18 

Typical Atrioventricular Bypass Tracts

OUTLINE
Types of Bypass Tracts, 599 Electrophysiological Testing, 623
Atrioventricular Bypass Tracts, 599 Baseline Observations During Sinus Rhythm, 623
Atrionodal Bypass Tracts, 599 Induction of Tachycardia, 633
Atrio-Hisian Bypass Tracts, 599 Tachycardia Features, 637
Atypical Bypass Tracts, 600 Diagnostic Maneuvers During Tachycardia, 641
Types of Preexcitation Syndromes, 600 Diagnostic Maneuvers During Sinus Rhythm After Tachycardia
Wolff-Parkinson-White Syndrome, 600 Termination, 648
Concealed Bypass Tracts, 600 Exclusion of Other Arrhythmia Mechanisms, 649
Lown-Ganong-Levine Syndrome, 600 Localization of the Bypass Tract, 649
Mahaim Variant of Preexcitation, 600 Pacing From Multiple Atrial Sites, 649
Pathophysiology, 600 Preexcitation Index, 649
Wolff-Parkinson-White Syndrome, 600 Effects of Bundle Branch Block During Orthodromic
Atrioventricular Bypass Tracts, 601 Atrioventricular Reentrant Tachycardia, 652
Atrioventricular Reentry, 602 Ventricular Entrainment During Orthodromic Atrioventricular
Other Arrhythmias Associated With Wolff-Parkinson-White Reentrant Tachycardia, 652
Syndrome, 603 Earliest Ventricular Activation Site During Anterograde Bypass
Epidemiology and Natural History, 606 Tract Conduction, 655
Wolff-Parkinson-White Pattern, 606 Earliest Atrial Activation Site During Retrograde Bypass Tract
Wolff-Parkinson-White Syndrome, 606 Conduction, 655
Sudden Death, 606 Atrial Electrogram Polarity Reversal During Retrograde Bypass
Associated Cardiac Abnormalities, 606 Tract Conduction, 656
Familial Wolff-Parkinson-White Syndrome, 606 Direct Recording of Bypass Tract Potential, 657
Concealed Bypass Tracts, 607 Local Atrioventricular (or Ventriculoatrial) Interval, 658
Clinical Presentation, 607 Ablation, 660
Initial Evaluation, 607 Target of Ablation, 660
Methods for Evaluation of Bypass Tract Refractory Ablation Technique: General Considerations, 661
Period, 607 Endpoints of Ablation, 662
Principles of Management, 608 Ablation of Left Free-Wall Bypass Tracts, 663
Acute Management, 608 Ablation of Right Free-Wall Bypass Tracts, 666
Chronic Management, 609 Ablation of Anteroseptal (Superoparaseptal) and Midseptal
Electrocardiographic Features, 612 Bypass Tracts, 667
Electrocardiography of Preexcitation, 612 Ablation of Posteroseptal (Inferoparaseptal) Bypass Tracts, 670
Supraventricular Tachyarrhythmias Associated With Ablation of Epicardial Bypass Tracts, 672
Wolff-Parkinson-White Syndrome, 614 Causes of Failed Bypass Tract Ablation, 673
Electrocardiographic Localization of the Bypass Tract, 614 Outcome, 674

TYPES OF BYPASS TRACTS
Bypass tracts (BTs) are remnants of the atrioventricular (AV) connec-
tions caused by incomplete embryological development of the AV annuli
and failure of the fibrous separation between the atria and ventricles.
There are several types of BTs, according to the structures they connect,
including AV, atrionodal, atrio-Hisian, atriofascicular, fasciculoventricular,
and nodofascicular BTs.1
Atrioventricular Bypass Tracts
AV BTs are strands of working myocardial cells connecting atrial and ven-
tricular myocardium across the electrically insulating fibrofatty tissues of
the AV junction bypassing the atrioventricular node (AVN)-His-Purkinje
system (HPS). In the older literature, these BTs were called Kent bundles,
although incorrectly (Kent described AVN-like tissue in the right atrial
[RA] free wall that did not connect to the ventricle). Thus the use of
the term bundle of Kent should be discouraged.
Atrionodal Bypass Tracts
Atrionodal BTs connect the atrium to the distal or compact AVN.
They have been called James fibers and are of uncertain physiological
significance.
Atrio-Hisian Bypass Tracts
Atrio-Hisian BTs connect the atrium to the His bundle (HB); these BTs
are rare.

