, 154, 154f with Fontan palliation, 207–8 juxtaposition of, 205
with retrograde right bundle ICE for treatment of, 71–73, 72f, 73f atrial arrhythmias
branch block, 154, 154f, 408 mechanisms of, 179–81 automatic compared with reen-
antihistamines, EAD and, 181t impulse initiation abnormalities trant, 563, 563t
aorta (Ao) resulting, 179, 180f after CHD surgery, 468–69, 468b,
air embolization into, 369, 369f impulse propagation abnormali- 468t
anatomy of, 367f, 368 ties, 179–81, 180f, 182f circumferential mapping catheter
intracardiac echocardiography reentry resulting in, 129–30, for, 379–80, 379f
imaging of, 65, 67f, 71, 72f 179–81, 180f, 182f ectopic beat in, 381, 381f
in LAO, 6f cellular mechanisms of, 199f, EG-P interval for, 135
puncture of 200f EnSite Array noncontact mapping
cause of, 364 drugs for, 196–99, 199f, 200f catheter for, 81
thrombus formation, 364, 364f with surgically corrected TOF, 213 intra-atrial activation in, 378–79,
in RAO, 6f tachycardia ablation and, 246 378f, 379f
superior vena cava and, 251, 251f triggered activity resulting in, 179, at left inferior pulmonary vein,
transseptal puncture of, bubbles in, 180f 377–78, 377f
363, 363f drugs for, 196, 197t, 198f S-P interval for, 135
aortic cusp, prepotentials in, 611, 611f arrhythmogenesis, 194, 196t with surgically corrected TOF, 213
aortic root arrhythmogenic right ventricular atrial cardinal veins, 677–78, 677f,
anatomy of, 367f, 368 cardiomyopathy, 343, 343f 678f
circumferential mapping catheter electrocardiogram of, 344, 344f atrial cycle length, QRS morphologies
in, 612, 612f epsilon wave in, 344, 344f and, 166, 168f
684 Index
atrial extrastimulus testing, 271f, 272 atypical AVNRT with, 524 mapping and ablation of, 22
H-V interval with, 354, 354f AVNRT with, 524–31, 525f, 526f, slow ventricular rates with, 491–94,
for paroxysmal palpitation, 396, 527f, 528f, 529f, 530f, 531f, 492f, 493f, 494f
396f, 397f, 398, 398f 533–34, 533f, 534f, 536–37, after TOF repair, 485
tachycardia induction in, 598f, 599 536f, 537f atrial flutter ablation
atrial fascicular pathways, 158f, 159 fluoroscopic and anatomic correla- approach to, 474, 474f
atrial fibrillation (AF) tion for, 24–49 associative and dissociative
as acquired channelopathy, 186, His bundle tachycardia with, maneuvers for, 228b
187t 531, 531f, 532t, 534–35, 534f, of cavotricuspid isthmus, 472, 472f
A-H interval in, 536, 536f 538–39, 538f, 539f difficulties with, 522b, 577
anomalous pulmonary vein and, isoproterenol administration and, fluoroscopy and electrogram cor-
232, 232f 529, 529f, 539 relation to, 24–49
arrhythmias associated with, 524, junctional tachycardia with, mapping for, 25–26
524b 524–34, 524b, 525f, 526f, 529f, subeustachian pouch and, 511, 511f
atrial flutter with, 387, 387f, 477 530f, 531f, 532f, 532t–533t, 533f, atrial-His (A-H) interval
atrial tachycardia and, 588f, 589 534f, 536–37, 536f in AF, 536, 536f
circumferential mapping for, 46, paroxysmal, 46–47, 49f, 61f, 62–64, of ART initiation with left-sided
48f, 49f 62f, 63f, 64f accessory pathway, 165, 166f
diagnosis of, 606, 606f pulmonary vein isolation for, 313, in atrial tachycardia, 619
electroanatomic mapping for, 76 313f in AVNRT, 637–38, 637f
Carto map of, 77, 78f tachyarrhythmias after, 576 in decremental atrial pacing,
with CartoMerge, 79, 79f tachycardia after, 562, 562f 114–15, 116f, 117f
H-A interval in, 525–28, 525f, 526f, ventricular pacing, 530, 530f, in differential atrial pacing,
527f, 528f, 533–34, 533f, 534f, 533–35, 533f, 534f 354–55, 354f, 355f
536f, 537 VT with, 530, 530f H-A interval and change in,
with heart block, 482, 482f atrial flutter. See also atypical atrial 618–19, 618f
H-H interval in, 525–27, 525f, 526f, flutter; cavotricuspid isthmus- in junctional tachycardia, 119
527f, 531, 531f, 534–35, 534f, dependent flutter; repaired in paroxysmal palpitation, 396,
537 CHD; typical atrial flutter 396f, 397f, 398, 398f
H-V interval in, 533, 533f, 535 activation during, 471, 471f prolongation of, 620, 620f
intrahisian sequence in, 525–27, AF with, 524 in right-sided accessory bypass
525f, 526f, 527f, 531, 531f, antiarrhythmic drugs for, 468, 468t tract, 350, 350f
534–35, 534f atrial fibrillation with, 387, 387f, 477 in wide QRS complex tachycardia,
junctional tachycardia with, conduction velocity in, 471 143, 146
ventricular fibrillation arising diagnosis of, 467, 467f with cycle length decreases, 156,
from, 540–42, 540f, 541f, 542f electroanatomic mapping for, 30, 158f
with left-sided AP, 300f, 301 32f, 370f, 371, 470, 470f with preexcitation, 155, 157f
paroxysmal, 245–46, 245f electrocardiographic manifesta- relative fi xity of, 145
pulmonary vein ablation for, 604 tions of, 490, 490b from right atrium, 155, 157f
in repaired CHD, 481 entrainment for, 470, 470f wobble in, 108, 108f, 109t
spontaneous induction of, 295, 295f Fontan approach to, 474–75, 474f, atrial myocardium, ablation catheter
SVC potential and, 588, 588f 475f in, 39, 39f
treatment of, ICE for, 71, 72f isoproterenol and, 387, 387f atrial pacing. See also decremental
V-A interval in, 533–34, 533f, 534f left atrium mapping in, 472, 472f atrial pacing; differential atrial
variable output pacing of, 309–10, macro-reentrant, 30–32, 32f pacing
309f, 310f mapping difficulties of, 522b for AF, 523–24, 523f, 536
at vein of Marshall, ablation of, after Mustard procedure, 485 atrial tachycardia and, 331, 331f,
268, 268f noncontact mapping for, 509, 509f 586, 586f
with wide-area circumferential after pulmonary vein isolation of SVC, 586, 586f
ablation, 43, 44f procedure, 567, 567f AV block and, 221, 221f
atrial fibrillation ablation pulmonary veins and, 477 block induced with, 222f, 223
atrial flutter with, 524 right atrial activation during, 29, 29f for dissociating potentials, 226,
atrial pacing, 523–24, 523f, 536 scar-related, 469, 469f 226f
atrial tachycardia with, 530, 530f, crista terminalis–related catheter from high right atrium, 155, 156f
577, 577f for, 27 for intrahisian block, 556, 556f
Index 685
junctional rhythm and, 648, 648f atrial septal defect, with IART, 203–4 atriofascicular pathway, with antidro-
for junctional tachycardia diagno- atrial tachycardia mic tachycardia, 154f, 155
sis, 118–19, 119f ablation of, 591–92, 591f atriotomy scar, atrial flutter and, 469
overdrive suppression and, 573–74, Fontan palliation followed by, atrioventricular (AV) block. See also
573f 209, 210t 2:1 AV block
for paroxysmal palpitation, 393, A-H interval in, 619 ablation near His bundle and,
393f atrial activation and, 644, 644f 594, 594f
preexcitation during, 220, 220f atrial cycle length and, 166–68, AVNRT with, 336, 336f
for PVC, 548f, 549 168f during pacing maneuver, 227, 227f
right-sided accessory bypass tract atrial fibrillation with, 530, 530f, preexcitation and, 221, 221f
and, 350, 350f 588f, 589 atrioventricular (AV) dissociation, in
right-sided accessory pathway and, after ablation for, 577, 577f wide QRS complex tachycar-
22–23, 23f atrial pacing and, 331, 331f, 586, 586f dia, 142–43
in RSPV, 383, 383f in CHD, 203–4, 204t atrioventricular (AV) nodal conduc-
supraventricular tachycardia in, with continued AV node reentry, tion. See also retrograde atrio-
331 411f, 414–17, 414f, 415f, 416f, ventricular nodal conduction
tachycardia initiation during, 331, 417f, 422 anatomy of, 364, 364f
331f diagnosis of, 90, 92f anomalies, 550f, 550t, 551
ventricular pacing and differential diagnosis of, 674–75, anteroseptal accessory pathway
in pathway potential analysis, 674f and, 623
121, 122f, 123f ectopic, sinus tachycardia differen- H-A interval with, 404
for wide QRS complex tachycar- tiation from, 328 in paroxysmal palpitation, 391–92,
dia diagnosis, 111–12 electroanatomic mapping for, 566, 391f, 399, 399f
for wide QRS complex tachycardia, 566f atrioventricular nodal reentry tachy-
111–13, 112b, 147–48, 148f H-A interval in, 617, 617f, 619 cardia (AVNRT). See also atyp-
A-A-V sequence, 112–13, 113f with left bundle branch block, 302, ical AVNRT; typical AVNRT
from anterolateral right atrium, 302f ablation of, 421–22, 421f, 422f
155, 157f macro-reentrant, 30–32, 32f amount of, 640, 640f
A-V-A sequence, 112–13, 113f Morady maneuver for, 97–98, 100f AF with, 524–31, 525f, 526f, 527f,
A-V-V-A sequence, 112–13, 113f in narrow QRS complex tachycar- 528f, 529f, 530f, 531f, 533–34,
at cycle length, 159, 160f, 165 dia, 86 533f, 534f, 536–37, 536f, 537f
with cycle length decreases, 156, paroxysmal narrow QRS complex A-H intervals in, 637–38, 637f
158f tachycardia electrograms and, atrial cycle length and, 166–68,
Mahaim fiber, 112, 114f 13, 14f 168f
Mahaim-like potentials on tri- with paroxysmal palpitation, 633, with atrial dissociation, 411f, 414–17,
cuspid annulus, 113, 115f 633f 414f, 415f, 416f, 417f, 422
with multielectrode catheter, reentrant, atrial pacing and, 331, atrial pacing and, 331, 331f
156, 158f 331f A-V intervals in, 637–38, 637f
with preexcitation, 155, 157f at right atrium, 245f, 246 catheter position for, 274, 274f
ventricular pacing with, 111–12 with right bundle branch block, coronary sinus activation and,
atrial potentials 151–53, 152f 323, 323f
in coronary sinus, 511, 511f proximal, 302f, 303 diagnosis of, 90, 90t, 92f, 150,
His bundle activation and, 626, of RSPV, 596t 287–88, 287f, 335, 335f
626f of SVC, atrial pacing and, 586, 586f distal coronary sinus PAC
left atrial appendage tachycardia V-A interval of, 411, 411f, 413t, 414 placement for, 153
and, 605, 605f ventricular and atrial electrograms earliest activation during, 12
on ligament of Marshall ridge, 308 in, 142 in Fontan patients, 209
PVC and, 231, 231f wide QRS complex tachycardia H-A interval during, 404t
tachycardia termination and, 333, and, 139t infrahisian block with, 638
333f left bundle branch block, 143, 144f junctional tachycardia compared
in vein of Marshall, 308 wobble and, 108 with, 640–41, 640f, 641f
ventricular potential overlap with, atrioesophageal fistula, 254–55, 255f with atrial dissociation, 417
222, 222f prevention of, 255 mapping for, 12, 13f
ventricular preexcitation and, atriofascicular bypass tract. See Morady maneuver for, 98, 100,
271f, 272 Mahaim fibers 101f, 102f
686 Index
atrioventricular nodal reentry tachy- His bundle in, 205 with pacing maneuvers, 32
cardia (AVNRT) (Cont.) atrioventricular (AV) valve point-to-point mapping for, 563,
in narrow QRS complex tachycar- aortic valve and, 52, 54f 563f
dia, 86 fluoroscopy and electrogram cor- prepotential and, 334, 334f
paroxysmal palpitation and, 667, 667f relation for, 52–54, 54f P wave in, 334, 573f, 574, 597, 597f
preexcitation index for, 88f atrium. See also left atrium; right reentrant compared with, 490, 490f
with 2:1 AV block, 418–21, 418f, atrium from right atrium, 561–62, 561f
419f, 420b, 420f, 421f during atrial flutter, electroana- of SVC, 587, 587f
typical compared with atypical, tomic mapping of, 30, 32f ventricular, reentrant ventricular
13, 14f coronary sinus mapping catheter tachycardia compared with,
V-A interval of, 411–14, 411f, in RAO projection and, 5–6, 7f 450t
412t–413t, 414f input to atrioventricular node, 13f A-V-A sequence, in atrial pacing for
wide QRS complex tachycardia morphologic anatomy of, 33, 33f wide QRS complex tachycardia
and, 111–12, 112f, 113f, 139t atypical atrial flutter diagnosis, 112–13, 113f
wobble and, 108, 108f ablation of, 22, 28–29, 29f A-V interval
atrioventricular node (AVN) CHD and, 502–3, 502f in AVNRT, 637–38, 637f
ablation of, accessory pathway mapping of, 22 V-A interval and, 638, 638f
ablation after, 21–22, 22f atypical AVNRT AVN. See atrioventricular node
action potential waveform of, AF with, 524 AVNRT. See atrioventricular nodal
176–77, 178f compared with typical, 13, 14f reentry tachycardia
adenosine and, 355 diagnosis of, 645, 645f AVRT. See atrioventricular recipro-
atrial input to, 13f H-A interval during, 404t cating tachycardia
automaticity in, 179 junctional tachycardia differentia- AVSD. See atrioventricular septal
in CHD, 204, 204t, 205–7 tion from, 119, 120t defect
coronary sinus activation and, 402, paroxysmal narrow QRS complex A-V-V-A sequence, in atrial pacing for
402f tachycardia electrograms and, wide QRS complex tachycardia
displacement of, 627 13, 14f diagnosis, 112–13, 113f
duplication of, 627 with paroxysmal palpitation, 633f, azygous continuation of IVC, 214
electrical abnormalities of, 629t 634 azygous vein, catheter placement in,
fast pathway and retrograde atrial activation 274, 274f
position of, 365, 365f sequence of, 640, 640f
wavefront propagation to, V-A interval of, 411–12, 411f, 412t, Bachmann bundle region, 249–50
320–21, 320f, 321f 413t, 414 catheter locations at, 32, 32f
inputs to, 319, 319f ventricular pacing for, 647, 647f fast pathway activation across, 321,
lateral extensions of, 627–28, 627f automatic atrial arrhythmias, reen- 321f
Mönckeberg sling with twin, trant compared with, 563, 563t interatrial conduction at, 602–3
206–7, 207f automaticity, 179 mapping of, 33
in paroxysmal palpitation, 394, arrhythmias resulting from, 179, tachycardias from, 327f, 328, 328f
394f 180f bidirectional Glenn, 208t
in pathway potential analysis, 121, drugs for, 194–95, 197f blind pouch. See dead-end pathway
122f automatic tachycardia, 308t, 519, 519f, Brugada syndrome, 182, 183t, 184f,
remnants of, 628, 628f 568, 568f 185f, 338f, 339. See also sudden
signal origination in, 222f, 223 ablation of, 451, 451f, 454, 454b, unexplained death syndrome
slow pathway wavefront propaga- 566, 566f possibility of, 343, 343f
tion to, 320, 320f site for, 574, 574f after procainamide injection, 339,
in wide QRS complex tachycardia, approach to, 590, 590f 339f
142–43 atrial pacing and, 331, 331f salient features of, 340, 340b
atrioventricular reciprocating tachy- in coronary sinus, 566f, 567 bubbles. See air bubbles; microbubbles
cardia (AVRT), 622, 622f left atrium and, 561–62, 561f, bundle branch aberrancy, in wide
diagnosis of, 90t, 92f 566f, 567 QRS complex tachycardia, 140
H-A interval during, 404t macroreentrant, 30–32, 32f bundle branch block. See also left
with paroxysmal palpitation, macroreentrant tachycardias com- bundle branch block; right
633–34, 633f pared with, 585 bundle branch block
atrioventricular septal defect (AVSD) near mitral annulus, 562, 562f antidromic activation and, 297,
AV node in, 204–5, 204t PAC during, 519, 576, 576f 297f
Index 687
conduction abnormalities of, 348, current sources and sinks, 188–89, of inappropriate sinus tachycar-
348f 189f dia, 77, 77f
QRS complex of, 296, 296f inherited cardiac channelopathies, of monomorphic ventricular
retrograde, 535 181, 183t tachycardia, 77, 77f
sinus rhythm with, 233, 233f Brugada syndrome, 182, 183t, of recurrent atrial fibrillation,
in wide QRS complex tachycardia, 184f, 185f 77, 78f
109, 109b catecholaminergic polymorphic of symptomatic monomorphic
bundle of His, ablation injury to, 10, 10f VT, 182, 183t, 185, 186f premature ventricular con-
bystander AV nodal conduction, conduction disease, 183t, 186 tractions, 77, 78f
pathway-to-pathway tachycar- familial AF, 183t, 185–86 catecholaminergic polymorphic VT,
dia with, 154, 154f long QT syndrome, 181–82, 183f, 182, 183t, 185, 186f
bystander pathway, 133f, 135. See also 183t catheter location/position
retrograde bystander accessory short QT syndrome, 182, 183t, for ablation, 24, 26f
pathway 184f in annulus, 28, 28f
ORT with, 154–55, 154f sick sinus syndrome, 186 at Bachmann bundle region, 32, 32f
stimulation response of, 135t sinus node dysfunction, 183t, 186 on fluoroscopy, 5, 6f, 7–8, 7f
in wide QRS complex tachycardia, ion channels, 173–75 for ischemic ventricular tachycar-
140, 150 cardiac action potentials and, dia, 49–50, 52f, 53f
bystander signals, AV node–like 176–77, 177f in left pulmonary vein, 38f, 39
tissue and, 23–24, 24f electrogenic membrane pumps for left-sided accessory pathway
bystander site, ablation at, 457–58, and exchanges, 175–76 ablation, 11, 12t
457f, 458f gating, 173, 174f in middle cardiac vein, 3, 4f, 17, 19f
structure of, 171, 172f clockwise torque test and, 20, 20f
cable theory, 187–88, 188f passive membrane properties, 187, counterclockwise torque and,
calcium (Ca 2+) channel blockers, 192f, 188f 18–20, 19f
193t refractoriness, excitability, and for outflow tract ventricular tachy-
automatic tachycardia and, 195 impulse propagation, 177–79 cardias ablation, 54–55, 56f
EAD and DAD suppression, 196, cardiac hypertrophy, as acquired for parahisian pacing, 15, 16f
198f cardiac channelopathy, 186–87, in paroxysmal narrow QRS com-
for reentrant arrhythmias, 199, 200f 187t plex tachycardia, 3, 4f
cannulation cardiac ion currents, 173–75 questions regarding, 59
atrial flutter and, 469 cardiac action potentials and, RAO and LAO projections for, 4, 5f
of middle cardiac vein, 266, 266f 176, 177f respiration and position of, 40, 40f
of posterolateral or posterior car- ICaL , 174 in right superior pulmonary vein,
diac vein, 265 ICa,T, 174 37, 37f
capture latency, 338 If, 175 for supraventricular tachycardia
significance of, 338t IK, 174–75 ablation, 11–13, 12f, 13f, 14f
during ventricular extrastimula- IK1, 175 systematic examination of, 59–60
tion, 337–38, 337f IKACh or IKAdo, 175 tendon of Todaro and, 12, 13f
cardiac channelopathies. See IKATP, 175 for ventricular pacing, for
acquired cardiac chan- INa, 173–74 supraventricular tachycardia,
nelopathies; inherited cardiac Ito, 174 15–17, 16f
channelopathies cardiac vein. See middle cardiac vein; for wide QRS complex tachycardia,
cardiac electrophysiology, 171 posterior cardiac vein; postero- 142
acquired cardiac channelopathies, lateral cardiac vein catheters
186, 187t cardinal veins, 677–78, 677f, 678f gain settings for, 8
atrial fibrillation, 186, 187t Carto 3 System, 77–78 names of, 217
cardiac hypertrophy, 186–87, 187t left atrial anatomic map with, 78, 78f numbering for, 8
heart failure, 186, 187t CartoMerge, 78–79, 79f catheter tip temperature
myocardial infarction, 187, 187t Carto RMT Electroanatomical ablation depth and, 263, 263f
cable theory, 187–88, 188f Mapping System, 78 blood flow and, 362
cardiac arrhythmia mechanisms, CartoSound, 79, 79f esophageal temperature and, 258,
179–81 Carto System, 76–79 258f
impulse initiation abnormalities composition of, 76–77 tissue temperature and, 257, 257f,
resulting in, 179, 180f map generation by, 77 362, 362f
688 Index
cavotricuspid annulus, atrial flutter channelopathies. See acquired cardiac compact AV node, ablation injury to,
and, 469 channelopathies; inherited 10, 10f
cavotricuspid isthmus (CTI) cardiac channelopathies computed tomography (CT)
ablation of, 388f, 389 channel state, antiarrhythmics and, CartoMerge with, 78–79, 79f
for atrial flutter, 472, 472f 192–93, 193f, 193t with electroanatomic mapping, 76
block with, 573, 573f CHD. See congenital heart disease with EnSite Verismo tool, 81
coronary sinus pacing, 571, 571f chest radiograph, heart on, 4, 5f concealed entrainment
difficulties with, 472b circumferential ablation definition of, 130, 133f
eustachian ridge and, 30, 31f at coronary sinus ostium, 574–75 key components of, 133–35, 133f
positioning for, 26–27, 27f electroanatomic map after, 575, pacing site in, 133
pseudoblock with, 28, 572, 572f 575f with repaired CHD, 484, 484f
pseudoconduction, 28, 572, 572f P wave after, 577 conductance, of ion channels, 172–73,
RAO projections for, 30, 31f of RSPV, 384f, 385, 606 173f, 173t
wavefronts in, 27f, 28 circumferential mapping catheter conduction block
catheter location in, 3, 4f, 59–60, (LASSO) CS catheter for, 570
60f in aortic root, 612, 612f with CTI ablation, 573, 573f
disposition of, with Mustard pro- for atrial arrhythmias, 379–80, 379f across eustachian ridge, 13
cedure, 210 atrial fibrillation and, 46, 48f, 49f between LIPV and mitral annulus,
longitudinal dissociation along, for atrial flutter, 477, 477f 323, 323f
390 fluoroscopy and electrogram cor- near interatrial septum, 30, 32f
multielectrode catheter across, 571, relation to, 51t noncontact mapping for assess-
571f in LVOT, 612, 612f ment of, 504, 504f
cavotricuspid isthmus-dependent in pulmonary veins, 41–42, 42f, conduction disease, 183t, 186
flutter, 490, 568, 568f 579, 579f conduction system
ablation of, 495, 495f respiration and position of, 40, 41f in CHD
algorithm for, 515, 515f in RSPV, 37–38, 37f, 38f AV node and His-Purkinje sys-
conduction through gap after, in superior vena cava, 232, 232f tem, 205–7
503, 503f for upper pulmonary vein map- heterotaxy syndromes, 205
difficulties with, 522b ping, 36, 37f sinus node, 205
eustachian ridge and, 501, 501f depth of, 43, 43f disorders of, with CHD, 203, 204t
fragmented potentials with, circumflex artery, left, ablation injury conduction tissue, remnant
498–500, 498f, 499f–500f to, 10–11, 10f, 11f associative and dissociative
high impedance in, 511, 511f circus movement, 130t maneuvers for, 228b
ICE for, 513, 513b, 513f CL. See cycle length in outflow tract, 235, 235f
linear drag approach to, 510, 510f class I antiarrhythmic drugs, 192f, conduction velocity, in atrial flutter,
pectinate muscles and, 512, 512f 193t 471
sheaths for, 513–14, 513f, 514f for atrial flutter, 468t congenital anomalies, ICE with, 71,
split and double potentials, 502, monitoring of, 199–201 73
502f classic atrio-pulmonary Fontan, 208t congenital heart disease (CHD), 203.
subeustachian pouch and, 511, classic Glenn, 208t See also repaired CHD
511f class III antiarrhythmic drugs, moni- ablation electrode in, 374, 374f
supraventricular tachycardia toring of, 192f, 193t, 201, 201f arrhythmias and substrates in, 203,
during, 518, 518f clockwise torque 204t
activation sequence along, 491, 491f on coronary sinus and catheter atrial tachycardias, 203–4, 204t
atrial activation sequence in, location, 20, 21f AV accessory pathways, 204,
491–94, 492f, 493f, 494f with femoral approach, 510 204t
block across, 506, 506f on intraventricular septum and AV block, 204, 204t
arrhythmia with, 516f, 517 catheter location, 20 sinus node dysfunction, 204,
multiple, 517, 517f on middle cardiac vein and cath- 204t
multiple arrhythmias, 516, 516f eter location, 20, 20f sudden cardiac death, 204, 204t
pacing from, 493, 493f for middle cardiac vein cannula- ventricular tachycardias, 204,
proximal coronary sinus pacing, tion, 266, 266f 204t
497, 497f coagulum formation, during ablation, atrial arrhythmia mechanisms
pseudoblock in, 497, 497f 363 with, 468b, 469
cc-TGA. See congenitally corrected common central pathway, 133, 133f atypical atrial flutter and, 502–3,
transposition of great arteries stimulation response of, 135t 502f
Index 689
conduction system in arrhythmias and arrhythmogenic dissection of, 304, 304f