599
600 CHAPTER 18  Typical Atrioventricular Bypass Tracts
Atypical Bypass Tracts
The term “atypical BTs” is used here to describe variants of BTs that
connect the atrium (atriofascicular BTs), AVN (nodofascicular and nodo-
ventricular BTs), or HB (fasciculoventricular BTs) to distal Purkinje
fibers or ventricular myocardium. In addition, this term encompasses
slowly conducting short AV BTs and long AV BTs. Although many of
those variants of BTs are sometimes referred to as “Mahaim fibers,” it is
more appropriate to describe them based on their anatomic connections.
TYPES OF PREEXCITATION SYNDROMES
Several patterns of preexcitation can occur, depending on the anatomy
of the BT and the direction in which impulses are conducted. Conduc-
tion from the atria to the ventricles normally occurs via the AVN-HPS.
Patients with preexcitation have an additional or alternative pathway,
the BT, which directly connects the atria and ventricles and bypasses
the AVN. The term syndrome is used when the anatomical variant is
responsible for tachycardia.
Wolff-Parkinson-White Syndrome
In the Wolff-Parkinson-White (WPW) syndrome, AV conduction occurs,
partially or entirely, through an AV BT, which results in earlier activa-
tion (preexcitation) of the ventricles than if the impulse had traveled
through the AVN.
Concealed Bypass Tracts
Concealed AV BTs refer to AV BTs that do not manifest anterograde
conduction and therefore do not result in ventricular preexcitation.
Because they do not result in alteration of the QRS complex in the
electrocardiogram (ECG), they cannot be detected by inspection of the
surface ECG; they are called concealed. However, the concealed BT can
conduct in a retrograde fashion, thereby creating a reentrant circuit
with impulses traveling from the atrium to the AVN, HPS, ventricle,
and then back to the atrium via the BT.
Lown-Ganong-Levine Syndrome
In the setting of Lown-Ganong-Levine (LGL) syndrome, preexcitation
purportedly occurs via atrio-Hisian BTs or, alternatively, no BT is present
and enhanced AVN conduction accounts for the ECG findings. The net
effect is a short PR interval without delta wave or QRS prolongation.
It is important to stress, however, that LGL is not a recognized syndrome
with an anatomical basis, but only an ECG description, and the use of
the term should be discouraged.
Mahaim Variant of Preexcitation
The so-called Mahaim variant of preexcitation does not typically result
in a delta wave because these pathways, which usually terminate in the
TABLE 18.1  Historical Description of Different Bypass Tracts
Eponymous
Pathway Anatomical Description
Kent bundle Clusters of nodal cells at nonseptal AV junction
James fiber Atriocompact nodal connection
Brechenmacher fiber Atrio-Hisian connection
Mahaim fiber Connection from compact AVN to ventricle
Paladino fiber Connection from proximal AVN to ventricle
AV, Atrioventricular; AVN, atrioventricular nodal; LGL, Lown-Ganong-Levine; WPW, Wolff-Parkinson-White.
conducting system or in the ventricular myocardium close to the con-
ducting system, conduct slowly, and the AVN-HPS has adequate time
to activate most of the ventricular muscle mass.
It is worth noting that some of the older literature refers to epony-
mous pathways that were originally anatomically described with sub-
sequent attempts made to correlate these structures with physiologic
findings. With more recent data from intracardiac recordings, many of
these correlations have been shown to be incorrect and thus the use of
the eponyms adds confusion to discussions about them. For instance,
the pathways described by Kent (AV nodal–like tissue at the free-wall
AV valve annulus) more resemble atriofascicular fibers than they do
typical AV fibers, and atriofascicular fibers in turn possess the physiol-
ogy initially (incorrectly) attributed to Mahaim fibers. Table 18.1 displays
some of the terminology; it is evident why use of eponymous terms is
discouraged.
PATHOPHYSIOLOGY
Wolff-Parkinson-White Syndrome
WPW pattern refers to the constellation of ECG abnormalities related
to the presence of a manifest AV BT (i.e., ventricular preexcitation:
short PR interval, delta wave, wide QRS complex) in asymptomatic
patients (Fig. 18.1). WPW syndrome refers to the combination of ven-
tricular preexcitation and either a documented tachyarrhythmia or
symptoms of a tachyarrhythmia.1
Because the AV BT typically conducts faster than the AVN, the onset
of ventricular activation is earlier than if depolarization occurred only
via the AVN, resulting in a shortened PR (P-delta) interval. Furthermore,
because the BT exhibits practically nondecremental conduction, the
early ventricular activation (i.e., P-delta interval) remains almost con-
stant at all atrial rates (Fig. 18.2).
Preexcited intraventricular conduction in WPW propagates from
the insertion point of the AV BT in the ventricular myocardium via
direct muscle-to-muscle conduction. This process is inherently slower
than ventricular depolarization resulting from rapid HPS conduction.
Thus, although the initial excitation of the ventricles (via the BT) occurs
earlier, it is followed by slower activation of the ventricular myocardium
than occurs normally. The net effect is that the QRS complex consists
of fusion between the early ventricular activation caused by preexcita-
tion with the later ventricular activation resulting from impulse propa-
gation through the AVN-HPS to the ventricles. The initial part of
ventricular activation resulting in the upstroke of the QRS complex is
slurred because of slow muscle-to-muscle conduction; this is termed
a delta wave.
Depending on the relative contribution from ventricular activation
by the normal AVN-HPS versus the manifest BT, a variable degree of
preexcitation occurs. The more rapid the conduction along the BT in
relation to the AVN, the greater the amount of myocardium depolarized
Proposed Physiological
Role/Syndrome Actual Physiologic Role
Anomalous AV connection/WPW syndrome None (possibly atriofascicular pathways)
LGL syndrome Enhanced AVN conduction
LGL syndrome Enhanced AVN conduction
Septal WPW pathways with decremental Probably none
conduction
Septal WPW pathways with decremental Probably none
conduction
 CHAPTER 18  Typical Atrioventricular Bypass Tracts
Normal QRS Preexcited QRS
delta
QRS
QRS
PRI PRI
Fig. 18.1  Ventricular Preexcitation. Three surface electrocardiogram
leads during normal sinus rhythm. The first sinus P wave is conducted
over the normal atrioventricular node-His Purkinje system (AVN-HPS),
resulting in a normal PR interval (PRI) and a normal QRS complex. The
second P wave is conducted over the AVN and a bypass tract (BT). AV
conduction over the BT is faster than over the AVN, resulting in preex-
citation of the ventricle and shortening of the PRI. Then, preexcited
intraventricular conduction propagates from the insertion point of the
BT in the ventricular myocardium via direct muscle-to-muscle (slow)
conduction, producing an initial slurred “delta” wave (shaded area of
the QRS complex). The rest of the QRS complex is produced by the
rapidly conducting HPS. Therefore the preexcited QRS results from
fusion between activation over the BT (which accounts for the initial
delta wave) and activation over the AVN-HPS (which accounts for the
rest of the QRS complex).
via the BT, resulting in a more prominent or wider delta wave and
increasing prolongation of the QRS complex duration.1
Atrioventricular Bypass Tracts
The cardiac skeleton consists of four rings of dense connective tissue
that surround the AV canals (mitral and tricuspid) and extend to the
origins of the aorta and the pulmonary trunk, providing structure and
support for the heart as well as electrical isolation between the atria
and the ventricles. The aortic valve occupies the central position with
the other valve rings attached to it. The right fibrous trigone includes
the triangular formation between the aortic valve and the medial parts
of the tricuspid and mitral valves, and it represents the largest thicken-
ing and strongest portion of the cardiac skeleton. Together with the
membranous septum, the right fibrous trigone constitutes the central
fibrous body (see Fig. 9.1).
The AV junctions are the areas of the heart where the atrial mus-
culature connects to the annuli of the mitral and tricuspid valves. The
AVN-HPS, which lies in the septal component of the AV junction, is
the only normal electrical connection between the atria and the ven-
tricles. The fibrous skeleton and AV valvular annuli (annulus fibrosus)
act as insulators to prevent electrical impulses from conducting to the
ventricles by any other route. The main function of the AVN is modula-
tion of atrial impulse transmission to the ventricles, thereby coordinating
atrial and ventricular contractions; it receives, delays, and conveys atrial
impulses to the ventricles.
601
AV BTs are aberrant muscle bundles that connect the atria to the
ventricles outside of the normal AV conduction system. AV BTs are
found most often in the parietal AV junctional areas, including the
paraseptal areas. They breach the insulation provided by the fibrofatty
tissues of the AV groove (sulcus tissue) and the hinge lines (fibrous
annulus) of the valves. They are rarely found in the area of fibrous
continuity between the aortic and mitral valves because in this area there
is usually a wide gap between the atrial myocardium and ventricular
myocardium to accommodate the aortic outflow tract. The remainder
of the AV groove may be divided into quadrants consisting of the left
free wall, right free wall, and posteroseptal and anteroseptal spaces. The
distribution of BTs within these regions is not homogeneous—46% to
60% of BTs are found within the left free-wall space; 25% are within the
posteroseptal space; 13% to 21% of BTs are within the right free-wall
space; up to 7% are within the right superoparaseptal (formerly called
anteroseptal) space; and less than 5% are located in the midseptum
(Fig. 18.3).
AV BTs are usually short and very thin muscular strands (typically
5 to 10 mm in length, with a maximal diameter of 0.1 to 7 mm) but
can occasionally exist as broad bands of tissue. They can course through
the AV groove at variable depths ranging from subepicardial to suben-
docardial locations. The AV BT can run in an oblique course rather
than perpendicular to the transverse plane of the AV groove. As a result,
the fibers can have an atrial insertion point that is transversely from
less than one to several centimeters removed from the point of ven-
tricular attachment. Some posteroseptal pathways insert into coronary
sinus (CS) musculature rather than atrial myocardium and can be
associated with the coronary venous system or diverticula from a CS
branch vein.
Multiple AV BTs occur in 5% to 10% of patients. BTs are defined
as multiple when they are separated by more than 1 to 3 cm at the AV
junction. The most common combination of widely spaced multiple
BTs is posteroseptal and right free-wall BTs. The incidence of multiple
BTs is particularly high in patients with antidromic atrioventricular
reentrant tachycardia (AVRT) (50% to 75%), patients in whom atrial
fibrillation (AF) resulted in ventricular fibrillation (VF), and patients
with Ebstein anomaly.
Although the majority (approximately 60%) of AV BTs conduct
both anterogradely and retrogradely (i.e., bidirectionally), some AV BTs
are capable of propagating impulses in only one direction. BTs that
conduct only in the anterograde direction are uncommon (less than
5%), often cross the right AV groove, and frequently possess decremental
conduction properties. On the other hand, BTs that conduct only in
the retrograde direction occur more frequently, accounting for 17% to
37% of all BTs. When the BT is capable of anterograde conduction,
ventricular preexcitation is usually evident during normal sinus rhythm
(NSR), and the BT is referred to as manifest. BTs capable of retrograde-
only conduction are referred to as concealed.
Because working myocardial cells make up the vast majority of AV
BTs, conduction over those BTs is mediated by the rapid inward sodium
current, similar to normal His-Purkinje tissue and atrial and ventricular
myocardium. Therefore AV BTs have rather constant anterograde and
retrograde conduction at all rates until the refractory period is reached,
at which time conduction is completely blocked. Thus conduction over
AV BTs usually behaves in an all-or-none fashion (i.e., nondecremental
conduction), although with careful measurement, there is often a small
amount of prolongation of conduction intervals (10 to 15 milliseconds)
over the BT when the pacing rate is just below that at which block
occurs. In contrast, the AVN, which depends on the slow inward calcium
current for generation and propagation of its action potential, exhibits
what has been called decremental conduction, whereby conduction time
of the impulse propagating through the AVN prolongs as the atrial
602 CHAPTER 18  Typical Atrioventricular Bypass Tracts