AV node and His-Purkinje sys- substrates in, 211–12 diverticulum of, 666, 666f
tem, 205–7 cardiac venous anatomy in, 211 fluoroscopy and electrogram cor-
heterotaxy syndromes, 205 clinical anatomy for, 212 relation for, 25t
sinus node, 205 with situs inversus, 206 intracardiac echocardiography
congenitally corrected transposi- congenital pulmonary atresia, from, 65
tion of great arteries cavotricuspid isthmus inser- isthmus catheters in, 28
anatomy of, 211 tion for, 60, 60f landmarks in RAO and LAO pro-
arrhythmias and arrhyth- contrast injection, for SVT, 275, 275f jections, 5–7, 7f
mogenic substrates in, 211–12 coronary arterial system, 11, 11f. See left atrium connection to, 324–25,
cardiac venous anatomy in, 211 also left coronary artery; right 324f
clinical anatomy for, 212 coronary artery left-sided epicardial accessory
CTI ablation and, 472, 472b aortic root relationship with, 368, pathway ablation from, 305–7,
dextrotransposition of great arter- 368t 305f, 306f
ies after intra-atrial baffle RVOT relative to, 430, 430f in macroreentrant tachycardias,
anatomy of, 209 coronary sinus (CS). See also distal 575, 575f
arrhythmias and arrhyth- coronary sinus; medial coro- mapping within, 308, 308f
mogenic substrate following, nary sinus; proximal coronary MCV junction with, 614, 614f
210 sinus myocardial sleeves of, 311, 312f
clinical anatomy for, 210–11 ablation of pacing from, 28
disposition of CTI with Mustard problems with, 662, 662f CTI ablation and, 571, 571f
procedure, 210 at roof, 574–75 in supraventricular tachycardia
surgical correction of, 209–10, activation of ablation, 25t
210t AV node vs. accessory pathway, variable output pacing from,
Ebstein anomaly 402, 402f 309–10, 309f, 310f
anatomy of, 212 distal-to-proximal, 322–23, 322f, ventricular electrogram on HRA
arrhythmias and arrhyth- 323f and, 6f, 8f, 9
mogenic substrates with, 212 in left atrial appendage tachycar- ventricular pacing at, 674, 674f
clinical anatomy for, 212–13 dia, 603, 603f ventricular signal in, 393, 393f
sudden death with, 212 to left atrium, 311, 312f coronary sinus beat, coronary sinus
surgical correction of, 212 in parahisian pacing, 91–92, 95f, recording catheter and, 9, 9f
medical treatments for, 468 96f coronary sinus mapping catheter
postoperative arrhythmias, 468, with paroxysmal narrow QRS atrial and ventricular electrograms
468t tachycardia, 13 and, 6–7, 7f
single-ventricle patients with with paroxysmal palpitation, ventricular and atrial in RAO pro-
Fontan palliation, 207–9 392, 392f jection and, 5–6, 7f
atrial tachycardia ablation after, in pathway potential identifica- coronary sinus ostium
209, 210t tion, 121, 123f coronary sinus and, 7, 7f
clinical anatomy for, 208–9 proximal-to-distal, 323, 323f isolation of, 574–75
common arrhythmias and in retrograde right bundle electroanatomic map after, 575,
arrhythmogenic substrate, branch block induction, 97, 99f 575f
207–8 variable sequences of, 15f isthmus catheters at, 28
Fontan connection anatomy, 207, ventricular pacing and, 333 pacing of, 388f, 389
208t, 209f anatomy of, 264, 264f coronary sinus recording catheter.
TOF annulus and, 61f, 62 See also distal coronary sinus;
anatomy of, 213 AP activation in, 307t mid coronary sinus electro-
arrhythmias and arrhyth- during atrial flutter, electroana- grams; proximal coronary
mogenic substrates with, 213 tomic mapping of, 30, 32f sinus
clinical anatomy for, 213 atrial potentials in, 511, 511f coronary sinus beat and, 9, 9f
surgical correction of, 213 automatic tachycardia in, 566f, paroxysmal narrow QRS complex
venous anomalies, 213 567 tachycardia and, 13–15, 14f,
interrupted IVC, 214 conduction block and catheter 15f
persistent LSVC, 213–14 for, 570 in typical intracardiac electro-
congenitally corrected transposition coronary sinus ostium and, 7, 7f gram, 8, 8f
of great arteries (cc-TGA) decremental pacing from, 114, 117f coronary venous system. See venous
anatomy of, 211 in dissected heart, 12, 13f system
690 Index
counterclockwise torque with increased preexcitation rate, for AVNRT, 98, 100, 101f, 102f
with femoral approach, 510 114, 116f difficult situations with, 100, 103
on middle cardiac vein and cath- with minimal preexcitation, 114, for orthodromic reciprocating
eter location, 18–20, 19f 116f tachycardia, 98, 101f
for middle cardiac vein cannula- decremental AV bypass tract, decre- for supraventricular tachycardia,
tion, 266, 266f mental atrial pacing and, 351t 97
crista terminalis, 252, 252f decremental retrograde-conducting V-A-H-V pattern, 100, 102f
P wave and, 574 pathway, 635, 635f V-A-V pattern, 100, 102f, 103f
slow pathway access past, 320–21, decremental ventricular pacing, ventricular pacing speed in, 100,
320f, 321f 103–4, 105f 103
crista terminalis–related catheter, for delayed afterdepolarization (DAD), for narrow QRS complex tachycar-
CTI ablation, 27, 27f arrhythmias and, 179, 180f dia, 86–90
crista terminalis tachycardia, differ- drugs for, 196, 197t, 198f accessory pathway, 89–90, 92f
ential diagnosis of, 595, 595f delayed rectifier potassium ion cur- atrial tachycardia, 90, 92f
CS. See coronary sinus rents (IK), 174–75 AVNRT, 90, 90t, 92f
CS d. See distal coronary sinus depolarization, antiarrhythmic block AVRT, 90t, 92f
CS m. See medial coronary sinus during, 193, 194f early activation in, 89, 90f, 91f
CS p. See proximal coronary sinus dextral retro-atrial cardinal veins, left bundle branch block and, 88
CT. See computed tomography 677–78, 677f, 678f preexcitation index, 86–87, 88b,
CTI. See cavotricuspid isthmus dextrocardia, 62–64, 63f 88f
current sources and sinks, 188–89, 189f dextrotransposition of great arteries PVC placement, 89, 89f, 90t
cycle length (CL) (D-TGA) retrograde His bundle deflection,
atrial pacing at tachycardia, 159, AV node and His bundle in, 205–6 86–88
160f after intra-atrial baffle sensed PVC placement, 85–86,
dominant loop and, 133 anatomy of, 209 87b, 87f
electroanatomic mapping and, 371 arrhythmias and arrhyth- timing of PVC placement, 88–89
isoproterenol and, 601 mogenic substrate following, ventricular pacing at apex, 88,
PVC and, 601, 601f 210 88f
of reentrant circuit, 470 clinical anatomy for, 210–11 ventricular pacing at base, 88, 89f
tachycardia and variation in, 241, disposition of CTI with Mustard parahisian pacing, 90–95
241f procedure, 210 algorithm for, 95, 98f
electroanatomic mapping of, 473, surgical correction of, 209–10, anatomy of, 90–91, 93f
473f 210t coronary sinus activation
of tachycardia in RSPV, 520, 520f diagnostic maneuvers, 85–86, 86b sequence, 91–92, 95f, 96f
electroanatomic mapping of, decremental ventricular pacing, His bundle capture, 91–92, 96f
520f, 521 103–4, 105f misconceptions of, 92, 95, 97f
V-H interval and tachycardia, 159, differential ventricular pacing, pitfalls with, 95, 97b
161, 162f, 165 104–6 QRS complex in, 91, 93f
of VT, 240, 240f accessory pathway in, 106, 107f retrograde right bundle branch
forms of, 104 block induction compared
DAD. See delayed afterdepolarization premise of, 104 with, 97, 100t
dead-end pathway, 133f, 135 from right ventricular apex, salient features of, 97b
in RVOT tachycardia, 433–34, 433f 105–6, 106f, 107f stimulus to A interval, 91, 94f
stimulation response of, 135t from ventricular base, 106, 106f, V-A interval, 91
decremental atrial pacing 107f pathway-related, 120–21
bypass tracts and, 350, 350f, for junctional tachycardia, 118–20 pathway potentials, 121, 121b,
351t–352t atrial pacing for, 118–19, 119f 122f, 123f, 124f, 125f, 125t
retrograde His bundle activation atypical AVNRT and, 119, 120t pathway slant, 121–27, 126b, 126f,
and, 400, 400f causes of, 118 127f
for wide QRS complex tachycardia ORT and, 119, 120t retrograde right bundle branch
diagnosis, 114–18, 147–48, 148f tachycardia termination, 119–20, block induction, 95, 98f
with adenosine, 114, 117f 120f atrial activation delay with, 97,
coronary sinus vs. right atrium, typical AVNRT and, 119, 120t 99f
114, 117f Morady maneuver, 97 coronary sinus activation, 97, 99f
effects of, 114, 115t algorithm for, 103, 104f parahisian pacing compared
fasciculoventricular tract, 115, 118f for atrial tachycardia, 97–98, 100f with, 97, 100t
Index 691
V-A interval in, 97 dominant loop, 133–35, 133f EnSite Array noncontact mapping
for wide QRS complex tachycardia, stimulation response of, 135t catheter, 81–82, 81f
108–18 double-inlet LV, 206 of esophagus, 258, 258f
accessory pathway in, 109–10, double potentials of Fontan conversion, 373, 373f
110f with ablation of CTI, 502, 502f ICE for, 71
atrial pacing for, 111–13, 112b, with electroanatomic mapping, 76 of macroreentrant tachycardias,
113f, 114f, 115f D-TGA. See dextrotransposition of 565, 565f
decremental atrial pacing for, great arteries magnetic, 76
114–18, 115t, 116f, 117f, 118f dual-chamber pacemaker, supraven- Carto 3 System, 77–78, 77f
goals for, 109 tricular tachycardia with, CartoMerge, 78–79, 79f
PACs placed during, 110–11, 112f 21–22, 22f Carto RMT Electroanatomical
wobble, 106–8 Dyna CT, 79, 80f Mapping System, 78
analyzing, 107–8, 108f CartoSound, 79, 79f
mechanism of, 106–7 early afterdepolarization (EAD) Carto System, 76–79, 77f, 78f
differential atrial pacing, 353, 353f arrhythmias and, 179, 180f Dyna CT, 79, 80f
adenosine and, 355, 355f drugs for, 196, 197t, 198f QwikStar, 79
A-H interval with, 354–55, 354f, conditions triggered by, 179, 181t magnetic navigation systems, 82–83
355f Ebstein anomaly Real-time Position Management,
differential ventricular pacing, 104–6 accessory pathway with, 204 82
accessory pathway in, 106, 107f anatomy of, 212 Sensei X Robotic Catheter
forms of, 104 arrhythmias and arrhythmogenic System, 82–83
for pathway slant identification, substrates with, 212 noncontact, 81–82, 81f
124–27, 126b, 126f, 127f AV node and His bundle in, 205 for pectinate muscle identification,
premise of, 104 clinical anatomy for, 212–13 513, 513f
from right ventricular apex, 105–6, sudden death with, 212 Real-time Position Management
106f, 107f surgical correction of, 212 System, 82
from ventricular base, 106, 106f, wide QRS complex tachycardia for reentrant arrhythmias, 370f,
107f and, 168–69, 169f 371, 564, 564f
difficult cases, 615–16, 616t ECG. See electrocardiogram for right ventricular tachycardia,
digitalis, Na+/K+ pump and, 175 ECG leads. See electrocardiographic 57, 57f
digoxin, for atrial flutter, 468t leads tachycardia cycle length on, 473,
diltiazem, for atrial flutter, 468t ectopic atrial tachycardia, sinus 473f, 520f, 521
dissociative maneuvers tachycardia differentiation ultrasound-based, 82
with ablation catheter, 224–25, 224f from, 328 for VT ablation, 459, 459f
ablation with, 225, 225f efficient sheath management, for electrocardiogram (ECG), for wide
arrhythmia cause and, 239, 239f transseptal puncture, 367, 367b QRS complex tachycardia,
to determine potential source, 228b EG-P interval, 135 138–40
determining source, 222f, 223, 228b EG-QRS interval, 133f, 135 electrocardiographic (ECG) leads,
for exercise-related VT, 233, 233f electrical impedance electroanatomic 8f, 9
PVC in, 227, 227f mapping, 80 electrodes, numbering for, 8
technique for, 226, 226f EnSite NavX, 80–81, 81f electrogenic membrane pumps and
two ventricular signals, 223, 223f LocaLisa Intracardiac Navigation exchanges, 175–76
ventricular signals in, 222, 222f System, 80 electrogram fractionation, in electro-
distal ablation catheter (ABL dis) electroanatomic mapping anatomic mapping, 75
signal deflection on, 223, 223f for arrhythmia ablation, 75 electrograms
in typical intracardiac electro- aspects of, 76 atrial flutter and, 24
gram, 8, 8f for atrial flutter, 30, 32f, 370f, 371, complex, 9f
distal coronary sinus (CS d) 470, 470f fluoroscopy correlation with, 9–10,
fast pathway activation, 14f for atrial tachycardia, 566, 566f 9f, 26, 26f
for LVOT ablation, 279 background on, 75–76 of paroxysmal narrow QRS com-
PAC from, 153 basic principles of, 76 plex tachycardia, 13, 14f
in parahisian pacing, 91, 95f after circumferential ablation at typical, 8, 8f
proximal coronary sinus electro- coronary sinus ostium, 575, electropharmacology, 192
grams and, simultaneous, 9, 9f 575f channel state and, 192–93, 193f, 193t
distal pairs of electrodes, numbering components of, 76 use dependence, 193–94, 194f, 195f,
for, 8 electrical impedance, 80–81, 81f 196f, 196t
692 Index
electrophysiology. See cardiac epicardial arrhythmogenic substrate, ventricular potentials and, 406–7
electrophysiology for VT, 632–33, 632f fascicular tachycardia
endocardial ablation epicardial bypass tract, 575 ablation of
for reentrant tachycardia, 262, 262f epicardial veins, 678 difficulty with, 446, 446t
for right ventricular tachycardia, epsilon wave, in arrhythmogenic not at earliest site of activation,
57, 57f right ventricular cardiomyopa- 631t
endocardial dissection, ICE of, 363, thy, 344, 344f with multiple connections to ven-
363f esophagus tricle, 596t
endocardial mapping, of Bachmann anatomy of, 40, 41f origination of, 632, 632f
bundle region, 33 ICE delineation of, 70f, 71 prepotential in, 406–7, 406f
energy delivery left atrium and pulmonary vein fascicular ventricular tachycardia
ablation depth and, 263, 263f and, 40, 41f, 254, 254f origin of, 58, 58f
in RVOT, 284, 284f location of, 253 with right bundle branch block,
EnSite Array noncontact mapping mapping systems for, 258, 258f 140, 140b
catheter, 81–82, 81f prevention of damage to, 256, 256f fasciculoventricular accessory path-
EnSite Fusion registration module, 81 endocardial temperature sensing, way, 550f, 551
EnSite NavX, 80–81, 81f 257, 257f fasciculoventricular bypass tract,
EnSite Verismo tool, 81 intracardiac ultrasonography for, decremental atrial pacing and,
entrainment 259, 259f 351t
for atrial flutter, 470, 470f, 472 temperature sensor for, 256 fasciculoventricular tract, 117, 118f
concealed eustachian ridge His extrasystole and, 406
definition of, 130, 133f activation past, 320–21, 320f, 321f in sinus rhythm, 115, 118f, 269,
key components of, 133–35, 133f anatomy of, 364, 364f 269f
pacing site and programmed stim- conduction block across, 13 fast pathway, 319
ulation, 134f–135f, 135, 135t in CTI ablation, 30, 31f, 501, 501f ablation catheter at, 319, 319f
pacing site and reentrant circuit, double potentials on isthmus map- activation propagation to slow
133 ping catheter and, 28–29, 29f pathway, 320–21, 320f, 321f
transient fast and slow pathway and, 320, 320f anatomy of, 320, 320f
criteria for, 130, 130b, 131f–132f retrograde fast pathway mapping delineation of, 676
definition of, 130 at, 622 fluoroscopic anatomy of, 13, 15f
entrainment mapping excitability, of cardiac cells, 178 fluoroscopy and electrogram cor-
in LA roof, 582–83, 582f exercise-related tachypalpitation, relation for, 25t
in left atrial appendage, 581, 581f epicardial ablation for, 260–61, location of, 12, 13f
from left atrium lateral roof, 584, 260f position of, 365, 365f
584f exercise-related VT, electrogram of, P wave and, 328
for macroreentrant tachycardias 57, 58f, 233, 233f in supraventricular tachycardia
ablation, 577–78, 580, 580f exit block, of left atrial appendage ablation, 11–12, 12f, 25t
P wave length with, 581–82, 581f, tachycardia, 604, 604f surrogate for, 12–13, 14f
582f exit site, in reentrant tachycardia, in ventricular pacing and tachycar-
steps for, 578b 452–54, 452f, 453f, 454f dia, 319
for tachycardia, 566 extracardiac total cavopulmonary fast pathway lesions, retrograde fast
in VT, 455–59, 455b, 455f, 456f, Fontan, 208t pathway conduction, 12
457f, 458f FAT. See focal atrial tachycardia
entrance block, of left atrial append- familial AF, 183t, 185–86 femoral approach, torque with, 510
age tachycardia, 604, 604f far-field potential femoral route, 59, 60f
epicardial ablation analysis of, 307t–308t for middle cardiac vein cannula-
for arrhythmia, 260–61, 260f in coronary sinus, 304–5, 304f tion, 266
in outflow tracts, 442–43, 442f, from LVOT, 251 figure-of-8, 130t
443f near-field potential timing with, antidromic tachycardia, 154f, 155
for outflow tract tachycardia, 237–38, 237f concealed entrainment compo-
56–57 in pulmonary vein, 311, 311f nents, 133–35, 133f
for reentrant tachycardia, 262, 262f QRS complex and, 223, 223f fluoroscopy
for right ventricular tachycardia, reversal of, 236, 236f of ablation catheter, 44, 45f,
57, 57f fascicular potentials 661–62, 661f
of ventricular fibrillation, 278–79 associative and dissociative atrial flutter and, 24
for VT, 262, 262f maneuvers for, 228b catheter location on, 5, 6f, 7–8, 7f
Index 693
with Dyna CT, 79, 80f for congenital pulmonary atresia, normal position in chest, 4, 5f
electrogram correlation with, 9–10, 60, 60f pericardium with, removed, 254,
9f, 26, 26f electroanatomic mapping of, 373, 254f
of fast pathway region, 13, 15f 373f position in open chest, 3, 4f
left atrial appendage on, 45–46, fenestrated, 372, 372f, 476, 476f RAO and LAO of, 6f
45f, 46t, 47f mapping sites for, 372, 372f subeustachian pouch in, 24, 26f
LSPV on, 45–46, 45f, 46t, 47f postoperative arrhythmias, 468, 468t superior view of, 33, 34f, 251, 251f
for more complex procedures, 4 single-ventricle patients with, transverse sinus in, 250, 250f
of paroxysmal narrow QRS com- 207–9 heart block
plex tachycardia, 3, 4f atrial tachycardia ablation after, atrial fibrillation with, 482, 482f
principles of, 3–10 209, 210t with right bundle branch escape,
of pulmonary veins, 34–36, 35f clinical anatomy for, 208–9 482f, 483–84, 484f
for supraventricular tachycardia, common arrhythmias and heart failure, as acquired cardiac
10, 25t arrhythmogenic substrate, channelopathy, 186, 187t
for ventricular electrogram on 207–8 hemi-Fontan, 208t
HRA, 6f, 8f, 9 Fontan connection anatomy, 207, hemodynamic catheterization, for
fluoroscopy and electrogram 208t, 209f tricuspid atresia, 468
correlation types of, 208t heterotaxy syndromes, 205
for atrial fibrillation ablation, fossa ovalis H-H interval. See His-His interval
24–49, 51t anatomy of, 364, 364f high right atrial (HRA) catheter
for AV valve, 52–54, 54f annulus and, 7, 7f atrial pacing from, 155, 156f
for circumferential mapping cath- catheter location in, 3, 4f fast pathway activation, 14f
eter, 51t fast pathway activation across, 321, proximal, 8, 8f
for congenital pulmonary atresia, 321f ventricular electrogram with, 6f,
60–62, 60f, 61f intracardiac echocardiography of, 8f, 9
for coronary sinus, 25t 65, 67f HIS. See His bundle catheter
for fast pathway exit site, 25t for localization of, 68–70, 70f His-atrial (H-A) interval
for ischemic ventricular tachycar- transseptal puncture and, 364, 364f in AF, 525–28, 525f, 526f, 527f, 528f,
dia ablation, 49–50, 52f, 53f fractionated potentials, with electro- 533–34, 533f, 534f, 536f, 537
for LIPV, 51t anatomic mapping, 76 A-H interval change with, 618–19,
for LSPV, 51t fragmented potentials, with abla- 618f
for middle cardiac vein, 25t tion of CTI, 498–500, 498f, in atrial tachycardia, 617, 617f, 619
for outflow tract ventricular tachy- 499f–500f with AV nodal conduction, 404
cardias, 54, 54f functional, univentricular heart, His bundle potential and, 401, 401f
for right ventricular tachycardia, electroanatomic mapping of, in junctional tachycardia, 120, 120f
57, 57f 370f, 371 in ORT, 402, 402f, 619
for RIPV, 51t functional reentry, 130t during pacing and tachycardia,
for RSPV, 51t funny ion currents (If ), 175 404t
for RVOT, 50–52, 53f fusion beats, VT and, 139–40 in paroxysmal palpitation, 401,
for semilunar valve, 52–54, 54f 401f
for superior vena cava, 51t gain settings for recording catheters, 8 prolongation of, 635, 635f
for SVT, 10–25, 25t ganglionated autonomic plexus, abla- with retrograde right bundle
for tricuspid annulus, 25t tion of, 251f, 252 branch block, 162, 163f, 164f
for vein of Marshall, 51t gap junction channels, 175–76 shortening of, 618, 618f
for ventricular pacing site, 25t gating, of ion channels, 173, 174f tachycardia
for ventricular tachycardia abla- GIRK channel. See inwardly rectify- termination of, 621, 621f
tion, 49–59 ing G-protein gated K+ channel with very short, 411–14, 411f,
focal arrhythmias, QwikStar for, 79 412t–413t, 414f
focal atrial tachycardia (FAT), in H-A interval. See His-atrial interval V-A interval compared with, 400
Fontan patients, 209 halo catheter, for mapping of tricus- during ventricular pacing, 403–4,
Fontan palliation pid annulus, 221 403f
ablation and, 475, 475b heart in wide QRS complex tachycardia,
arrhythmia after, 478, 478f on chest radiograph, 4, 5f 143, 146, 157–59, 158f
for atrial flutter, 474–75, 474f, inferior view of, 614, 614f Ebstein anomaly and, 168–69,
475f morphologic anatomy of atria in, 169f
common type of, 372, 372f 33, 33f wobble in, 109t
694 Index
His bundle activation. See also in ventricular pacing, 16, 16f IART. See intra-atrial reentrant
antegrade His bundle activa- in wide QRS complex tachycardia, tachycardia
tion; retrograde His bundle 141, 142f ICaL. See L-type calcium ion currents
activation His bundle tachycardia, 596t ICa,T. See T-type calcium ion currents
atrial potential and, 626, 626f AF with, 531, 531f, 532t, 534–35, ICD. See implantable cardioverter-
mitral annulus and, 623 534f, 538–39, 538f, 539f defibrillator
RSPV activation and, 602–3 His extrasystoles, 405–6, 405f, 481, ICE. See intracardiac
His bundle catheter (HIS) 481f echocardiography
atrial and ventricular electrograms His-His (H-H) interval idiopathic aneurysm, ablation of,
and, 6–7, 7f in AF, 525–27, 525f, 526f, 527f, 531, ICE–assisted, 71, 73, 73f
atrial potential on, 623, 623f 531f, 534–35, 534f, 537 If. See funny ion currents
AV block and, 221, 221f in junctional tachycardia, 619 IK. See delayed rectifier potassium ion
in interatrial septum, 32, 32f in wide QRS complex tachycardia, currents
in right side of heart, 25, 26f 146 IK1. See strong inward rectifier potas-
septum and, 35 wobble in, 109t sium ion currents
signal origination in, 222f, 223 His p. See proximal His bundle IKACh. See inwardly rectifying
on typical intracardiac electro- His-Purkinje system G-protein gated potassium ion
gram, 8, 8f action potential waveform of, 177, currents
in wobble, 108, 108f 178f IKAdo. See inwardly rectifying
His bundle potential automaticity in, 179 G-protein gated potassium ion
atrial activation sequence and, in CHD, 205–7 currents
403–4, 403f His-ventricular (H-V) interval IKATP. See inward rectifier potassium
double, 653, 653f in AF, 533, 533f, 535 ion currents
fast pathway and, 622 with atrial and ventricular poten- implantable cardioverter-defibrillator
H-A interval and, 401, 401f tial overlap, 222, 222f (ICD)
missing, 668–72, 668f, 669f, 670f, with atrial extrastimulus, 354, Holter tracing of, 278, 278f
671f, 672f 354f for VT, 204
in paroxysmal palpitation, 394–95, in decremental atrial pacing, impulse initiation abnormalities, arrhyth-
394f, 395f 114–15, 116f, 117f mias resulting from, 179, 180f
in PVC, 543–53, 543f, 544f, 545f, with differential atrial pacing, 353, impulse propagation
546f, 547f, 548f, 549f, 550f, 353f, 355, 355f arrhythmias due to abnormalities
550t, 551f, 552f, 553b prolongation of, 635, 635f in, 179–81, 180f, 182f
ventricular potential and, 641–42, in PVC, 543–44, 543f, 544f cable theory for, 187–88, 188f
641f, 642f in right-sided accessory bypass of cardiac cells, 178–79
His bundle reentry, 553–58, 553f, 554f, tract, 349, 349f current sources and sinks, 188–89, 189f
555f, 556f, 557f, 558f, 558t in wide QRS complex tachycardia, INa. See sodium ion currents
His bundle region 143, 146–47 inappropriate sinus tachycardia,
accessory pathway ablation near, Ebstein anomaly and, 168–69, Carto map of, 77, 77f
219–20, 219f 169f incisional reentry, 469f
antegrade 2-for-1 conduction to, with preexcitation, 155, 157f incremental atrial pacing, for wide
650, 650f from right atrium, 155, 157f QRS complex tachycardia
AV block and ablation near, 594, wobble in, 108, 109t diagnosis, 147–48, 148f
594f Holter tracing inferior vena cava (IVC)
locating with pacing maneuver, of ICD, 278, 278f ablation at, 61
271, 271f of QRS complex with left bundle ablation catheter in, 24, 26f
in parahisian pacing, 91–92, 96f, 330 branch block, 348, 348f anatomy of, 364, 364f
in paroxysmal palpitation, 394, 394f HRA. See high right atrial azygous continuation of, 214
proximal, activation of, 12–13, 14f catheter with hemiazygos continuation, 214
retrograde fast pathway conduc- HRA prox. See proximal high right interrupted, 214
tion and, 12 atrial electrogram infradiaphragmatic venous mapping,
septum in LAO projection and, H-V interval. See His-ventricular 273, 273f
5–6, 7f interval infrahisian block, 143
septum penetration by, 283, 283f hypokalemia, EAD and, 181t with AVNRT, 638
tachycardia origination in, 632, hypomagnesemia, EAD and, infrahisian conduction disease, diagnosis
632f 181t of, 341, 341f
Index 695
inherited cardiac channelopathies, intracardiac thrombus assess- inwardly rectifying G-protein gated
181, 183t ment, 71, 71f potassium ion currents (IKACh,
Brugada syndrome, 182, 183t, 184f, pericardial eff usion recognition, IKAdo), 175
185f 70f, 71 inwardly rectifying K+ (Kir) channels,
catecholaminergic polymorphic procedural complication assess- 171, 172f
VT, 182, 183t, 185, 186f ment, 70f, 71, 71f inward rectifier potassium ion currents
conduction disease, 183t, 186 specific arrhythmia treatment, (IKATP), 175
familial AF, 183t, 185–86 71–73, 72f, 73f ion channels
long QT syndrome, 181–82, 183f, transseptal catheterization, cardiac action potentials and,
183t 68–70, 70f 176–77, 177f, 178f
short QT syndrome, 182, 183t, 184f in CartoSound, 79 cardiac ion currents, 173–75
sick sinus syndrome, 186 of catheter position during respira- conductance of, 172–73, 173f, 173t
sinus node dysfunction, 183t, 186 tion, 40, 41f electrogenic membrane pumps and
inner loop, 133, 133f of circumferential catheter posi- exchanges, 175–76
stimulation response of, 135t tion, 43, 43f gating, 173, 174f
interatrial conduction, at Bachmann for CTI ablation, 513, 513b, 513f structure of, 171, 172f
bundle, 602–3 of endocardial dissection, 363, 363f subunits of, 176
interatrial flutter, 577, 577f for esophagus protection, 259, ischemic cardiomyopathy, capture
ablation of, 574–75 259f latency in, 338
interatrial septum general settings, views and orienta- ischemic ventricular tachycardia
anatomy of, 364, 364f tions of, 65–68, 66f, 67f, 68f, catheter positioning for, 49–50, 52f
conduction block near, 30, 32f 69f with right bundle branch block,
in electroanatomic map, 30, 32f intravascular ultrasound compared 140, 140b
ICE of, 366, 366f with, 65 isolation procedure, 608t–609t
mapping of, 32, 32f of right atrium, 366, 366f, 610, 610f at superior vena cava-right atrial
intercaval ablation line, 474, 474f for transseptal puncture, 365–66, junction, 233, 233f
intermittent accessory pathway con- 366f isoproterenol
duction, with antegrade 2-for-1 types of, 65 AF and, 529, 529f, 539
phenomenon, 228–29, 228f intracardiac thrombus atrial cycle length and, 601
intermittent wide complex beats, aorta puncture and, 364, 364f atrial flutter and, 387, 387f
543–49, 543f, 544f, 545f, 546f, extraction of, 363, 363f junctional rhythm with, 386, 386f
547f, 548f, 549f, 550f, 550t, ICE for assessment of, 71, 71f for left atrial appendage tachycar-
551–53, 551f, 552f, 553b intravenous heparinization for, 363 dia, 607, 607f
internal jugular venous route, for during left atrial ablation, 362–63, with parahisian pacing, 359, 359f
middle cardiac vein cannula- 362f tachycardia with, 236, 236f, 595,
tion, 266, 266f intrahisian block, procainamide 595f
intra-atrial baffle, D-TGA after administration and, 556, 556f isthmus catheter, for CTI ablation,
anatomy of, 209 intrahisian conduction disease, 26–28, 27f
arrhythmias and arrhythmogenic 654–55, 654f, 655f isthmus mapping catheter, double
substrate following, 210 intrahisian reentry, 553–58, 553f, 554f, potentials on, 28–29, 29f
clinical anatomy for, 210–11 555f, 556f, 557f, 558f, 558t Ito. See transient outward potassium
disposition of CTI with Mustard intrahisian sequence, in AF, 525–27, ion currents
procedure, 210 525f, 526f, 527f, 531, 531f, IVC. See inferior vena cava
surgical correction of, 209–10, 210t 534–35, 534f
intra-atrial reentrant tachycardia intravascular ultrasound, intracardiac J-point elevation, 338f, 339
(IART), 203–4, 204t echocardiography compared after procainamide injection, 339,
atrial switch operation followed with, 65 339f
by, 210 intravenous heparinization, throm- junctional escape beats, typical
in Fontan patients, 209 bogenic complications and, AVNRT echo beats and, 640,
intracardiac echocardiography (ICE) 363 640f
during ablation, 361, 361f intraventricular septum, catheter junctional rhythm, 335, 335f
of left atrium, 362–63, 362f location in, clockwise torque atrial pacing and, 648, 648f
of ventricular myocardium, 362 and, 20 with isoproterenol, 386, 386f
applications of, 65 inwardly rectifying G-protein gated in left atrial appendage tachycar-
esophagus delineation, 70f, 71 K+ (GIRK) channel, 171 dia, 604, 604f
696 Index
junctional rhythm (Cont.) lateral tunnel total cavopulmonary circumferential ablation of, 606,
retrograde atrial activation Fontan, 208t 606f
sequence during, 639, 639f lateral view exit block of, 604, 604f
sinus rhythm competing with, for anatomic structure evaluation, 3 isoproterenol for, 607, 607f
591–92, 591f RAO projection and, 4, 5f left atrium (LA)
junctional tachycardia LCC. See left coronary cusp ablation at, 251
ablation of, not at earliest site of leading circle, 130t ICE during, 362–63, 362f
activation, 631t left anterior descending artery, RVOT pulmonary vein conduction
AF with, 524–34, 524b, 525f, 526f, and, 53 block, 44, 45f
529f, 530f, 531f, 532f, 532t–533t, left anterior oblique (LAO) projection activation of
533f, 534f, 536–37, 536f anatomic landmarks in, 5–7, 7f from coronary sinus, 311, 312f
ventricular fibrillation arising of Carto map, during monomor- distal-to-proximal, 322, 322f
from, 540–42, 540f, 541f, 542f phic ventricular tachycardia, right atrium and, 597, 597f
atypical AVNRT differentiation 77, 77f anatomy of, 40, 41f
from, 119, 120t of CartoSound map, 79, 79f atrial flutter and mapping of, 472,
AVNRT compared with, 640–41, catheter location and, 3, 4f, 5, 6f, 472f
640f, 641f 7–8, 7f automatic tachycardia and, 561–62,
with atrial dissociation, 417 cavotricuspid isthmus location on, 561f, 566f, 567
causes of, 118 28 Carto 3 System map of, 78, 78f
with CHD, 479, 479f of circumferential mapping Carto map of, during recurrent
diagnostic maneuvers for, 118–20 catheter atrial fibrillation, 77, 78f
atrial pacing for, 118–19, 119f in LSPV and LIPV, 38–39, 38f CartoMerge map of, 79, 79f
tachycardia termination, 119–20, in RSPV, 37–38, 38f CartoSound map of, 79, 79f
120f on fluoroscopy, 4–5, 6f coronary sinus connection to,
H-H interval in, 619 of heart, 6f 324–25, 324f
intrahisian reentry in, 553–58, for left atrial appendage tachycar- EnSite NavX map of, 81, 81f
553f, 554f, 555f, 556f, 557f, 558f, dia, 605, 605f entrainment mapping in, 582–83,
558t of LSPV and left atrial appendage, 582f
ORT differentiation from, 119, 120t 46, 46t, 47f esophagus and, 254, 254f