Ventricular preexcitation Normal QRS

I I

II II

III III

aVR aVR

aVL aVL

aVF aVF

V1 V1

V2 V2

V3 V3

V4 V4

V5 V5

V6 V6

Fig. 18.2  Wolf-Parkinson-White Electrocardiogram (ECG) Pattern. Surface ECG of normal sinus rhythm
with ventricular preexcitation (left) and without preexcitation (right) in the same patient.

Supero- Anterior cycle length (CL) shortens. Thus AV conduction is more rapid through
Anterior paraseptal
Anterolateral the AV BT than through the AVN, a difference that is exaggerated at
Anterolateral
His faster heart rates. This difference has potentially great clinical impor-
tance. A primary function of the AVN is to limit the number of impulses
conducted from the atria to the ventricles, which is particularly important
AV node Mitral Orifice
Lateral Lateral during fast atrial rates (e.g., AF or atrial flutter [AFL]) when only a
Tricuspid Orifice fraction of impulses are conducted to the ventricles, whereas the remain-
Midseptal
der are blocked in the AVN. However, in the presence of nondecrementally
conducting AV BTs with short refractory periods, these arrhythmias
Coronary sinus Posterolateral
can lead to very fast ventricular rates that can degenerate into VF.
Posterolateral Posteroseptal Posterior
Posterior
Atrioventricular Reentry
Fig. 18.3  Locations of Atrioventricular (AV) Bypass Tracts by Ana-
tomical Region. Tricuspid and mitral valve annuli are depicted in a left AVRT is a macroreentrant tachycardia with an anatomically defined
anterior oblique view. Locations of the coronary sinus, AV node, and circuit that consists of two distinct pathways, the normal AV conduction
His bundle are shown. AV bypass tractts may connect atrial to ventricular system and an AV BT, linked by common proximal (atrial) and distal
myocardium in any of the regions shown. (From Miller JM, Zipes DP. (ventricular) tissues. If sufficient differences in conduction time and
Therapy for cardiac arrhythmias. In: Libby P, Bonow R, Mann DL, et al., refractoriness exist between the normal conduction system and the BT,
eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. a properly timed premature impulse of atrial or ventricular origin can
8th ed. Philadelphia: WB Saunders; 2007:779–830.) initiate reentry. AVRTs are the most common (80%) tachycardias associ-
ated with the WPW syndrome. AVRT is divided into orthodromic and
antidromic according to the direction of conduction in the AVN-HPS
(Fig. 18.4). Orthodromic indicates normal direction (anterograde) of
conduction over AVN-HPS during AVRT.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts
Orthodromic AVRT Antidromic AVRT
AVN AVN
HB BT HB BT
RB LB RB LB
Preexcited AT Preexcited AVNRT
AVN AVN
BT BT
HB HB
RB LB RB LB
Fig. 18.4  Bypass Tract–Related Tachycardias. Schematic representa-
tion of the reentrant circuit during orthodromic atrioventricular reentrant
tachycardia (AVRT), antidromic AVRT, preexcited atrial tachycardia (AT),
and preexcited atrioventricular nodal reentrant tachycardia (AVNRT) using
a left-sided bypass tract (BT). HB, His bundle; LB, left bundle branch;
RB, right bundle branch.
Orthodromic Atrioventricular Reentrant Tachycardia
In orthodromic AVRT, the AVN-HPS serves as the anterograde limb of
the reentrant circuit (i.e., the pathway that conducts the impulse from
the atria to the ventricles), whereas an AV BT serves as the retrograde
limb (see Figs. 18.4 and 18.5). Approximately 50% of BTs participating
in orthodromic AVRT are manifest (able to conduct bidirectionally)
and 50% are concealed (able to conduct retrogradely only). Therefore
a WPW pattern may or may not be present on the surface ECG during
NSR. When preexcitation is present, the delta wave seen during NSR
is lost during orthodromic AVRT because anterograde conduction during
the tachycardia occurs over the normal AV conduction system, and not
via the BT (i.e., the ventricle is not preexcited). Orthodromic AVRT
accounts for approximately 90% to 95% of AVRT episodes in patients
with a manifest BT and 35% of all paroxysmal supraventricular tachy-
cardias (SVTs).1
Antidromic Atrioventricular Reentrant Tachycardia
Antidromic AVRT is a preexcited AVRT whereby an AV BT serves as
the anterograde limb and the AVN-HPS serves as the retrograde limb
of the reentrant circuit (see Figs. 18.4 and 18.5). Consequently, the QRS
complex during antidromic AVRT is fully preexcited (i.e., the ventricles
are activated totally by the BT with no contribution from the normal
conduction system). The BT involved in the antidromic AVRT circuit
must be capable of anterograde conduction and, therefore, preexcitation
is typically observed during NSR. Other, less frequent, forms of preex-
cited AVRT utilize one AV BT as the anterograde conduction and a
second BT for retrograde conduction or a combination of one BT plus
the AVN-HPS in either direction (eFig. 18.1).1
Clinically, antidromic AVRT is much less frequent than orthodromic
AVRT, occurring in less than 5% of patients with WPW syndrome, and
can be induced in the electrophysiology (EP) laboratory in less than
10%. The low prevalence of antidromic AVRT is related to the EP prop-
erties of the AVN, because good retrograde ventriculoatrial (VA)
603
conduction is required to sustain tachycardia. Clinical presentation,
sex, age, and orthodromic AVRT induction appear similar in patients
with and without inducible antidromic AVRT. Patients with antidromic
AVRT induction more frequently have BTs with more rapid conduction
properties than other WPW patients.2
Susceptibility to antidromic AVRT appears to be facilitated by a
distance of at least 4 cm between the BT and the normal AV conduction
system. Consequently, most antidromic AVRTs use a lateral (right or
left) BT as the anterograde route for conduction. Because posteroseptal
BTs are in close proximity to the AVN, those BTs are rarely part of
antidromic AVRT if the other limb is the AVN and not a second free-
wall BT. Up to 50% to 75% of patients with spontaneous antidromic
AVRT have multiple BTs (manifest or concealed), which may or may
not be utilized as the retrograde limb during the tachycardia.2
Permanent Junctional Reciprocating Tachycardia
Permanent junctional reciprocating tachycardia (PJRT) is a rare form
of nearly incessant orthodromic AVRT mediated by a concealed, ret-
rogradely conducting AV BT that has slow and decremental conduction
properties. Conduction properties of this retrograde BT are slower than
the anterograde conduction properties of the AVN and those of typical
fast BTs found in patients with AVRT. The BT in PJRT is most often
located in the posteroseptal region, although other portions of the AV
groove can also harbor this unusual pathway. Because these BTs are
almost always concealed and have slow conduction, all elements neces-
sary for reentry are present at all times, and thus PJRT can be present
much of the time (i.e., incessant), with only short interludes of sinus
rhythm. The incessant nature of PJRT can result in tachycardia-induced
cardiomyopathy.1,3
Other Arrhythmias Associated With
Wolff-Parkinson-White Syndrome
Atrial tachycardia (AT), AFL, AF, and atrioventricular nodal reentrant
tachycardia (AVNRT) can all coexist with a BT. In these preexcited
tachycardias, the BT serves as a bystander route for ventricular or atrial
activation, and is not required for the initiation or maintenance of the
arrhythmia.
Atrioventricular Nodal Reentrant Tachycardia
and Atrial Tachycardia
Both AVNRT and AT can use the bystander BT to transmit impulses
to the ventricle (see Fig. 18.4). When AVNRT occurs in the WPW syn-
drome, the arrhythmia can be difficult to distinguish from AVRT without
EP testing.
Atrial Fibrillation
The overall incidence of AF in patients with WPW syndrome varies
from 12% to 39%. AF is typically paroxysmal. Persistent AF is rare in
these patients. AF is most common in patients with anterogradely con-
ducting BTs. Patients with antidromic AVRT, multiple BTs, and BTs
that have a short anterograde effective refractory period (ERP) are more
prone to develop AF. In individuals with WPW, AF is often preceded
by AVRT that degenerates into AF (Fig. 18.6).
The frequency with which intermittent AF occurs in patients with
the WPW syndrome is striking because of the low prevalence of coex-
isting structural heart disease or other predisposing factors for AF.
This observation suggests that the AV BT itself can be related to the
genesis of AF, supported by the fact that when the BT is ablated, AF may
not recur.
The mechanisms by which AVRT precipitates AF are not well under-
stood. The rapid atrial rate can cause disruption in atrial activation and
reactivation, creating an EP substrate conducive to AF. The observation
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 603.e1

II

V1

HRA

H A H A H A H H A H A H
His

CSprox

CSdist

RVA
l–– 300 msec ––l

eFig. 18.1  Preexcited Atrioventricular Reentrant Tachycardia. The anterograde limb of the reentry circuit
in mediated by a right lateral bypass tract (BT), as indicated by the preexcited QRS morphology. The retro-
grade limb of the circuit is mediated by a left lateral BT, as indicated by the eccentric atrial activation sequence.
A, Atrial electrogram; CSdist, distal coronary sinus; CSprox, proximal coronary sinus; H, His bundle potential;
HRA, high right atrium; RVA, right ventricular apex.
604 CHAPTER 18  Typical Atrioventricular Bypass Tracts

NSR

I aVR V1 V4

II
aVL V2 V5

III aVF V3 V6

Antidromic AVRT Orthodromic AVRT

I I

II II

III III

aVR aVR

aVL aVL

aVF aVF

V1 V1

V2 V2

V3 V3

V4 V4

V5 V5

V6 V6
Fig. 18.5  Orthodromic and Antidromic Atrioventricular Reentrant Tachycardias (AVRTs) in a Patient
With a Bidirectional Left Posteroseptal Bypass Tract (BT). Ventricular preexcitation is evident during normal
sinus rhythm (NSR). The narrow complex tachycardia represents orthodromic AVRT using the BT as the
retrograde limb of the reentrant circuit. Antidromic AVRT utilizes the BT for anterograde atrioventricular
conduction, resulting in wide complex tachycardia.

that most patients with BT and AF who undergo BT ablation are cured
of both AVRT and AF is compatible with this hypothesis. Another pos-
sibility is that the complex geometry of networks of BTs predisposes to
AF by fractionation of the activation wavefronts. Localized reentry has
been recorded in some patients, using direct recordings of the activa-
tion of the BTs. Hemodynamic changes, atrial stretch caused by atrial
contraction against closed AV valves during ventricular systole, can
also play a role. Ablation of the BT can cure AF in more than 90% of
patients; however, vulnerability to AF persists in up to 56%, and the
response to atrial extrastimulation (AES) is also unaltered by ablation.
AF in younger WPW patients is usually associated with the BT and
is unlikely to occur after ablation; in contrast, older patients may have
recurrence of AF from causes unrelated to the BT. Nonetheless, recent
studies have challenged the role of BT ablation in modulating the risk
of AF particularly in adult patients, and show persistently higher rates
of AF in WPW patients (hazard ratio, 4.77) compared with the general
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 605

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Antidromic AVRT Preexcited AF NSR

Fig. 18.6  Antidromic Atrioventricular Reentrant Tachycardia (AVRT) Converting Into Nonsustained
Preexcited Atrial Fibrillation (AF). Normal sinus rhythm (NSR) follows. Preexcitation is mediated via a left
anterior bypass tract.