typical AVNRT differentiation of middle cardiac vein catheter intracardiac echocardiography of,
from, 119, 120t location, 17, 19f 65, 67f, 71, 72f
V-A interval of, 411, 411f, 412t, clockwise torque and, 20, 20f linear ablation across, 246
413t, 414 counterclockwise torque and, macroreentrant tachycardias in,
variants of, 532t–533t, 558t 18–20, 19f 566f, 567
ventricular and atrial electrograms of outflow tract ventricular tachy- mechanical rotational ultrasound
in, 143 cardias, 54–55, 56f of, 66f
wide QRS complex tachycardia of pulmonary veins, 34, 35f noncoronary cusp and, 283, 283f
and, 139t right and left determinations with, perforation into, 282, 282f
4, 5f phased-array transducer imaging
K ATP channel. See adenosine triphos- of right ventricular tachycardia, of, 66f
phate–sensitive K+ channel 57, 57f roof fibers of, 250
+
K channel blockers. See potassium septum in, 5 tachycardias from, 327f, 328, 328f
channel blockers left atrial appendage (LAA) transseptal puncture and air
kinetics of recovery from Na+ channel ablation of, 604, 604f bubbles in, 367, 367f
blockers, 193, 195f entrainment mapping in, 581, 581f vein of Marshall and, 47–49, 50f, 51t
Kir channels. See inwardly rectifying on fluoroscopy, 45–46, 45f, 46t, left atrium apex (LAA), normal posi-
K+ channels 47f tion in chest, 4, 5f
intracardiac echocardiography of, left atrium–coronary sinus connec-
LA. See left atrium 71, 72f tions, activation through, 13
LAA. See left atrial appendage; left isolation of, 599–600, 599f, 600f, left atrium lateral wall
atrium apex 609t accessory pathway ablation near,
Lancisi fibers, 433–34, 433f LSPV proximity to, 45–46, 46f 219–20, 219f
LAO projection. See left anterior left atrial appendage tachycardia, 601, entrainment mapping from, 584,
oblique projection 601f 584f
LASSO. See circumferential mapping ablation of, 604, 604f left atrium septum, accessory path-
catheter activations in, 602–3, 602f, 603f way ablation near, 219–20, 219f
Index 697
left bundle branch block. See also left-sided accessory pathway. See for supraventricular tachycardia,
antegrade left bundle branch also left lateral accessory 15–17, 16f
block; retrograde left bundle pathway left ventricular free wall. See left free
branch block ablation of, 11, 12t wall
atrial pacing and, 220, 220f AF with, 300f, 301 left ventricular outflow tract (LVOT)
atrial tachycardia with, 302, 302f ART initiation with, 165, 165f, 166f ablation of, 279
in infrahisian conduction disease, endocardial, 303, 303f access for, 279
341, 341f epicardial, ablation of, 305–7, 305f, circumferential mapping catheter
in mitral isthmus ventricular 306f in, 612, 612f
tachycardia, 461, 461f Morady maneuver for lateral, 98, coronary vasculature and, 280,
in narrow QRS complex tachycar- 101f 280f
dia diagnosis, 88 ORT with, 289–90, 289f, 290f far-field ventricular potentials
QRS complex with, 348, 348f retrograde conduction and, 408, from, 251
in wide QRS complex tachycar- 408f mapping of, 428, 428f, 438–40,
dia, 140–41, 141b, 143, 144f, left-sided fascicle-related tachyar- 438f, 439f, 440f, 443, 443f
449–51, 449f, 450t rhythmia, 58–59, 58f catheter positioning during, 610,
left bundle branch block tachycardia, left-sided His bundle variant, 668, 610f
initiation of, during ventricu- 668f RVOT and, 54, 55f
lar pacing, 165, 166f left superior fascicles, 433–34, 433f left ventricular outflow tract
left circumflex artery, ablation injury left superior pulmonary vein (LSPV) tachycardia
to, 10–11, 10f, 11f anatomy of, 35 difficulty ablating, 436–42, 436f,
left coronary artery angiogram of, 36, 37f 437f, 438f, 439f, 440f, 441f,
RVOT and, 53 circumferential mapping of, 38–39, 442f, 446, 446t
VT in, 282, 282f 38f epicardial origin in, 442–43, 442f,
left coronary cusp (LCC) depth of, 43, 43f 443f
Carto map of, during symptomatic on fluoroscopy, 45–46, 45f, 46t, 47f with right bundle branch block,
monomorphic PVC, 77, 78f fluoroscopy and electrogram cor- 140, 140b
low-output pacing in, 611, 611f relation to, 51t left ventricular tachycardia, with left
left free wall (LFW) injection of, 35, 35f bundle branch block, 141, 141b,
AP ablation on, 269–70 intracardiac echocardiography of, 142f
drainage of, 265 65, 67f, 71, 72f levotransposition of great arteries
preexcitation index for, 88f left atrial appendage proximity to, (L-TGA)
left heterotaxy. See polysplenia 45–46, 46f AV node in, 204, 204t, 206
syndrome location of, 40, 41f twin, 207
left inferior pulmonary vein (LIPV) passive conduction at, 245f, 246 His bundle in, 206
ablation at, 50, 52f, 569–70, 569f left superior vena cava (LSVC) with pulmonary valve hypoplasia,
atrial arrhythmias, 377–78, 377f persistent, 213–14 206
circumferential mapping of, 38–39, vein of Marshall and, 311, 311f with septal malalignment, 206
38f left ventricle (LV) LFW. See left free wall
conduction block between mitral activation of ligament of Marshall ridge, atrial
annulus and, 323, 323f accessory pathway and, 137, 138f potentials on, 308
fluoroscopy and electrogram cor- VT and, 137, 138f LIPV. See left inferior pulmonary vein
relation to, 51t Carto map of, during monomor- LMO. See left main ostium
intracardiac echocardiography of, phic ventricular tachycardia, LocaLisa Intracardiac Navigation
65, 67f, 68f, 71, 72f 77, 77f System, 80
location of, 40, 41f CartoSound map of, 79, 79f longitudinal dissociation, along
tachycardia origins in, 574 on chest radiograph, 4, 5f cavotricuspid isthmus, 390
left lateral accessory pathway double-inlet, 206 long QT syndrome, 181–82, 183f, 183t
Morady maneuver for, 98, 101f intracardiac echocardiography of, EAD and, 181t
typical AVNRT and, 318 68, 69f lower-loop conduction, 389–90, 389f,
left main ostium (LMO), ICE of, 71, in LAO, 6f 571, 571f
72f normal position in chest, 4, 5f LPA. See left pulmonary artery
left midseptal accessory pathway, 596t retrograde aortic approach to, LSPV. See left superior pulmonary vein
left pulmonary artery (LPA), intracar- 61–62 LSVC. See left superior vena cava
diac echocardiography of, 68f ventricular pacing from L-TGA. See levotransposition of great
left pulmonary vein tachycardia, 596t importance of, 18t arteries
698 Index
L-type calcium ion currents (ICaL), 174 Real-time Position Management, mid-diastolic potentials, with electro-
LV. See left ventricle 82 anatomic mapping, 76
LVOT. See left ventricular outflow Sensei X Robotic Catheter System, middle cardiac vein (MCV)
tract 82–83 ablation catheter in, 24, 26f
magnetic resonance imaging (MRI) ablation of, 264, 614
macrolide antibiotics, EAD and, 181t CartoMerge with, 78–79, 79f accessory pathway in, 659, 659f,
macroreentrant atrial flutter, 30–32, with electroanatomic mapping, 76 663, 663f
32f with EnSite Verismo tool, 81 anatomy of, 264, 264f
macroreentrant automatic tachycar- Mahaim fiber–related antidromic cannulation of, 266, 266f
dia, 30–32, 32f tachycardia, 407–8, 407f catheter location in, 3, 4f, 17, 19f
macroreentrant left atrial flutter, 577, ablation of, not at earliest site of clockwise torque and, 20, 20f
577f activation, 631t counterclockwise torque and,
macroreentrant right atrial flutter, Mahaim fibers, 116–17, 118f 18–20, 19f
577, 577f ablation of, 632, 632f CS junction with, 614, 614f
macroreentrant tachycardias. See also adenosine and, 355 fluoroscopy and electrogram cor-
atrial flutter antidromic reciprocating tachycar- relation for, 25t
ablation of, 577–78 dia with, 154f, 155 PCV compared with, 264
entrainment mapping for, diagnosis of, 150 in supraventricular tachycardia
577–78, 580, 580f His bundle potential and, 544, ablation, 25t
approach to, 590, 590f 546–47, 546f, 549 midseptum, ventricular pacing at,
automatic tachycardias compared location of, 627 642, 642f
with, 585 as wide QRS complex tachycardia missing His bundle potential, 668–72,
circuit mapping for, 565 on ablation catheter, 113, 114f 668f, 669f, 670f, 671f, 672f
coronary sinus in, 575, 575f for PAC placement during, 111, mitral annulus
electroanatomic mapping of, 565, 112f ablation at, 569–70, 569f
565f Mahaim-like fibers, 627 ablation catheter and, 11, 11f
in left atrium, 566f, 567 Mahaim tachycardia, H-A interval automatic tachycardia near, 562,
mapping systems for, 508, 508f during, 404t 562f
PACs during, 576, 576f mapping catheter catheter location in, 3, 4f
QwikStar for, 79 coronary sinus conduction block between LIPV
in right atrium, 566f, 567 atrial and ventricular electro- and, 323, 323f
magnetic electroanatomic mapping, grams and, 6–7, 7f earliest activation in, 623
76 ventricular and atrial in RAO intracardiac echocardiography of,
Carto 3 System, 77–78 projection and, 5–6, 7f 65, 67f
left atrial anatomic map with, EnSite Array noncontact, 81–82, mapping of, 277, 277f
78, 78f 81f VT and, 300, 300f
CartoMerge, 78–79, 79f respiration and position of, 40, 40f mitral isthmus ablation line, 569, 569f
Carto RMT Electroanatomical two ventricular signals on, 223, bidirectional block for, 570
Mapping System, 78 223f mitral isthmus-dependent flutter, 562,
CartoSound, 79, 79f Marfan syndrome, Carto map of, 77, 562f, 568, 568f
Carto System, 76–79 77f mitral isthmus ventricular tachycar-
composition of, 76–77 maximum diastolic potential (MDP), dia, 449f, 451, 461, 461f
during inappropriate sinus drugs for, 194–95, 197f moderator band, VT at, 632, 632f
tachycardia, 77, 77f MCV. See middle cardiac vein modified atriopulmonary Fontan,
map generation by, 77 MDP. See maximum diastolic 208t
during monomorphic ventricular potential Mönckeberg sling, twin AV nodes
tachycardia, 77, 77f mechanical rotational ultrasound, 65 with, 206–7, 207f
of recurrent atrial fibrillation, of left and right atrium, 66f monomorphic ventricular tachycar-
77, 78f medial coronary sinus (CS m), fast dia, Carto map of, 77, 77f
of symptomatic monomorphic pathway activation, 14f Morady maneuver
premature ventricular con- microbubbles algorithm for, 103, 104f
tractions, 77, 78f during ablation, 257, 257f atrial pacing compared with, 111
Dyna CT, 79, 80f ICE of, 361, 361f for atrial tachycardia, 97–98, 100f
QwikStar, 79 tissue vaporization and, 362 for AVNRT, 98, 100, 101f, 102f
of tricuspid annulus, 221 mid coronary sinus electrograms, as difficult situations with, 100, 103
magnetic navigation systems, 82–83 earliest, 9–10, 9f one-to-one entrainment for, 333
Index 699
for orthodromic reciprocating Na+/Ca 2+ exchange. See sodium/cal- nodofascicular accessory pathway,
tachycardia, 98, 101f cium exchange 549, 550f, 551, 553
for supraventricular tachycardia, Na+ channel blockers. See sodium nodofascicular bypass tract, decre-
97 channel blockers mental atrial pacing and, 352t
V-A-H-V pattern, 100, 102f Na+/K+ pump. See sodium/potassium nodofascicular tachycardia, diagnosis
V-A-V pattern, 100, 102f, 103f pump of, 150
ventricular pacing speed in, 100, narrow QRS complex tachycardia nodofascicular tract, 117, 118f
103 causes of, 86, 467 nodoventricular accessory pathway,
for wide QRS complex tachycardia, diagnostic maneuvers for, 86–90 550f, 551
151 accessory pathway, 89–90, 92f nodoventricular bypass tract, decre-
wobble with, 107 atrial tachycardia, 90, 92f mental atrial pacing and, 352t
MRI. See magnetic resonance AVNRT, 90, 90t, 92f nodoventricular conduction, inter-
imaging AVRT, 90t, 92f mittent, 228–29, 228f
multielectrode catheter early activation in, 89, 90f, 91f nodoventricular tachycardia, diagno-
for atrial flutter ablation, 25–26, 27f left bundle branch block and, 88 sis of, 150
double potentials on, 28–29, 29f preexcitation index, 86–87, 88b, nodoventricular tract, 117, 118f
across CTI, 571, 571f 88f noncontact electroanatomic mapping,
in left upper pulmonary vein, 315, PVC placement, 89, 89f, 90t 81–82, 81f
315f retrograde His bundle deflection, in RVOT tachycardia, 426, 426f
for mitral annulus mapping, 569 86–88 noncontact mapping
for pathway potential identifica- sensed PVC placement, 85–86, for conduction block assessment,
tion, 121, 122f 87b, 87f 504, 504f
for pathway slant identification, timing of PVC placement, 88–89 with counterclockwise atrial flut-
124–25 ventricular pacing at apex, 88, ter, 509, 509f
placement along tricuspid annulus, 88f noncoronary cusp, left atrium and,
22 ventricular pacing at base, 88, 89f 283, 283f
for mapping, 221 junctional tachycardia in, 118, numbering, for electrodes, 8
for wide QRS complex tachycardia, 540–42, 540f, 541f, 542f
142 paroxysmal oblique pericardial sinus, 253–54,
Mustard procedure electrograms of, 13, 14f 253f, 254f
atrial flutter and, 485 fluoroscopy of, 3, 4f ablation catheter at, 256, 256f
disposition of CTI with, 210 premature ventricular contractions mapping at, 33
postoperative arrhythmias, 468t during, 85 pericardial eff usion with, 259, 259f
myocardial infarction P waves in, 636f, 637 open chest, heart position in, 3, 4f
as acquired cardiac channelopathy, rapid, fluoroscopic anatomy for, ORT. See orthodromic reciprocating
187, 187t 10–11, 10f, 11f, 12t tachycardia
atrial fibrillation with, 482, 482f R-P interval of, 643, 643f orthodromic AV reciprocating
VT ablation after, 451, 451f, 454b, V-A interval of, 633–34, 633f tachycardia
460, 460f near-field potential diagnosis of, 287–88, 287f
automatic tachycardia, 451, 451f, analysis of, 307t–308t H-V interval in, 535
454, 454b in coronary sinus, 304–5, 304f V-A interval of, 414
difficulty with, 462–65, 462f, with exercise-related VT, 57–58, orthodromic AV reentrant
463f, 464f, 465f 58f, 233, 233f tachycardia
electroanatomic mapping, 459, far-field potential timing with, diagnosis of, 150
459f 237–38, 237f in narrow QRS complex tachycar-
entrainment mapping, 455–59, after fragmented potential, 235, dia, 86
455b, 455f, 456f, 457f, 458f 235f wobble and, 108, 108f
mitral isthmus ventricular tachy- in left atrial appendage tachycar- orthodromic reciprocating tachycar-
cardia, 449f, 451, 461, 461f dia, 605, 605f dia (ORT)
reentrant tachycardia, 451–54, from pulmonary artery, 237, 237f antegrade left bundle branch block
451f, 452f, 453f, 454b, 454f in pulmonary vein, 311, 311f during, 161, 163f
scar tissue and, 465, 465f reversal of, 236, 236f with bystander accessory pathway,
myocardial sleeves, 234, 234f tachycardia termination and, 239, 154–55, 154f
of coronary sinus, 311, 312f 239f, 241, 241f diagnosis of, 290, 290f
myocardial tissue, superior to pulmo- ventricular potential and, 242, 242f with left-sided accessory path-
nary valve, 234, 234f near-simultaneous activation, 596t way, 289, 289f
700 Index
orthodromic reciprocating tachycar- sudden-onset, sudden-offset, 317f, ventricular signal in, 393, 393f
dia (ORT) (Cont.) 318, 318f passive membrane properties, 187,
with right-sided accessory path- with wide QRS complex tachycar- 188f
way, 287–88, 287f dia, 151–53, 152f patent foramen ovale, ICE for detec-
H-A interval in, 402, 402f, 619 parahisian pacing, 90–95 tion of, 70
junctional tachycardia differentia- accessory pathway and, 277–78, pathway length (PL)
tion from, 119, 120t 277f in different reentrant models, 130t
Morady maneuver for, 98, 101f algorithm for, 95, 98f of reentrant circuit, 129, 129f
recurrent, 21, 22f anatomy of, 90–91, 93f pathway potentials
wide QRS complex tachycardia catheter placement for, 15, 16f on ablation catheter, 224, 224f
and, 111–12, 112f, 113f, 139t conclusions with, 359, 359f near-field, 224f, 225
outer loop, 133, 133f coronary sinus activation sequence diagnostic maneuvers for, 121,
stimulation response of, 135t in, 91–92, 95f, 96f 121b, 125t
outflow tract ventricular tachycardias His bundle capture, 91–92, 96f coronary sinus activation in, 121,