population despite catheter ablation of the BT.4 Trends of increased
risk of AF in ablated WPW patients suggest that mechanisms other
than those directly related to the presence of a BT, such as underlying
atrial myopathy, may play a role in AF genesis.
Atrial Flutter
About 4% of WPW patients present with AFL. AFL is the most common
(60%) regular preexcited tachycardia in patients with WPW syndrome.
AFL is caused by a macroreentrant circuit within the RA and therefore
exists independently of the BT, and AFL does not have the same causal
association to AV BTs as AF. In some patients with WPW syndrome
who develop AFL, AVRT is often the initiating event. This relationship
can be mediated by contraction-excitation feedback into the atria during
the AVRT.
AFL, like AF, can conduct anterogradely via a BT causing a preexcited
tachycardia. Depending on the various refractory periods of the normal
and pathological AV conduction pathways, AFL can potentially conduct
1:1 to the ventricles during a preexcited tachycardia, making the arrhyth-
mia difficult to distinguish from VT (see Fig. 12.10).
Ventricular Fibrillation and Sudden Cardiac Death
The mechanism of sudden cardiac death (SCD) in patients with WPW
is likely the occurrence of AF or AFL with a very rapid ventricular rate,
which provokes VF. Although the frequency with which AF with rapid
AV conduction via a BT degenerates into VF is unknown, the incidence
of SCD in patients with WPW syndrome is rather low, ranging from
0% to 0.39% annually in several large case series. The trigger for AF in
this population of patients is generally an episode of AVRT. In fact,
most patients who have been resuscitated from VF secondary to pre-
excitation have a previous history of AVRT, AF, or both. Nonetheless,
SCD can be the first manifestation of WPW syndrome.5
Several factors can help identify the patient with WPW who is at
increased risk for VF, including symptomatic AVRT, septal location of
the BT, presence of multiple BTs, and male gender. In addition, the risk
of SCD associated with WPW appears highest in the first two decades
of life.1 Nonetheless, it is clear that the most important factor for the
occurrence of VF in these patients is the ability of the BT to conduct
rapidly to the ventricles. This is best measured by determining the
shortest and average preexcited R-R intervals during AF or, alternatively,
606 CHAPTER 18  Typical Atrioventricular Bypass Tracts
by measuring the anterograde ERP of the BT. If the BT has a very short
anterograde ERP (less than 250 milliseconds), a rapid ventricular response
can occur with degeneration of the rhythm to VF. A short preexcited
R-R interval during AF (≤220 milliseconds) appears to be a sensitive
clinical marker for identifying children at risk for SCD, although its
positive predictive value in adults is only 19% to 38%.5
Drug therapy can be an additional determinant of the risk of VF in
patients with preexcitation. Several pharmacological agents can poten-
tially enhance BT conduction and increase the ventricular rate during
AF and, hence, increase the risk of VF (see later).
Ventricular Tachycardia
Coexisting VT is uncommon in patients with WPW syndrome because
structural heart disease is very infrequent in this young patient popula-
tion. Naturally, older patients are subject to coronary artery and other
diseases that can cause VT.
EPIDEMIOLOGY AND NATURAL HISTORY
Wolff-Parkinson-White Pattern
The prevalence of WPW pattern on the surface ECG is 0.1% to 0.3%
in the general population.1 The prevalence is increased to 0.55% among
first-degree relatives of affected patients, suggesting a familial compo-
nent. The annual incidence of newly diagnosed cases of preexcitation
in the general population was substantially lower (0.004%) in a diverse
population of residents from Olmsted County, Minnesota, 50% of whom
were asymptomatic. The incidence in men is twice that in women,
and is highest in the first year of life, with a secondary peak in young
adulthood.5
The WPW pattern on the surface ECG can be intermittent and can
even permanently disappear with loss of anterograde but preserved
retrograde conduction. Loss of preexcitation has been observed in up
to 31% of adults and in 0% to 33% of children and adolescents over
a 5-year time period. Intermittent and persistent loss of preexcitation
may indicate that the BT has a relatively longer baseline ERP, which
makes it more susceptible to age-related degenerative changes and varia-
tions in autonomic tone.6
Wolff-Parkinson-White Syndrome
The prevalence of the WPW syndrome is substantially lower than that
of the WPW ECG pattern. At present, it is estimated that approximately
65% of adolescents and 40% of adults over 30 years of age with a WPW
pattern on a resting ECG are asymptomatic.5
The occurrence of arrhythmias is related to the age at the time
preexcitation is discovered and can vary with location and EP properties
of the BT. AVRT manifests early in life, with an average of more than
10 years separating the time of clinical presentation of AVRT versus
that of AVNRT.1 Up to 70% of children (8 to 12 years of age) who are
asymptomatic at the time of diagnosis of WPW ECG pattern remain
asymptomatic over median follow-up of 57 months. About 30% even-
tually develop an arrhythmic event, which can be potentially life-
threatening in approximately 10% of patients. In contrast, only a minority
(10%) of adults who are asymptomatic at the time of diagnosis of
ventricular preexcitation develop cardiac arrhythmias over median
follow-up of 67 months, which can be potentially life-threatening in
approximately 5% of patients. The vast majority of patients in whom
preexcitation is first uncovered after the age of 40 remain asymptomatic.5
In a large meta-analysis, the annual risk of developing SVT was 0.25%
of WPW patients.7
A male predominance among WPW patients has been observed.
Furthermore, men tend to have a higher incidence of antidromic AVRT,
more prevalent left-sided BTs, and shorter anterograde BT ERP. Also,
men usually present with AVRT at an older age than women. In contrast,
women were found to have a higher prevalence of multiple BTs, ortho-
dromic AVRT, and right-sided BTs. In addition, Asians appear to have
right free-wall BTs substantially more frequently than other races.8,9
Sudden Death
The incidence of SCD among patients with asymptomatic preexcitation
is difficult to ascertain. A large meta-analysis (including 1869 patients
with asymptomatic ventricular preexcitation from 20 studies with 11,722
patient-years of follow-up) found a total of 10 cases of SCD, with SCD
rates between 0 and 4.5 events per 1000 person-years of follow-up, and
an overall risk of SCD in adults and children of 2.5 per 1000 person-
years (or 3% to 4% over a lifetime). Italian studies reported all but one
SCD event.6,7
In general, children seem to have a numerically higher event rate
than adults. The majority of victims were between the ages of 10 and
40 years. Patients with WPW who are most susceptible to SCD are
symptomatic; however, SCD can be the first event in patients with
asymptomatic preexcitation.7 Several characteristics have been reported
among patients who experienced potentially life-threatening events,
including younger age (less than 30 years), male gender, history of AF,
prior syncope, associated congenital or other heart disease, and familial
WPW. Low-risk WPW patients also showed a characteristic EP profile
(older age, lower tachyarrhythmia inducibility, longer anterograde refrac-
tory ERP of BTs, and low likelihood of baseline retrograde BT conduc-
tion or multiple BTs).7
Associated Cardiac Abnormalities
Most patients with AV BTs do not have coexisting structural cardiac
abnormalities, except for those that are age related. The association of
ventricular preexcitation with structural congenital heart defects is well
recognized. Up to 20% of children with WPW also have congenital
heart disease. Associated congenital abnormalities, when present, are
more likely to be right sided than left sided. Ebstein anomaly is the
congenital lesion most strongly associated with the WPW syndrome.
As many as 10% of such patients have one or more BTs; most of these
are located in the right free-wall or the right posteroseptal space. Ven-
tricular preexcitation has also been described in patients with transposi-
tion of great arteries, pulmonary atresia, patent ductus arteriosus,
tetralogy of Fallot, total anomalous pulmonary venous return, and
ventricular septal defects.5,6
Familial Wolff-Parkinson-White Syndrome
Typically, WPW syndrome occurs sporadically; however, in a minor-
ity of cases it is inherited. A familial form of WPW has infrequently
been reported and is usually inherited as an autosomal dominant trait.
Among patients with the WPW syndrome, 3.4% have first-degree rela-
tives with a preexcitation syndrome. The genetic cause of a rare form
of familial WPW syndrome has been described. The clinical phenotype
is characterized by the presence of preexcitation on the ECG, frequent
SVTs (including AF), progressive conduction system disease, and left
ventricular (LV) hypertrophy (distinct from sarcomeric hypertrophic
cardiomyopathy). Patients typically present in late adolescence or the
third decade with syncope or palpitations. Premature SCD occurred
in 10% of patients. Paradoxically, by the fourth decade of life, progres-
sion to advanced SND or AV block (with the loss of preexcitation)
requiring pacemaker implantation was common. Approximately 80%
of the patients older than 50 years had chronic AF. Causative mutations
in the PRKAG2 gene were identified in these families. The PRKAG2
gene encodes the gamma-2 regulatory subunit of the adenosine mono-
phosphate (AMP)–activated protein kinase, which is a key regulator
of metabolic pathways, including glucose metabolism. The penetrance
 CHAPTER 18  Typical Atrioventricular Bypass Tracts
of the disease for WPW syndrome was complete, but the expression
was variable. The described phenotype of this syndrome is similar to
the autosomal recessive glycogen storage disease, Pompe disease. Given
the function of the AMP-activated protein kinase and this similarity, the
PRKAG2 syndrome is likely a cardiac-specific glycogenosis syndrome.
This syndrome thus belongs to the group of genetic metabolic cardiomy-
opathies, rather than to the congenital primary arrhythmia syndromes.
The annulus fibrosus, which normally insulates the ventricles from the
atria, is thinned and disrupted by glycogen-filled myocytes, and these
anomalous microscopic AV connections, rather than morphologically
distinct BTs, appear to provide the anatomic substrate for ventricular
preexcitation. Of note, certain mutations in PRKAG2 have been associ-
ated with nodoventricular BTs.10
Another genetic form of WPW syndrome is associated with muta-
tions in the bone morphogenetic protein-2 (BMP2) gene, which belongs
to the class of transforming growth factor, The TGF-β-superfamily of
proteins, and is involved in the development of the annulus fibrosus.
This syndrome is characterized by variable cognitive deficits and dys-
morphic features in addition to ventricular preexcitation.11
Concealed Bypass Tracts
The true prevalence of concealed BTs is unknown because, unlike the
situation with the WPW ECG pattern, these BTs are concealed on the
surface ECG and are only expressed during AVRT; only symptomatic
patients undergo EP testing. As noted, orthodromic AVRT accounts for
approximately 95% of AVRTs and 35% of all paroxysmal SVTs, and
50% of the BTs that participate in orthodromic AVRT are concealed.
SVTs using a concealed BT have no gender predilection and tend to
occur more frequently in younger patients than in those with AVNRT;
however, significant overlap exists. PJRT most often occurs in early
childhood, although clinically asymptomatic patients presenting later
in life are not uncommon.
CLINICAL PRESENTATION
The majority of patients with preexcitation are asymptomatic and are
discovered incidentally on an ECG obtained for unrelated reasons. When
symptomatic arrhythmias occur in the WPW patient, the disorder is
called the WPW syndrome. The two most common types of arrhythmias
in the WPW syndrome are AVRT and AF. Patients with AVRT experi-
ence symptoms characteristic of paroxysmal SVT with abrupt onset
and termination, including rapid and regular palpitations, chest pain,
dyspnea, presyncope, and rarely, syncope. Episodes can last from seconds
to several hours. Symptoms are usually mild and short-lived and ter-
minate spontaneously or with vagal maneuvers. However, occasionally
patients present with disabling symptoms, especially in the presence of
structural heart disease.1,12
AVRT, which in general is well tolerated by the patient when addi-
tional heart disease is absent, can deteriorate into AF; the latter can be
a life-threatening arrhythmia if the BT has a short anterograde refractory
period, resulting in very fast ventricular rates, with possible degenera-
tion into VF and SCD. The incidence of SCD in patients with the WPW
syndrome has been estimated to range from 0.15% to 0.39% over a
3- to 10-year follow-up. It is unusual for cardiac arrest to be the first
symptomatic manifestation of WPW syndrome. Conversely, in about
50% of cardiac arrest cases in WPW patients, it is the first manifestation
of WPW syndrome.
PJRT commonly presents as a frequently recurring or incessant
tachycardia that is refractory to drug therapy and can lead to tachycardia-
induced cardiomyopathy and heart failure symptoms.
Rarely, significant ventricular preexcitation during NSR can result
in ventricular dysfunction secondary to dyssynchronous ventricular
607
contraction. Improvement of left ventricular ejection fraction has been
described after ablation of septal BTs in pediatric patients.5
INITIAL EVALUATION
History, physical examination, and 12-lead ECG constitute an appropri-
ate initial evaluation. In patients with brief, self-terminating episodes
of palpitations, an event recorder is the most effective way to obtain
ECG documentation. Also, echocardiographic examination is recom-
mended to exclude structural heart disease.
Several other noninvasive tests have been proposed as useful for
evaluating symptomatic patients and risk-stratifying patients for SCD
risk. However, the sensitivity and specificity of noninvasive testing have
been shown to be limited. Invasive EP testing may be considered in
patients with arrhythmias and those with a WPW ECG pattern when
noninvasive testing does not lead to the conclusion that the anterograde
ERP of the BT is relatively long. However, a strategy to perform an EP
study for all asymptomatic patients with the WPW ECG pattern for
the purpose of risk stratification is still controversial and not widely
accepted.
Methods for Evaluation of Bypass Tract
Refractory Period
Demonstration of Intermittent Preexcitation
Intermittent preexcitation has historically been thought to confer a
lower risk of SCD than persistent preexcitation. Observation of inter-
mittent loss of the preexcitation pattern on ambulatory monitoring or
serial ECGs is generally correlated with a long BT anterograde ERP.
The longer refractory period of the BT decreases the frequency of mani-
fest preexcitation during NSR and is expected to lower the risk of
mediating rapid preexcited ventricular activation during AF. Neverthe-
less, EP studies in symptomatic patients with intermittent preexcitation
found that 10% to 24% can have BTs capable of conducting at rapid
rates during AF (with anterograde ERP or shortest preexcited R-R interval
less than 250 milliseconds), perhaps related to autonomic influences.
However, similar findings have not yet been demonstrated in asymp-
tomatic patients with intermittent preexcitation.13,14
Intermittent preexcitation can be observed on ambulatory monitor-
ing in up to 67% of patients. It is important, however, to distinguish
intermittent preexcitation from inapparent preexcitation (see later) and
from a bigeminal ventricular rhythm with a long coupling interval.1,5
Although intermittent preexcitation is a predictor of poor anterograde
conduction through the BT, it has rarely been observed in some patients
with cardiac arrest. Furthermore, the presence of intermittent preexcita-
tion does not predict retrograde conduction properties of the BT nor
preclude the development of AVRT.5
Loss of Preexcitation During Exercise
Demonstration of a sudden loss of preexcitation (indicated by abrupt
loss of the delta wave associated with prolongation of the PR interval