ablation for, 50–52, 53f importance of, 18t 123f
catheter placement for, 54–55, 56f misconceptions of, 92, 95, 97f electrogram separation, 121, 125f
epicardial, 56–57 pitfalls with, 95, 97b multielectrode catheter place-
electrograms for, 55, 56f QRS complex in, 91, 93f ment for, 121, 122f
fluoroscopy and electrogram cor- retrograde atrioventricular nodal sensed PAC placement, 121, 124f
relation for, 54, 54f conduction and, 330, 330f, sensed ventricular pacing in, 121,
isolation procedure for, 608t 646, 646f 122f, 123f
LVOT tachycardia retrograde right bundle branch VA block in, 121, 124f
difficulty ablating, 436–42, 436f, block induction compared in paroxysmal palpitation, 393–94,
437f, 438f, 439f, 440f, 441f, with, 97, 100t 393f, 394f
442f, 446, 446t salient features of, 97b pathway-related diagnostic maneu-
epicardial origin in, 442–43, stimulus to A interval, 91, 94f vers, 120–21
442f, 443f V-A interval, 91, 358, 358f pathway potentials, 121, 121b, 125t
RVOT tachycardia paravenous pacing, of RSPV, 383–84, coronary sinus activation in, 121,
difficulty ablating, 423–36, 423f, 383f, 384f 123f
424b, 424f, 425f, 426f, 427f, parietal pericardium, 254, 254f electrogram separation, 121, 125f
428f, 429f, 430f, 431f, 432f, paroxysmal atrial fibrillation, 245–46, multielectrode catheter place-
433f, 434f, 435f, 446, 446t 245f ment for, 121, 122f
epicardial origin in, 442–43, ablation for, 46–47, 49f, 61f, 62–64, sensed PAC placement, 121, 124f
442f, 443f 62f, 63f, 64f sensed ventricular pacing in, 121,
with RV dysplasia, 444–45, 444f, paroxysmal narrow QRS complex 122f, 123f
445b, 445t tachycardia VA block in, 121, 124f
treatment of, ICE for, 71–73, 72f, electrograms of, 13, 14f pathway slant, 121–24
73f fluoroscopy of, 3, 4f differential pacing for, 124–27,
overdrive suppression supraventricular tachycardia with, 126b, 126f, 127f
atrial pacing and, 573–74, 573f 649, 649f pathway slant
of tachycardia, 575 paroxysmal palpitation, 299, 299f of AP, 293, 293f
atrial extrastimulus testing for, diagnostic maneuvers for, 121–24
PAC. See premature atrial 396, 396f, 397f, 398, 398f differential pacing for, 124–27,
contractions atrial pacing for, 393, 393f 126b, 126f, 127f
pace-mapping, of RVOT tachycardia, AV nodal conduction with, 391–92, pathway-to-pathway tachycardia, 153
434–36, 434f, 435f 391f with antegrade AV nodal
pacing maneuvers AVNRT and, 667, 667f bystander, 154–55, 154f
automatic tachycardia with, 32 diagnosis of, 489, 489f atrial cycle length and, 166–68,
AV block during, 227, 227f His bundle potential in, 394–95, 168f
His bundle region location with, 394f, 395f with bystander AV nodal conduc-
271, 271f pathway potentials in, 393–94, tion, 154, 154f
for wide QRS complex tachycardia, 393f, 394f diagnosis of, 109–10, 110f
147–48, 148f preexcitation and, 391–92, 391f with retrograde right and left
palpitations. See also paroxysmal loss of, 399, 399f bundle branch block, 154, 154f
palpitation tachycardia with, 633–34, 633f PCV. See posterior cardiac vein
exercise and, 327, 327f ventricular pacing for, 392, 392f pectinate muscles, 252, 252f
Index 701
CTI ablation and, 512, 512f lateral left ventricle drainage, 265, premature atrial contractions (PAC)
electroanatomic mapping for, 513, 265f for antidromic tachycardia, at dis-
513f posteroseptal (PS) region tal coronary sinus, 153
pericardial eff usions ablation at, 630, 630f automatic tachycardia and, 519,
ICE recognition of, 70f, 71 preexcitation index for, 88f 576, 576f, 585, 585f
intracardiac echocardiography postexcitation, with ventricular pac- for AVNRT, at distal coronary
imaging of, 65 ing, 333 sinus, 153
with oblique sinus, 259, 259f postoperative arrhythmias, 468, 468t circumferential mapping catheter
superior vena cava perforation and, postpacing interval (PPI), 133f, 135 for, 379–80, 379f
253 potassium (K+) channel blockers, 192f, diagnosis of, 287–88, 287f
pericardial reflection, 250 193t ectopic beat in, 381, 381f
pericardial sac, RVOT and, 285, EAD and DAD suppression, 196, EnSite Array noncontact mapping
285f 198f catheter for, 81–82, 81f
pericardial space for reentrant arrhythmias, 198, fusion during placement of, 140
catheter in, 248, 248f 199f intra-atrial activation in, 378–79,
locations of, 249, 249f reverse rate-dependent effect of, 378f, 379f
pericardium 194, 196f for junctional tachycardia diagno-
with heart removed, 254, 254f PPI. See postpacing interval sis, 118–19, 119f
posterior surface of, 249, 249f P-P intervals, in Brugada syndrome, at left inferior pulmonary vein,
peri–sinus node region, tachycardias 343, 343f 377–78, 377f
from, 327f, 328, 328f precaval bundle, 252, 252f in macroreentrant tachycardias,
permanent junctional reciprocating preexcitation. See also antegrade 585, 585f
tachycardia (PJRT), 89, 91f, preexcitation; ventricular with paroxysmal palpitation, 391f,
327f, 328, 328f preexcitation 392
atrial pacing and, 331–32, 331f, during atrial pacing, 220, 220f for pathway potential identifica-
332f atrioventricular block and, 221, tion, 121, 124f
H-A interval during, 404t 221f for preexcited reciprocating
phase 4 diastolic depolarization, diagnosis of, 269, 269f tachycardia, at distal coronary
drugs for, 194, 197f with differential atrial pacing, 353, sinus, 153
phased-array transducer imaging, 65 353f reentrant tachycardia and, 519,
of left and right atrium, 66f in dissociating potentials, 226, 226f 576, 576f
phrenic nerve, 252f, 253 His extrasystoles and, 405f, 406 at RSPV, 379–80, 379f, 382, 382f
PI. See preexcitation index loss of, 223, 223f for VT, at distal coronary sinus,
pinging with PAC, 392 153
for macroreentrant tachycardias paroxysmal palpitation and, in wide QRS complex tachycardia,
ablation, 578 391–92, 391f 85, 110–11, 148, 149f
method of, 578b PVC and, 546–47, 546f, 547f V advancement and antegrade
PJRT. See permanent junctional recip- retrograde His activation and, 399, His advancement with, 150
rocating tachycardia 399f V advancement and QRS mor-
PL. See pathway length in right-sided accessory bypass phology change with, 150
point-to-point mapping tract, 347, 347f V advancement with, 149–50
for automatic tachycardia ablation sinus rhythm with, 393, 393f V and A advancement with,
site, 563, 563f supraventricular tachycardia with, 149
for premature beat origin, 585 449–50, 449f algorithm for, 112f
polysplenia syndrome, 205 preexcitation index (PI), for narrow antegrade His with, 110–11
posterior cardiac vein (PCV) QRS complex tachycardia V and AV node advancement
ablation of, 264, 614 diagnosis, 86–87, 88b, 88f with, 150
cannulation of, 265 preexcited atrial fibrillation, accessory decremental properties of, 111
MCV compared with, 264 pathway ablation for, 21–22, V delay with, 150
posterior mitral annular tachycardia, 22f tachycardia resetting, 111
differential diagnosis of, 595, preexcited reciprocating tachycardia, termination of, 148–49
595f distal coronary sinus PAC ventricular activation sequence,
posterolateral cardiac vein placement for, 153 110
ablation of, 264 preexcited tachycardias ventricular electrograms with,
anatomy of, 264, 264f diagnosis of, 299, 299f 110
cannulation of, 265 Mahaim fiber in, 116 wobble with, 107
702 Index
premature ventricular contractions for intrahisian block, 556, 556f anatomy of, 40, 41f
(PVC) for intrahisian conduction disease, arrhythmogenicity of, 313, 313f
annulus mapping of, 628 655, 655f associative and dissociative
atrial cycle length and, 601, 601f propranolol, for atrial flutter, 468t maneuvers for, 228b
atrial pacing for, 548f, 549 prosthetic closure device atrial flutter and, 477
atrial signal and, 231, 231f atrial flutter around, 469, 469f Carto 3 map of, 78, 78f
in AVNRT, 420, 420b, 420f transseptal puncture with, 275–76, circumferential mapping in, 579,
in dissociating potentials, 227, 227f 366, 366f, 369, 369f, 370t 579f
electrogram of, 229, 229f prosthetic valves, ablation catheter catheter for, 41–42, 42f
fusion during placement of, 140 and, 276, 276f esophagus and, 254, 254f
His bundle potential in, 543–53, proximal ablation catheter (ABL fluoroscopy of, 34–36, 35f
543f, 544f, 545f, 546f, 547f, prox), in typical intracardiac intracardiac echocardiography of,
548f, 549f, 550f, 550t, 551f, electrogram, 8, 8f 65, 67f
552f, 553b proximal coronary sinus (CS p) isolation procedure for, 608t
intermittent, 228–29, 228f activation of, 12–13, 14f junctional rhythm with, 386, 386f
in narrow QRS complex tachycar- distal coronary sinus electrograms left atrium ablation and conduc-
dia diagnosis and, simultaneous, 9, 9f tion block of, 44, 45f
early activation in, 89, 90f, 91f fast pathway activation, 14f multielectrode catheter in, 315,
placement of, 89, 89f, 90t in parahisian pacing, 91, 95f 315f
sensed, 85–86, 87b, 87f proximal high right atrial electro- in pericardium, 249, 249f
timing of, 88–89 gram (HRA prox), 8, 8f potential of, 307t
in pathway potential identification, proximal His bundle (His p), activa- close to ostium, 311, 311f
121, 122f, 123f tion of, 12–13, 14f contamination of, 308t
in RVOT, 229, 229f proximal pairs of electrodes, number- right atrium pacing and, 314, 314f
activation in, 610, 610f ing for, 8 separation from right atrium, 313f,
QRS complex and, 292, 292f PS region. See posteroseptal region 314, 314f
sinus rhythm with right bundle pseudoblock superior vena cava connection of,
branch block and, 239, 239f with atrial flutter at CTI, 497, 497f 232, 232f
antegrade, 230, 230f with CTI ablation, 28, 572, 572f variable output pacing into,
symptomatic monomorphic, Carto pseudoconduction, 389–90, 389f 309–10, 309f, 310f
map of, 77, 78f with CTI ablation, 28, 572, 572f vein of Marshall and, 47–49, 50f,
tachycardia reset with, 405, 405f, pseudointerval, 403, 403f, 406 51t
589, 589f pulmonary arteries pulmonary vein stenosis, 37, 37f
tachycardia termination and, 333, anatomy of, 40, 41f pulmonary vein tachycardia, 562,
333f beginning of, 427, 427f 562f
for unknown potential, 665, 665f bifurcation of, 251, 251f ablation of, not at earliest site of
ventriculoatrial conduction after, intracardiac echocardiography activation, 631t
601, 601f from, 65 atrial fibrillation with, 480, 480f
in wide QRS complex tachycardia, near-field potential from, 237, 237f puncture, of aorta
150–51 pulmonary valve cause of, 364
Ebstein anomaly and, 168–69, beginning of, 427, 427f thrombus formation, 364, 364f
169f circumferential ablation around, PVC. See premature ventricular
wobble with, 107 240 contractions
PR interval hypoplasia, L-TGA with, 206 P wave
in infrahisian conduction disease, myocardial tissue superior to, 234, in atrial flutter, 491–94, 492f, 493f,
341, 341f 234f 494f
in right-sided accessory bypass RVOT isolation at, 52, 243, 243f in atrial tachycardias, 378–79, 378f
tract, 347, 347f, 350, 350f pulmonary vein isolation procedure, with right bundle branch block,
R-P interval identical to, 636f, 637 atrial flutter after, 567, 567f 151–53, 152f
in SVT, 592f, 593 pulmonary vein ostium, circumfer- in automatic tachycardia, 334, 573f,
in wide QRS complex tachycardia, ential mapping catheter at, 36, 574, 597, 597f
139 37f after circumferential ablation, 577
Prinzmetal phenomenon, 269, 269f pulmonary veins crista terminalis and, 574
decremental atrial pacing and, 352t ablation of, for AF, 604 in entrainment mapping
procainamide injection AF ablation, 34, 34f in LA roof, 582–83, 582f
Brugada syndrome after, 339, 339f and isolation of, 313 in left atrial appendage, 581, 581f
Index 703
from left atrium lateral roof, 584, left bundle branch block in, epicardial and endocardial ablation
584f 140–41, 141b for, 262, 262f
fast pathway and, 328 right bundle branch block in, PAC and, 519
in infrahisian conduction disease, 140, 140b at right upper pulmonary vein,
341, 341f QT-prolonging drugs, 197t 245f, 246
in narrow QRS complex tachycar- QwikStar, 79 scenarios for, 129, 129f
dia, 636f, 637 reentry
in PACs, 378–79, 378f RA. See right atrium concealed entrainment, 130, 133f
positivity of, 593, 593f RAO projection. See right anterior definition of, 129–30, 129f
reentrant arrhythmias and, 334, oblique projection incisional, 469f
334f rapid narrow QRS complex tachycar- intrahisian, 553–58, 553f, 554f,
with retrograde fast pathway con- dia, fluoroscopic anatomy for, 555f, 556f, 557f, 558f, 558t
duction, 636 10–11, 10f, 11f, 12t with septal patch–related scar, 469f
in sinus tachycardia, 327f, 328, RBBB. See right bundle branch block transient entrainment, 130
328f RCA. See right coronary artery types of, 130, 130t
stimulus compared with local, Real-time Position Management refractoriness, of cardiac cells,
581–82, 581f, 582f (RPM) System, 82 177–78
in SVT, 592f, 593 rectification, of ion channels, 173, 173f regional wall motion abnormalities,
recurrent atrial fibrillation, Carto ICE recognition of, 70f, 71
QRS complex map of, 77, 78f remnant conduction tissue
accessory pathway and, 296, 296f recurrent orthodromic reciprocating associative and dissociative
of AF with left-sided AP, 300f, 301 tachycardia, 21, 22f maneuvers for, 228b
in arrhythmogenic right ventricu- recurrent pacemaker-mediated in outflow tract, 235, 235f
lar cardiomyopathy, 344–45, tachycardia, accessory pathway repaired CHD
344f, 345f ablation for, 21–22, 22f ablation in
during atrial fibrillation, 295, 295f recurrent tachyarrhythmia, 561–62, approach to, 474, 474f
in Brugada syndrome, 343, 343f 561f concealed entrainment, 484, 484f
bundle branch block and, 296, 296f reentrant arrhythmias, 129–30, heart block with right bundle
far-field–like potential and, 223, 179–81, 180f, 182f, 478f, 479 branch escape, 482f, 483–84,
223f automatic compared with, 563, 484f
and generation of next, 240, 240f 563t transposition of great arteries,
in infrahisian conduction disease, cellular mechanisms of, 199f, 200f 485, 485f
341, 341f circuits for, 564, 564f atrial fibrillation in, 481
with left bundle branch block, 348, drugs for, 196–99, 199f, 200f atrial flutter, 467, 467f
348f electroanatomic mapping for, 370f, atrial fibrillation and, 477
in parahisian pacing, 91, 93f 371, 564, 564f Fontan approach to, 474–75, 474f,
of preexcited tachycardias, 299, maps of, 510, 510f 475f
299f prepotential and, 334, 334f inducement of, 470, 470f
of right-sided accessory bypass TOF surgical correction and, 486, mapping of, 472–73, 472f
tract, 347, 347f 486f mechanisms of, 468b, 469
RVOT PVC and, 292, 292f reentrant circuit medication efficacy for, 468, 468t
of VT, 296, 296f arrhythmia origin in, 470 prevention and treatment of, 474,
at mitral annulus, 300, 300f CL of, 470 474f
in wide QRS complex tachycardia, PL of, 129, 129f pulmonary veins and, 477
152, 297, 297t–298t WL of, 129, 129f scars and, 469, 469f
QRS complex tachycardia. See narrow reentrant tachycardia, 561–62, 561f cavotricuspid isthmus ablation,
QRS complex tachycardia; ablation of, 451–54, 451f, 452f, 453f, 472, 472b
wide QRS complex tachycardia 454b, 454f, 566, 566f electroanatomic mapping for, 470,
QRS morphologies not at earliest site of activation, 470f
atrial cycle length and, 166, 168f 631t analysis of, 470–71
with isoproterenol, 236, 236f site for, 574, 574f of scars, 473–74, 473f
SVT and, 142 atrial pacing and, 331, 331f junctional tachycardia with, 479,
of wide QRS complex tachycardia, automatic compared with, 490, 479f
140–41 490f pulmonary vein tachycardia, 480,
Ebstein anomaly and, 168–69, automatic ventricular tachycardia 480f
169f compared with, 450t reentrant arrhythmia, 478f, 479
704 Index
repaired CHD (Cont.) differential diagnosis for, 651, 651f use dependence compared with,