and normalization of the QRS) during exercise is consistent with block
in the BT and is consistent with a long BT ERP (greater than 300 mil-
liseconds). Importantly, rapid AVN conduction during exercise can
potentially mask persistent preexcitation. Therefore only abrupt and
complete loss of preexcitation during exercise should be sought as a
surrogate of a long anterograde ERP of the BT.5
Loss of preexcitation during exercise is a good predictor that the
patient is not at risk for VF even during sympathetic stimulation.
However, the frequency of block in the BT during exercise is low (approxi-
mately 10% to 20%), and thus sensitivity of this test is poor. On the
other hand, persistence of preexcitation during exercise stress has a
sensitivity of 96% but a specificity of only 17% in predicting either a
608 CHAPTER 18  Typical Atrioventricular Bypass Tracts
shortest preexcited R-R less than 250 milliseconds during AF or a BT
ERP of less than 250 milliseconds (positive predictive value of 40%
and negative predictive value of 88%).5
Bypass Tract Conduction Block in Response to
Antiarrhythmic Agents
When the administration of ajmaline (1 mg/kg IV over 3 minutes) or
procainamide (10 mg/kg IV over 5 minutes) results in complete block
of the BT during NSR, a long anterograde ERP (greater than 270 mil-
liseconds) of the BT is likely. The shorter the BT ERP, the less likely it
would be blocked by these drugs. Also, the amount of ajmaline required
to block conduction over the BT correlates with the duration of the
anterograde ERP of the BT. However, the incidence of BT block in
response to these drugs is low and, although the occurrence of block
predicts a long ERP of the BT, failure to produce block does not neces-
sarily suggest a short ERP. Moreover, pharmacological testing is carried
out at rest and therefore does not indicate what effect the drug will
have on the BT ERP during sympathetic stimulation, such as exercise,
emotion, anxiety, and recreational drug use. Importantly, the specificity
of loss of preexcitation after administration of sodium blockers is poor
compared to the shortest preexcited R-R intervals during inducible AF.
Given these limitations, pharmacologic challenge is no longer routinely
utilized.5
Evaluation of Ventricular Response During Atrial Fibrillation
During spontaneous or induced AF, the propensity for rapid AV con-
duction can be judged by the interval between consecutively preexcited
QRS complexes. A mean preexcited R-R interval greater than 250 mil-
liseconds and a shortest preexcited R-R greater than 220 milliseconds
predict low risk for SCD, with a negative predictive value of more than
95%; however, the positive predictive value is low (20%).5
Response of Preexcitation to Transesophageal
Atrial Stimulation
There is good correlation between the value of the anterograde ERP of
the BT obtained during single-test programmed atrial stimulation and
atrial pacing at increasing rates and the ventricular rate during AF.
Programmed electrical stimulation of the atrium can be performed by
the transesophageal route and the value of the anterograde ERP of the
BT can be determined.
Electrophysiological Testing
Programmed atrial stimulation is used to evaluate the anterograde ERP
of the BT. Because BT refractoriness shortens with decreasing pacing
cycle length (PCL), the ERP should be determined at multiple PCLs
(preferably ≤400 milliseconds). In addition, atrial stimulation should
be performed close to the BT atrial insertion site to obviate the effect
of intraatrial conduction delay. Incremental-rate atrial pacing is per-
formed to determine the maximal rate at which 1:1 conduction over
the BT occurs. Induction of AF should be performed to determine the
average and the shortest R-R interval during preexcited AF. Atrial and
ventricular stimulation is also performed to evaluate inducibility of
AVRT as well as the number and location of BTs.5
A shortest preexcited R-R interval less than 220 to 250 milliseconds
during AF has been shown to be the best discriminator of those at risk
of VF, with a high sensitivity (88% to 100%) and a high negative pre-
dictive value for identifying children and young adults with WPW
syndrome at risk for VF. However, the positive predictive value is low
(19% to 38%), largely due to the very low incidence of SCD in these
patients. Also, a shortest preexcited R-R interval less than 250 millisec-
onds during AF has been noted in 20% to 26% of asymptomatic
adults with a WPW pattern, and in up to 67% when isoproterenol is
administered. Thus, although isoproterenol raises the sensitivity of
invasive EP testing, it markedly reduces the specificity.5
On the other hand, BT ERP less than 240 milliseconds appears to
significantly correlate with only AVRT inducibility, but as an isolated
variable, it is less predictive of life-threatening events and exhibits sig-
nificant overlap between WPW patients with VF and those without VF.
The presence of multiple BTs and the ability to induce sustained AVRT,
especially when AVRT spontaneously degenerates into AF, have been
proposed to predict risk of malignant ventricular arrhythmias. The lack
of retrograde conduction over the BT appears to be at lower risk for
SCD. However, the predictive value of these criteria remains limited
and significant overlap exists.1,5
PRINCIPLES OF MANAGEMENT
Acute Management
Symptomatic Patients With Concealed Bypass Tracts
Patients with orthodromic AVRT utilizing a concealed BT are treated
in a similar fashion as those with paroxysmal SVT. Vagal maneuvers
(including Valsalva and carotid sinus massage) are the first-line inter-
vention for acute conversion of the tachycardia; though the overall
success rate is limited (approximately 28%). If SVT persists, adenosine
is recommended, and it offers a success rate of 90% to 95%. For refrac-
tory tachycardia, IV diltiazem, verapamil, or beta-blockers can terminate
orthodromic AVRT in the majority of patients. Synchronized cardiover-
sion is recommended for hemodynamically unstable patients and for
those refractory or intolerant to drug therapy (Fig. 18.7).1
Symptomatic Patients With Manifest Bypass Tracts
In patients with manifest preexcitation during NSR presenting with
AVRT (orthodromic or antidromic), vagal maneuvers are the first-line
intervention for tachycardia termination (see Fig. 18.7). For persistent
SVT, adenosine is recommended. Importantly, adenosine should be
used with caution because it can induce AF with a rapid ventricular
rate in the presence of an anterogradely conducting BT. This is unusual
and should not be viewed as a contraindication to adenosine use, but
one should be prepared for emergency cardioversion before administer-
ing adenosine to SVT patients.1
For refractory AVRT, IV diltiazem, verapamil, or beta-blockers can
be considered to block conduction in the AVN, which represents either
the retrograde or anterograde limb in the AVRT circuit. AVN blocking
drugs, however, are ineffective in patients with preexcited AVRT that
utilizes two separate BTs for anterograde and retrograde conduction.
Drug treatment directed at the BT (ibutilide, procainamide, flecainide)
may also be considered. When drug therapy fails or hemodynamic
instability is present, electrical cardioversion should be considered.
It is important to note that IV diltiazem and verapamil can result
in hemodynamic collapse if the AVRT does not terminate or AF is
induced with rapid conduction over the BT degenerating to VF, and one
must be prepared for immediate electrical cardioversion if that occurs
(see later).
Preexcited Atrial Fibrillation
In patients with AF or AFL, ventricular preexcitation, and rapid ven-
tricular response, prompt direct-current cardioversion is recommended,
especially when hemodynamic compromise is present. IV procainamide
or ibutilide to restore NSR or slow the ventricular rate may be considered
in hemodynamically stable patients. Both drugs slow BT conduction.
Importantly, drugs that preferentially slow AVN conduction without
prolonging BT refractoriness (such as verapamil, diltiazem, beta-blockers,
adenosine, oral or IV digoxin, and IV amiodarone) can accelerate the
ventricular rate and potentially precipitate hemodynamic collapse and
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 609