surgical procedures and arrhyth- distal-to-proximal, 142f, 143 196t
mias, 468, 468t in paroxysmal palpitation, 395, reverse transseptal approach, 61–62
tachypalpitations with, 467, 467f 395f, 395t, 398–99, 398f, 399f right anterior oblique (RAO)
repolarization, antiarrhythmic block proximal-to-distal, 145, 145f projection
during, 193, 194f in sinus tachycardia, 329, 329f anatomic landmarks in, 5–7, 7f
resetting of tachycardia, 86, 87f tachycardia reset and, 405, 405f annulus in, 5
respiration, catheter position and, 40, in wide QRS complex tachycardia, of Carto map, during monomor-
40f 143–45, 144f, 145f phic ventricular tachycardia,
retrograde accessory pathway, decre- retrograde His bundle deflection 77, 77f
mental pacing for, 103–4, 105f for narrow QRS complex tachycar- of CartoSound map, 79, 79f
retrograde aortic approach, 61–62 dia diagnosis, 86–88 catheter location and, 3, 4f, 5, 6f,
retrograde atrial activation sequence with ventricular pacing, 16, 16f 7–8, 7f
of atypical AVNRT, 640, 640f retrograde left bundle branch block cavotricuspid isthmus location on,
in junctional rhythm, 639, 639f pathway-to-pathway tachycardia 28
retrograde atrioventricular nodal with, 154, 154f of circumferential mapping
conduction, 330, 330f, 335, 358, tachycardia and V-H interval, 161, catheter
358f 162f in LSPV and LIPV, 38–39, 38f
atrial activation sequence and, 294 retrograde pulmonary venography, of in RSPV, 37, 37f
decremental pacing for, 103–4, 105f right inferior vein, 41, 42f for CTI ablation, 30, 31f
parahisian pacing and, 646, 646f retrograde right bundle branch on fluoroscopy, 4–5, 6f
in retrograde right bundle branch block of heart, 6f
block induction, 95, 97, 99f, antegrade right bundle branch for left atrial appendage tachycar-
100t block with, 656, 656f dia, 605, 605f
during ventricular pacing, 13, 15, antegrade conducting accessory of LSPV and left atrial appendage,
15f pathway with, 658, 658f 45f, 46, 46t
retrograde bundle branch block, 535 antidromic tachycardia with, 154, of middle cardiac vein catheter
retrograde bystander accessory path- 154f location, 17, 19f
way, antidromic tachycardia His bundle activation and, 329, clockwise torque and, 20, 20f
with, 154, 154f 329f counterclockwise torque and,
retrograde conducting accessory induction of, 95, 98f 18–20, 19f
pathway atrial activation delay with, 97, of outflow tract ventricular tachy-
in parahisian pacing, 92, 96f, 97b 99f cardias, 54–55, 56f
in paroxysmal palpitation, 401, coronary sinus activation, 97, 99f profi le view with, 4, 5f
401f parahisian pacing compared right atrial activation map, 81–82, 81f
retrograde conduction with, 97, 100t right atrial automatic tachycardia,
AVN and, 330, 330f, 335, 358, 358f V-A interval in, 97 mapping and ablation of, 22
left-sided accessory pathway and, pathway-to-pathway tachycardia right atrium (RA)
408, 408f with, 154, 154f activation of
with retrograde right bundle retrograde conduction with, 162, during atrial flutter, 29, 29f
branch block, 162, 163f, 408 163f, 408 left atrium and, 597, 597f
ventricular extrastimulus and, 356, in sinus tachycardia, 329, 329f atrial pacing
356f during ventricular pacing, 162–63, pulmonary vein potentials and,
retrograde fast pathway conduction 164f 314, 314f
earliest activation during, 12 ventricular tachycardia VT with, for wide QRS complex tachycar-
exits of, 638 distal, 303 dia from, 155, 157f
mapping of, 622 V-H interval with, 162, 163f, 164f atrial tachycardia at, 245f, 246
P waves with, 636 in wide QRS complex tachycar- automatic tachycardia from,
retrograde His bundle activation dia, 159, 161f 561–62, 561f
accessory pathways and, 400, 400f retrograde transaortic approach, 59, Carto map of, during inappropri-
antegrade compared with, 156, 60f ate sinus tachycardia, 77, 77f
158f retrograde V-A Wenckebach, 622, CartoSound map of, 79, 79f
associative and dissociative 622f on chest radiograph, 4, 5f
maneuvers for, 228b reverse rate-dependent effect decremental pacing from, 114,
decremental atrial pacing and, 400, of potassium channel blockers, 117f
400f 194, 196f ICE probe in, 366, 366f, 610, 610f
Index 705
intracardiac echocardiography location of, 40, 41f anterior surface of, 248, 248f
and, 65, 66f, 67f, 68f retrograde pulmonary venography Carto map of, during monomor-
isolation procedure at, 233, 233f of, 41, 42f phic ventricular tachycardia,
macroreentrant tachycardias in, right interventricular septal position, 77, 77f
566f, 567 17, 19f CartoSound map of, 79, 79f
mechanical rotational ultrasound right midseptal accessory pathway, dysplasia, RVOT tachycardia with,
of, 66f 596t 444–45, 444f, 445b, 445t
normal position in chest, 4, 5f right pulmonary artery (RPA) in fast pathway activation, 14f
phased-array transducer imaging intracardiac echocardiography of, intracardiac echocardiography
of, 66f 65, 67f and, 65, 66f, 67f, 69f
pulmonary vein separation from, in univentricular AV connection, in LAO, 6f
313f, 314, 314f 372, 372f normal position in chest, 4, 5f
RAO projection of, 6f, 319, 319f right-sided accessory bypass tract RAO projection of, 6f, 319, 319f
right bundle branch block (RBBB). decremental atrial pacing and, 350, ventricular pacing from
See also antegrade right bundle 350f, 351t–352t importance of, 18t
branch block; retrograde right diagnosis of, 347, 347f for supraventricular tachycardia,
bundle branch block H-V interval in, 349, 349f 15–17, 16f
in arrhythmogenic right ventricu- right-sided accessory pathway right ventricular apex
lar cardiomyopathy, 345, 345f atrial pacing with, 22–23, 23f normal position in chest, 4, 5f
atrial tachycardia with, 151–53, mapping and ablation of, 22 ventricular pacing from, 105–6,
152f ORT with, 287–88, 287f, 290, 290f 106f, 107f
proximal, 302f, 303 with paroxysmal palpitation, 391f, differential pacing, 238, 238f
in Brugada syndrome, 338f, 339, 392 importance of, 18t
339f right-sided fascicle-related tachyar- in narrow QRS complex tachy-
in infrahisian conduction disease, rhythmia, 58–59, 58f cardia diagnosis, 88, 88f
341, 341f right superior fascicles, 433–34, 433f near-field and far-field potentials,
in mitral isthmus ventricular right superior pulmonary vein 238, 238f
tachycardia, 461, 461f (RSPV) for supraventricular tachycardia,
sinus rhythm with, 239, 239f activation of, 598, 598f 15–17, 16f
for supraventricular tachycardia, His bundle activation and, 602–3 right ventricular base, ventricular
17, 17f, 18t anatomy of, 35 pacing from, 357, 357f
ventricular activation and, 137, atrial pacing in, 383, 383f right ventricular outflow tract
138f atrial tachycardia of, 596t (RVOT)
ventricular pacing at apex with, circumferential ablation of, 384f, ablation of, catheter position for,
642, 642f 385, 606 50–51, 53f, 279, 284, 284f
in wide QRS complex tachycardia, circumferential mapping of, 36–37, anterior surface of, 248, 248f
140, 140b 37f aortic valve and, 54, 55f
right bundle branch escape, heart depth of, 43, 43f ending of, 427, 427f
block with, 482f, 483–84, 484f on fluoroscopy, 44, 45f energy delivery in, 284, 284f
right bundle ectopy, PVC and, 546, fluoroscopy and electrogram cor- fluoroscopy and electrogram cor-
546f, 549, 551–53, 551f, 552f, relation to, 51t relation for, 50–52, 53f
553b intracardiac echocardiography of, intracardiac echocardiography
right coronary artery (RCA) 65, 67f, 68f imaging of, 65, 66f, 67f, 71,
ablation injury to, 10, 10f location of, 40, 41f 72f
catheter, placement on annulus, PAC at, 379–80, 379f, 382, 382f isolation of, 243, 243f
222, 222f paravenous pacing of, 383–84, LVOT and, 54, 55f
mapping of tricuspid annulus and, 383f, 384f mapping and anatomy of, 426–30,
221 reentrant tachycardia at, 245f, 246 426f, 427f, 428f, 429f, 430f, 437,
RVOT and, 53 superior vena cava muscle connec- 437f, 439–40, 439f, 440f, 443,
right heterotaxy. See asplenia tion to, 383, 383f, 585 443f
syndrome tachycardia origins in, 520–21, pericardial sac and, 285, 285f
right inferior pulmonary vein (RIPV) 520f, 521f pulmonary valve, 52
fluoroscopy and electrogram cor- right ventricle (RV) PVC in, 229, 229f, 542–44, 542f,
relation to, 51t accessory pathway ablation near, 543f, 544f
intracardiac echocardiography of, 219–20, 219f activation in, 610, 610f
65, 67f activation of, VT and, 137, 138f QRS complex and, 292, 292f
706 Index
right ventricular outflow tract reentry, 469f 2:1 AV block in, 601
tachycardia septum. See also interatrial septum; sinus tachycardia
difficulty ablating, 423–36, 423f, intraventricular septum differential diagnosis of, 592–93,
424b, 424f, 425f, 426f, 427f, catheter localization on, 7–8, 7f 592f
428f, 429f, 430f, 431f, 432f, His bundle catheter and, 35 exclusion of, 327–28, 327f, 328f
433f, 434f, 435f, 446, 446t in LAO projection and, 5–6, 7f inappropriate, Carto map of, 77,
epicardial origin in, 442–43, 442f, His bundle penetration of, 283, 77f
443f 283f retrograde His bundle potential,
with RV dysplasia, 444–45, 444f, in LAO projections, 5, 6f 329, 329f
445b, 445t VT origination within, 632, 632f situs inversus, cc-TGA with, 206
right ventricular recording catheter short QT syndrome, 182, 183t, 184f slow pathway, 319, 319f
(RV prox), 8f, 9 sick sinus syndrome, 186 ablation catheter in, 24, 26f
right ventricular tachycardia Singh Vaughan Williams classifica- ablation of, 648, 648f
electroanatomic map of, 57, 57f tion system, 191, 192f, 193t anatomy of, 320, 320f
fluoroscopy and electrogram cor- single-ventricle patients delineation of, 676
relation for, 57, 57f AV node and His bundle in, 206 fast pathway activation propaga-
with left bundle branch block, 141, with Fontan palliation, 207–9 tion to, 320–21, 320f, 321f
141b atrial tachycardia ablation after, linear ablation of, 639, 639f
RIPV. See right inferior pulmonary 209, 210t location of, 12, 13f
vein clinical anatomy for, 208–9 wavefront propagation to AVN,
RPA. See right pulmonary artery common arrhythmias and 320, 320f
R-P interval arrhythmogenic substrate, slow pathway lesions, location of, 12
of narrow QRS complex tachycar- 207–8 sodium/calcium (Na+/Ca 2+) exchange,
dia, 643, 643f Fontan connection anatomy, 207, 175
PR interval identical to, 636f, 637 208t, 209f sodium (Na+) channel blockers,
in sinus tachycardia, 327f, 328, 328f sinus arrhythmia, in Brugada syn- 191–92, 192f, 193t
in tachycardias, 407 drome, 343, 343f antiarrhythmics and, 192, 193f,
RPM System. See Real-time Position sinus node 193t
Management System action potential waveform of, 176, capture latency and, 338
RSPV. See right superior pulmonary 178f kinetics of recovery from, 193,
vein automaticity in, 179 195f
RV. See right ventricle in CHD, 205 for reentrant arrhythmias, 198–99,
RVOT. See right ventricular outflow dysfunction of, 183t, 186 199f, 200f
tract with CHD, 204, 204t use-dependent, 193, 195f
RV prox. See right ventricular record- juxtaposition of, 205 sodium ion currents (INa), 173–74
ing catheter modification of, crista terminalis– sodium/potassium (Na+/K+) pump,
ryanodine receptors, 176 related catheter for, 27 175
sinus rhythm S-P interval, 135
scar-related atrial flutter, 469, 469f with antegrade right bundle spiral waves, 130t
crista terminalis–related catheter branch block, 230, 230f split potentials, with ablation of CTI,
for, 27 atrial activation sequence during, 502, 502f
mapping and ablation of, 22 9, 9f S-QRS interval, 133f, 135
scar-related tachycardia, 307t with bundle branch block, 233, 233f ST elevation, in Brugada syndrome,
secundum atrioseptal defect, postop- fasciculoventricular tract in, 115, 338f, 339–40
erative arrhythmias, 468t 118f, 269, 269f strong inward rectifier potassium ion
semilunar valve, fluoroscopy and junctional rhythm competing with, currents (IK1), 175
electrogram correlation for, 591–92, 591f subeustachian pouch
52–54, 54f in left atrial appendage tachycar- ablation catheter in, 24, 26f
Senning repair, postoperative dia, 604, 604f atrial flutter ablation and, 511, 511f
arrhythmias, 468t with left atrial appendage tachycar- mapping of, 25–26, 27f
Sensei X Robotic Catheter System, dia, 606–7, 606f, 607f location in heart, 24, 26f
82–83 with preexcitation, 393, 393f subunits, of ion channels, 176
septal malalignment, L-TGA with, with right bundle branch block, subxiphoid pericardial approach, 253,
206 239, 239f 253f
septal patch–related scar right-sided accessory bypass tract for annular automatic tachycardia,
atrial flutter and, 469 and, 349, 349f 264
Index 707
for left-sided epicardial accessory differential diagnosis for, 449–51, diagnostic maneuvers during,
pathway ablation, 305–7, 305f, 449f 85–86, 86b
306f electrical isolation for, 614, 614f decremental pacing, 103–4, 105f
sudden cardiac death, in CHD, 204, fluoroscopic anatomy for, 10, 25t differential pacing, 104–6, 106f,
204t fluoroscopy and electrogram cor- 107f
sudden-onset, sudden-offset palpita- relations for, 10–25, 25t junctional tachycardia, 118–20,
tions, 317f, 318, 318f with left bundle branch block, 119f, 120b, 120f
sudden unexplained death syndrome, 140–41, 141b Morady maneuver, 97–103
340, 340f medication-resistant, 287, 287f for narrow QRS complex tachy-
superior cavopulmonary anastomosis, with paroxysmal narrow QRS cardia, 86–90
208t complex tachycardia, 649, 649f parahisian pacing, 90–95
superior vena cava (SVC) PR prolongation and, 139, 592f, 593 pathway potentials, 121, 121b,
anatomy of, 364, 364f QRS morphologies and, 142 122f, 123f, 124f, 125f, 125t
anomalous pulmonary vein con- with right bundle branch block, pathway-related, 120–21
nection to, 232, 232f 140, 140b pathway slant, 121–27, 126b, 126f,
aorta and, 251, 251f ventricular pacing during, 15–17, 127f
atrial fibrillation 16f, 97 retrograde right bundle branch
circumferential mapping from, ablation, 25t block induction, 95, 97, 98f
46, 48f, 49f algorithm for, 103, 104f for wide QRS complex tachycar-
potential of, 588, 588f SVC. See superior vena cava dia, 108–18
atrial tachycardia of, atrial pacing S-V interval, in wide QRS complex wobble, 106–8, 108f, 109t
and, 586, 586f tachycardia entrainment mapping for, 566
automatic tachycardia of, 587, with preexcitation, 155, 157f with isoproterenol, 236, 236f, 595,
587f from right atrium, 155, 157f 595f
circumferential mapping catheter SVT. See supraventricular tachycardia LIPV origins of, 574
in, 232, 232f S wave mapping sequence for, 30, 32f
fluoroscopy and electrogram cor- in arrhythmogenic right ventricu- near-field potential and termina-
relation to, 51t lar cardiomyopathy, 345, 345f tion of, 239, 239f, 241, 241f
isolation procedure for, 233, 233f, in Brugada syndrome, 343, 343f with paroxysmal palpitation,
609t in infrahisian conduction disease, 633–34, 633f
medial perforation of, 251 341, 341f resetting of, 86–87, 87f
nerves associated with, 252f, 253 symptomatic monomorphic prema- with PAC placement during wide
PAC in, 585 ture ventricular contractions, QRS complex tachycardia, 111
pericardial eff usions and perfora- Carto map of, 77, 78f with PVC, 405, 405f, 589, 589f
tion of, 253 syncope, in infrahisian conduction retrograde His bundle activation
in pericardium, 249, 249f disease, 341, 341f and, 405, 405f
RSVP muscle connection to, 383, syncytial myocardium, 613, 613f R-P interval in, 407
383f, 585 RSPV origins of, 520–21, 520f, 521f
transseptal needle in, 369, 369f tachyarrhythmia termination of, 621, 621f
in univentricular AV connection, after ablation of AF, 576 V-A interval of, 411–14, 411f,
372, 372f recurrent, 561–62, 561f 412t–413t, 414f
vein of Marshall and, 574 tachycardia. See also specific tachypalpitations
ventricular electrogram on HRA tachycardias exercise-related, epicardial ablation
and, 6f, 8f, 9 ablation of, 246 for, 260–61, 260f
supra-aortic valvar focus, of ventricu- atrial extrastimulus testing and, with tricuspid atresia, 467, 467f
lar fibrillation, 281, 281f 598f, 599 tendon of Todaro (TT)
supravalvar aortic tachycardia, abla- after atrial fibrillation ablation, catheter location behind, 12, 13f,
tion of, not at earliest site of 562, 562f 622
activation, 631t atrial pacing and initiation of, 331, fast pathway lesions behind, 12
supravalvar muscle tissue potentials, 331f slow pathway lesions in front of, 12
associative and dissociative atrial potential and termination of, tenting, during transseptal puncture,
maneuvers for, 228b 333, 333f 366, 366f
supraventricular tachycardia (SVT) automatic, 308t tetralogy of Fallot (TOF)
during ablation of CTI, 518, 518f cycle length variation in, 241, 241f anatomy of, 213
in atrial pacing, 331 electroanatomic mapping of, 473, arrhythmias and arrhythmogenic
contrast injection for, 275, 275f 473f substrates with, 213
708 Index
tetralogy of Fallot (TOF) (Cont.) transverse pericardial sinus, 247, 247f with atypical manifestation, 637,
AV node and His bundle in, 205 ablation catheter at, 33, 34f, 256, 637f
clinical anatomy for, 213 256f compared with atypical, 13, 14f
IART with, 203–4 anatomic relationships of, 249, diagnosis of, 30–32, 32f, 620, 620f,
surgical correction of, 213 249f 636, 636f
atrial flutter after, 485 Bachmann bundle region in, echo beats, junctional escape beats
postoperative arrhythmias, 468t 249–50 and, 640, 640f
reentrant arrhythmias, 486, 486f catheter entry into, 250–51, 251f H-A interval during, 404t
VT with, 204, 486–87, 487b in heart dissection, 250, 250f junctional tachycardia differentia-
thebesian vein tricuspid annulus tion from, 119, 120t
catheter placement in, 274, 274f anatomy of, 364, 364f paroxysmal narrow QRS complex
contrast injection in, 274, 274f fluoroscopy and electrogram cor- tachycardia electrograms and,
threshold potential of AP upstroke, relation for, 25t 13, 14f
drugs for, 194, 197f Mahaim fibers along, 627, 627f with paroxysmal palpitation, 633f,
thrombogenic stroke, 369, 369f Mahaim-like potentials on, 113, 634
thrombus. See intracardiac thrombus 115f sinus tachycardia differentiation
tissue temperature, tip temperature mapping of, 221, 221f, 624, 624f from, 328
and, 257, 257f, 362, 362f multielectrode catheter placement V-A interval of, 411–12, 411f, 412t,
tissue vaporization, microbubbles along, 22 414, 414f
and, 362 in supraventricular tachycardia
TOF. See tetralogy of Fallot ablation, 25t ultrasound-based catheter localiza-
tonic block, 193, 194f tricuspid atresia tion, 82
torsades de pointes, 197t AV node and His bundle in, 206 univentricular AV connection, 372,
transient entrainment hemodynamic catheterization for, 372f
criteria for, 130, 130b, 131f–132f 468 unknown potential, 664–66, 664f,
definition of, 130 tachypalpitations with, 467, 467f 665f
transient hypotension, ICE recogni- tricuspid valve upper common pathway block, 417,
tion of, 70f, 71 ablation from, 61 422
transient outward potassium ion cur- ICE positioning through, 71, 72f use-dependent block, 193, 194f
rents (Ito), 174 tricuspid valve procedure, postopera- of Na+ channel blockers, 193–94,
transseptal catheterization tive arrhythmias, 468t 195f
complications of, 367b triggered activity, arrhythmias and, reverse use dependent compared
for exercise-related VT, 58, 58f 179, 180f with, 196t
with ICE, 68–70, 70f drugs for, 196, 197t, 198f
for left-sided epicardial accessory TT. See tendon of Todaro VA block
pathway ablation, 305–7, 305f, T-type calcium ion currents (ICa,T), in pathway potential identification,
306f 174 121, 124f
transseptal puncture T-wave inversion in sinus tachycardia, 329, 329f
of aorta in arrhythmogenic right ventricu- V-A-H-V pattern, in Morady maneu-
anatomy for, 364, 364f lar cardiomyopathy, 345, 345f ver, 100, 102f
bubbles in, 363, 363f in Brugada syndrome, 338f, V-A interval. See ventriculoatrial
thrombus formation, 364, 364f 339–40, 343, 343f interval
atrial cardinal veins and, 677–78, 2:1 AV block variable output pacing, of atrial fibril-
677f, 678f AVNRT with, 418–21, 418f, 419f, lation, 309–10, 309f, 310f
attempt of, 365, 365f 420b, 420f, 421f V-A-V pattern
difficult situations for, 370t in sinus rhythm, 601 in Morady maneuver, 100, 102f,
efficient sheath management for, 2-for-1 phenomenon, in AVNRT, 524 103f
367, 367b typical atrial flutter in wide QRS complex tachycardia,
fossa ovalis and, 364, 364f ablation of, 22, 490f, 491 151
ICE for, 365–66, 366f mapping of, 22 vein of Marshall, 250
incorrect location of, 367, 367f systems for, 508, 508f ablation at, 267, 267f, 574
with prosthetic closure device, typical AV bypass tract, decremental for AF, 268, 268f
275–76, 366, 366f, 369, 369f, atrial pacing and, 351t for paroxysmal atrial fibrillation,
370t typical AVNRT, 317f, 318, 318f 46–47, 49f
superior vena cava and, 369, 369f ablation of, not at earliest site of atrial potentials in, 308
tenting during, 366, 366f activation, 631t electrically active conduction, 596t
Index 709
fluoroscopy and electrogram cor- ventricular base. See also right ven- differential pacing
relation to, 51t tricular base from right ventricular apex,
isolation procedure for, 609t differential ventricular pacing 105–6, 106f, 107f
left atrium and, 47–49, 50f, 51t from, 106, 106f, 107f from ventricular base, 106, 106f,
left superior vena cava and, 311, ventricular pacing at, 642, 642f 107f
311f for narrow QRS complex tachy- earliest activation during, 12
pulmonary veins and, 47–49, 50f, cardia, 88, 89f fast pathway in, 319
51t ventricular electrograms fluoroscopy and electrogram cor-
activation and, 315, 315f coronary sinus mapping catheter relation for, 25t
SVC and, 574 and, 6–7, 7f H-A interval during, 403–4, 403f
vein of Marshall ostium on high right atrial catheter, left bundle branch block tachycar-
isolation at, 574, 574f 8f, 9 dia initiation during, 165, 166f
mapping of, 679, 679f with PAC placement during wide location for, 15
venoluminal vessel, catheter place- QRS complex tachycardia, 110 importance of, 18t
ment in, 274, 274f ventricular extrastimulation, 337–38, at midseptum, 642, 642f
venous anatomy, 264, 264f 337f, 408, 408f in Morady maneuver, speed of,
venous anomalies, with CHD, 213 retrograde conduction and, 356, 100, 103
interrupted IVC, 214 356f in narrow QRS complex tachycar-
persistent LSVC, 213–14 V-A interval with, 356, 356f dia diagnosis
venous system, 11, 11f ventricular fibrillation at apex, 88, 88f
ablation of, 264 with Brugada syndrome, 340 at base, 88, 89f
anatomy of, 264, 264f electroanatomic mapping for, 76 for orthodromic reciprocating
infradiaphragmatic mapping of, epicardial ablation of, 278–79 tachycardia, 98, 101f
273, 273f junctional tachycardia leading to, for paroxysmal palpitation, 392,
LVOT and, 280, 280f 540–42, 540f, 541f, 542f 392f
ventricle. See also left ventricle; right supra-aortic valvar focus of, 281, in pathway potential analysis
ventricle 281f coronary sinus activation during,
catheter localization on, 7, 7f ventricular arrhythmias and, 338 121, 123f
coronary sinus mapping catheter during ventricular extrastimula- sensed, 121, 122f, 123f
in RAO projection and, 5–6, tion, 337–38, 337f postexcitation with, 333
7f ventricular looping, 206 retrograde AV nodal conduction
ventricular activation sequence ventricular myocardium during, 13, 15, 15f
accessory pathway and, 137, 138f, ablation of, ICE of, 362 retrograde right bundle branch
294 in parahisian pacing, 330 block during, 162–63, 164f
with PAC placement during wide ventricular myocytes, action potential from right ventricular apex, 238, 238f
QRS complex tachycardia, 110 waveform of, 177, 178f V-A interval with, 357, 357f
pathway slant of, 122–24 ventricular pacing. See also decre- from right ventricular base, V-A
with right and left stimulation, 137, mental ventricular pacing; interval with, 357, 357f
138f differential ventricular pacing for supraventricular tachycardia,
right bundle branch block and, 137, for AF, 530, 530f, 533–35, 533f, 15–17, 16f, 97
138f 534f ablation, 25t
in right-sided accessory bypass at apex, 642, 642f algorithm for, 103, 104f
tract, 349, 349f with RBBB, 642, 642f typical AVNRT and, 636, 636f
VT and, 137, 138f atrial activation sequence during, in VT, 455–59, 455b, 455f, 456f,
ventricular apex 622, 622f 457f, 458f
position and orientation of, 62f, atrial pacing and ventricular potential
63, 63f AV nodal conduction and, 329, ablation catheter for, 224, 224f
ventricular pacing at, 642, 642f 329f accessory pathway and, 220, 220f
for narrow QRS complex tachy- in pathway potential analysis, atrial potential overlap with, 222, 222f
cardia, 88, 88f 121, 122f, 123f in coronary sinus, 393, 393f
with RBBB, 642, 642f for wide QRS complex tachycar- fascicular potentials and, 406–7
ventricular arrhythmias dia diagnosis, 111–12 fragmented, 228–29, 228f
EnSite Array noncontact mapping for atypical AVNRT, 647, 647f His bundle potential and, 641–42,
catheter for, 81 at base, 642, 642f 641f, 642f
ventricular fibrillation and, 338 at coronary sinus, 674–75, 674f from left ventricle, 228–29, 228f
ventricular tachycardia and, 338 CS activation and, 333 near-field potential and, 242, 242f
710 Index
ventricular preexcitation, atrial with surgically corrected TOF, 204, V-H interval
potential and, 271f, 272 213 of ART initiation with left-sided
ventricular septal defect (VSD), AV ventricular activation and, 137, accessory pathway, 165, 166f
node and His bundle in, 205 138f with atrial fascicular pathways,
ventricular signals, detection of two, ventricular and atrial electrograms 158f, 159
223, 223f in, 142 of atrial pacing at CL of tachycar-
ventricular tachycardia (VT) ventricular arrhythmias and, 338 dia, 159, 160f
ablation of, 451, 451f, 454b, 460, during ventricular extrastimula- in differential pacing, 106, 106f
460f tion, 337–38, 337f with retrograde right bundle
automatic tachycardia, 451, 451f, wide QRS complex tachycardia branch block, 162, 163f, 164f
454, 454b and, 111–12, 112f, 113f, 139t with right bundle branch block, 17,
difficulty with, 462–65, 462f, ventricular tachycardia ablation 17f, 18t
463f, 464f, 465f concealed entrainment and, 133 tachycardia and
electroanatomic mapping, 459, fluoroscopic and electrogram cor- cycle length and, 159, 161, 162f,
459f relations for, 49–59 165
entrainment mapping, 455–59, ICE–assisted, 71, 73f retrograde left bundle branch
455b, 455f, 456f, 457f, 458f ventriculoatrial conduction, after block and, 161, 162f
mitral isthmus ventricular tachy- PVC, 601, 601f in ventricular pacing at His
cardia, 449f, 451, 461, 461f ventriculoatrial (V-A) interval, 550t bundle, 16–17, 16f
reentrant tachycardia, 451–54, in AF, 533–34, 533f, 534f in wide QRS complex tachycardia,
451f, 452f, 453f, 454b, 454f with atrial fascicular pathways, 147, 157, 158f
scar tissue and, 465, 465f 158f, 159 change in, 159, 161f
AF with, 530, 530f in atrial tachycardia with right Ebstein anomaly and, 168–69, 169f
annulus mapping of, 628 bundle branch block, 152–53, long, 159, 160f
in CHD, 204, 204t 152f voltage, in electroanatomic
cycle length of, 240, 240f A-V interval and, 638, 638f mapping, 75
differential diagnosis for, 449–51, in differential pacing, 106, 106f voltage-gated Ca 2+ channels, 171, 172f
449f, 450t H-A interval compared with, 400 voltage-gated K+ channels, 171, 172f
distal coronary sinus PAC place- in Mahaim fiber–related antidro- voltage-gated Na+ channels, 171, 172f
ment for, 153 mic tachycardia, 407f, 408 VSD. See ventricular septal defect
ECG and, 139 of narrow QRS complex tachycar- VT. See ventricular tachycardia
EG-QRS interval for, 135 dia, 633–34, 633f V-V interval
electroanatomic mapping for, 76 during ORT with antegrade left A-A interval and, 638, 638f
epicardial ablation for, 262, 262f bundle branch block, 161, in wide QRS complex tachycardia,
epicardial arrhythmogenic sub- 163f 146
strate for, 632–33, 632f in parahisian pacing, 91,
exercise-related, electrogram of, 57, 358, 358f wavelength (WL)
58f, 233, 233f with retrograde right bundle in different reentrant models, 130t
fast pathway in, 319 branch block, 162, 163f of reentrant circuit, 129, 129f
fusion beats and, 139–40 in tachycardia, 620, 620f wide-area circumferential ablation,
within interventricular septum, with very short, 411–14, 411f, atrial fibrillation with, 43, 44f
632, 632f 412t–413t, 414f wide complex beats, intermittent,
with left bundle branch block, 141, in typical AVNRT, 620, 620f 543–49, 543f, 544f, 545f, 546f,
141b, 142f with ventricular extrastimulation, 547f, 548f, 549f, 550f, 550t,
in left main coronary artery, 282, 356, 356f 551–53, 551f, 552f, 553b
282f with ventricular pacing wide QRS complex tachycardia, 137
mitral annulus and, 300, 300f from right ventricular apex, 357, A-A interval in, 146
at moderator band, 632, 632f 357f A-H interval in, 143, 146
monomorphic, Carto map of, 77, from right ventricular base, 357, changes in, 156, 158f
77f 357f relative fi xity of, 145
QRS complex of, 296, 296f in wide QRS complex tachycardia, with antegrade conducting acces-
readily ablatable, difficulty ablat- 157–59, 158f sory pathway, 154–55, 154f
ing, 446, 446t ventriculophasic arrhythmia, 601, approach to, 142
with retrograde right bundle 601f atrial pacing for
branch block, distal, 303 vertebral column, on fluoroscopy, 5, from anterolateral right atrium,
S-QRS interval for, 133f, 135 6f 155, 157f
Index 711
at cycle length, 159, 160f ECG and monitoring data for, premature ventricular contractions
with cycle length decreases, 156, 138–40 during, 150–51
158f H-A interval in, 143, 146, 157–59, QRS complex in, 152, 297,
with multielectrode catheter, 158f 297t–298t
156, 158f H-H interval in, 146 QRS morphologies of, 140–41
with preexcitation, 155, 157f H-V interval in, 143, 146–47 retrograde His bundle activation
atrioventricular relationship to, intracardiac intervals, 143 in, 143–45, 144f, 145f
142–43 left bundle branch block in, right bundle branch block in, 140,
catheter placement and recording 140–41, 141b 140b
of, 142 Morady maneuver for, 151 V-A interval in, 157–59, 158f
causes of, 109, 109b, 137, 138f, 139t morphology of, 138f, 140–41, 140b, V-A-V pattern in, 151
clinical features of, 137–38 141b, 141f, 142f V-H interval of, 147, 157, 158f
diagnostic maneuvers for, 108–18 pacing maneuvers for, 147–48, 148f change in, 159, 161f
accessory pathway in, 109–10, palpitations with, 151–53, 152f cycle length of, 159, 161, 162f,
110f paroxysmal palpitation, 299, 299f 165
atrial pacing for, 111–13, 112b, precordial QRS concordance, long, 159, 160f
113f, 114f, 115f 141–42 retrograde left bundle branch
decremental atrial pacing for, premature atrial contractions dur- block and, 161, 162f
114–18, 115t, 116f, 117f, 118f, ing, 85, 148, 149f V-V interval in, 146
147–48, 148f V advancement and antegrade with Wolff-Parkinson-White syn-
goals for, 109 His advancement with, 150 drome, 153, 154f
incremental atrial pacing, V advancement and QRS mor- WL. See wavelength
147–48, 148f phology change with, 150 wobble, 106–8
PACs placed during, 110–11, V advancement with, 149–50 analyzing, 107–8, 108f
112f V and A advancement with, 149 for junctional tachycardia diagno-
differential diagnosis for, 449–51, V and AV node advancement sis, 118
449f, 450t with, 150 Wolff-Parkinson-White syndrome
driver of, 145–47 V delay with, 150 electrocardiogram with, 219, 219f
Ebstein anomaly and, 168–69, 169f termination of, 148–49 tachycardias with, 153, 154f

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MAYO CLINIC SCIENTIFIC PRESS OXFORD UNIVERSITY PRESS

Oxford New York

Copyright ©2014 by Mayo Foundation for Medical Education and Research.

Published by Oxford University Press, Inc.

Oxford is a registered trademark of Oxford University Press

Library of Congress Cataloging-in-Publication Data

Samuel J. Asirvatham, MD Dorothy J. Ladewig

INTRODUCTION This fluoroscopic image is from the RAO projection (ver-

What does the electrophysiologist performing complex

Figure 1.9 Typical intracardiac electrogram obtained during a sinus beat.

Figure 1.10 Complex electrograms on the coronary sinus catheter (arrows).

sinus (CS 11,12). Th is fi nding strongly suggests that the ear-

FLUOROSCOPIC ANATOMY RELEVANT

the coronary veins or with high energy along the annulus

HRA His His p

an alternate location is necessary occasionally. In fact, the

Figure 1.22 Right anterior oblique view with catheters placed

(see below). This concept of the ventricular pacing site affect-

Figure 1.32 A diverticulum occurring between the middle cardiac

the EP laboratory for EP study and radiofrequency abla-

No connection with atrium

Conduction via rapidly

The posterior orientation of the multielectrode mapping Fossa ovalis

on both sides of the septum) is needed to defi ne which

intracardiac ultrasound) (see Chapter 2) placed also in the

Figure 1.62 Intracardiac ultrasound image obtained

(perforation occurs if undue pressure is applied). The cath-

2. On the endocardial surface at the same location

the circumflex coronary artery or one of its branches. The

FLUOROSCOPIC ANATOMY AND

The catheter positioning in the RAO and LAO views for a

infarction and the mitral annulus (mitral isthmus ventricu-

artery. This region of the heart may be considered a quadrilat-

1. The pulmonic valve and right ventricular outflow tract

Figure 1.78 In this left anterior oblique view, catheters inserted

These important relationships should be kept in mind

circumferential mapping catheter has been placed. It has

Figure 1.88 For both right- and left-sided fascicle-related

Considering the heart in the standard orthogonal fluo-

Figure 2.4 Imaging of the left-sided pulmonary veins obtained

For closer examination of the pericardial structures for Transseptal Catheterization

Figure 2.11 Top panel, Intracardiac echocardiographic image

structure. In our laboratory, with routine use of ICE to guide

of transient hypotension, a pericardial scan quickly excludes

Use of ICE to Guide Treatment

In several specific arrhythmias, ICE is particularly useful to

Figure 2.14 Use of intracardiac echocardiography (ICE) to

INTRODUCTION Single-channel electrograms have been replaced by multi-

information sensed by the field sensor at the tip of the map-

calculated using a proprietary algorithm. This current-based

The 26-electrode mapping and ablation catheter QwikStar

ELECTRICAL IMPEDANCE electric currents with slightly different frequencies of about

Figure 3.10 Th is right atrial activation map was created using