Orthodromic AVRT Chronic Management

Symptomatic Patients With Concealed Bypass Tracts
Catheter ablation is considered first-line therapy (class I) for patients
Vagal maneuvers with paroxysmal SVT involving a concealed BT (i.e., orthodromic AVRT).
and/or IV adenosine However, because concealed BTs are not associated with an increased
(class I)
risk of SCD in these patients, catheter ablation can be presented as one
of a number of potential therapeutic approaches, including pharma-
If ineffective
or not feasible
cological therapy and clinical follow-up alone. When pharmacological
therapy is selected for patients with concealed BTs, it is reasonable to
consider a trial of beta-blocker therapy, diltiazem, or verapamil (Fig.
18.8). These agents are effective for preventing recurrent tachycardia
Hemodynamically in approximately 50% of patients. Antiarrhythmic agents may be con-
stable
sidered for patients with refractory tachycardia; however, the risk and
benefits of these drugs should be carefully considered.1
Yes No
Symptomatic Patients With Manifest Bypass Tracts
Catheter ablation is considered the treatment of choice for patients
Synchronized
Preexcitation cardioversion with WPW syndrome—that is, patients with manifest preexcitation
on resting (class I) along with documented arrhythmias (antidromic or orthodromic AVRT
ECG or preexcited AF) or symptoms consistent with cardiac arrhythmias.
Catheter ablation is curative in more than 95% of patients with a rela-
Yes No tively low complication rate (about 3%), and it also obviates the unwanted
side effects of pharmacological therapy.1
For patients with WPW syndrome who are not candidates for, or
IV beta-blockers, IV beta-blockers,
IV diltiazem, or IV diltiazem, or
prefer not to undergo catheter ablation, antiarrhythmic drugs to block
IV verapamil IV verapamil BT conduction are considered (see Fig. 18.8). Class IC agents such as
(class IIb) (class IIa) flecainide and propafenone (in patients without structural heart disease
or ischemic heart disease), and class III drugs, such as sotalol and dofeti-
lide, may be considered. Oral amiodarone is a last resort therapy, given
If ineffective or not feasible the associated risks of long-term therapy. In general, antiarrhythmic
drug therapy can offer symptomatic improvement in up to 90% of
patients, although complete disappearance of symptoms is observed in
Synchronized only 30%.1
cardioversiona Chronic oral beta-blocker, verapamil, and diltiazem may be used
(class I)
for the treatment of patients with WPW syndrome, particularly if their
BT has been demonstrated to be incapable of rapid anterograde con-
Fig. 18.7  Acute Treatment of Orthodromic Atrioventricular Reentrant
duction. However, these agents must be used with caution and after a
Tachycardia (AVRT). aFor rhythms that break or recur spontaneously,
synchronized cardioversion is not appropriate. IV, Intravenous. (From discussion with the patient concerning the potential risk of rapid con-
Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline duction over the BT if AF develops. Digoxin, on the other hand, should
for the management of adult patients with supraventricular tachycardia: be avoided because it can shorten the refractory period of the BT and,
a report of the American College of Cardiology/American Heart Associa- hence, is potentially harmful in patients with manifest BTs.1
tion Task Force on Clinical Practice Guidelines and the Heart Rhythm
Society. J Am Coll Cardiol. 2016;67:e27–e115.) Asymptomatic Patients With Manifest Bypass Tracts
Asymptomatic young WPW patients have about 30% risk of becoming
symptomatic, and a very small, but definite risk of life-threatening
arrhythmias and SCD. Therefore, in the recent Pediatric and Congenital
VF in high-risk patients. Several mechanisms are probably involved; Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS)
hypotension produced by some of those medications is followed by expert consensus document on treatment of asymptomatic young WPW
a sympathetic discharge that enhances BT conduction. Furthermore, subjects, risk stratification is recommended to identify a potential sub-
slowing or blocking conduction through the AVN prevents competitive group of patients with BTs with “high-risk” properties that may confer
concealed retrograde conduction into the BT by normally conducted an increased risk for lethal cardiac arrhythmias and in whom the risk-
beats and, as a result, can potentially enhance conduction over the BT. to-benefit ratio favors prophylactic ablation (Fig. 18.9).5
In addition, the rapid and irregular ventricular rate, hypotension, and Initial risk stratification utilizes noninvasive testing (e.g., Holter
sympathetic discharge probably result in fractionation of the ventricu- monitoring, exercise stress testing) to ascertain true loss of preexcitation
lar wavefront and VF. Also, digoxin increases the ventricular rate by at physiological heart rates. Complete and abrupt loss of preexcitation
shortening BT refractoriness. Lidocaine, for reasons that are unclear, during exercise testing or intermittent loss of preexcitation during ECG
has also been associated with degeneration of AF into VF. It is occa- or ambulatory monitoring, indicate long anterograde ERP of the BT
sionally used in patients with WPW who have a wide QRS complex and help identify patients at low risk of rapid conduction over the BT
tachycardia that might be misinterpreted as VT. Unlike the IV route and SCD (Box 18.1).5,15
of administration, chronic oral amiodarone therapy can slow or block Inability to clearly demonstrate absolute loss of ventricular preex-
BT conduction.1 citation on noninvasive testing warrants consideration for transesophageal
610 CHAPTER 18  Typical Atrioventricular Bypass Tracts

Orthodromic AVRT

Preexcitation
on resting
ECG
Yes No

Ablation Ablation
candidate, willing to candidate, pt prefers
undergo ablation ablation

No Yes Yes No

Flecainide or Amiodarone, Flecainide or Amiodarone,

beta-blockers Catheter Beta-blockers,
propafenone propafenone digoxin,
diltiazem, ablation diltiazem, or
(in the absence (in the absence dofetilide,
dofetilide, sotalol, (class I) verapamil
of SHD) of SHD) or sotalol
or verapamil (class I) (class IIb)
(class IIa) (class IIa)
(class IIb)

If ineffective, If ineffective,
consider ablation consider ablation
Fig. 18.8  Ongoing Management of Orthodromic Atrioventricular Reentrant Tachycardia (AVRT). Drugs
listed alphabetically. pt, Patient; SHD, structural heart disease (including ischemic heart disease). (From Page
RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the management of adult patients with
supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task
Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2016;67:e27–e115.)

Baseline electrocardiogram

Persistent manifest Intermittent

preexcitation preexcitation
Fig. 18.9  Management Algorithm for Young
Asymptomatic Patients With Wolf-Parkinson-
White Electrocardiogram Pattern. aPatients unable
to perform an exercise stress test should undergo Exercise stress testa Follow in cardiology
risk stratification with an electrophysiological study. with counseling
b
Prior to invasive testing, patients and their parents/ regarding symptom
awareness
guardians should be counseled on the risks and
benefits of proceeding with invasive studies, risks
of observation only, and risks of medication strat- Persistent or uncertain loss Abrupt and clear loss of
egy. cPatients participating at moderate- to high-level of manifest preexcitation manifest preexcitation
competitive sports should be counseled concerning
the risk-benefit of ablation. dIn the absence of induc-
ible atrial fibrillation, the shortest preexcited R-R
interval determined by rapid atrial pacing is a rea- Diagnostic transesophageal or
sonable surrogate. SPERRI, Shortest pre-excited intracardiac electrophysiology studyb,c
R-R interval SVT, supraventricular tachycardia. (From
Cohen MI, Triedman JK, Cannon BC, et al. PACES/
HRS expert consensus statement on the manage-
ment of the asymptomatic young patient with a
Wolff-Parkinson-White [WPW, ventricular preexcita- SPERRI in atrial fibrillation >250 msec SPERRI in atrial
tion] electrocardiographic pattern. Heart Rhythm. Inducible SVT
and absence of inducible SVTc,d fibrillation ≤250d
2012;9:1006–1024.)

Follow in cardiology May consider ablation

with counseling based on pathway Discuss Discuss
regarding symptom location and/or patient risk/benefits of risk/benefits of
awareness characteristics ablation ablation
(class IIA) (class IIB) (class IIA) (class IIB)
 CHAPTER 18  Typical Atrioventricular Bypass Tracts
BOX 18.1  Findings Suggestive of Lower
Risk of Life-Threatening Events in Wolff-
Parkinson-White Patients
• Intermittent loss of the preexcitation pattern on ambulatory monitoring or
serial electrocardiograms
• Abrupt and complete loss of preexcitation during exercise
• Loss of preexcitation after administration of sodium blockers
• Mean preexcited R-R interval >250 msec and shortest preexcited R-R
>220 msec during atrial fibrillation
• Anterograde effective refractory period of the bypass tract <240 msec
or intracardiac EP testing. However, the benefits and risk of invasive
risk stratification should be based on individual considerations such
as age, gender, occupation, and athletic involvement, and should be
thoroughly discussed with the patient or, in the case of a child, with
the parents. Given the low risk associated with invasive EP testing (0.1%
to 1%), it is reasonable to consider this approach for risk stratification
in asymptomatic WPW patients. Several EP findings help identify high-
risk patients who may benefit from catheter ablation, including: (1)
shortest preexcited R-R interval less than 250 milliseconds during induced
AF; (2) the presence of multiple BTs; (3) spontaneous degeneration of
induced AVRT into preexcited AF; and (4) BT anterograde ERP less
than 240 milliseconds.1 The critical obligatory condition for VF is the
presence of a short anterograde functional refractory period of the BT,
which is best reflected in the shortest R-R interval between preexcited
beats in AF.5,16 Although the ability to induce sustained AVRT has been
considered by some as a potential risk factor, this has not been sup-
ported by recent studies.2
The role of isoproterenol challenge during EP testing has not yet
been clearly defined. Isoproterenol administration can significantly
shorten the shortest preexcited R-R interval and, as a result, increase
the proportion of asymptomatic patients in the “high-risk” category.
Thus some investigators suggested the use of a more stringent threshold
for the shortest preexcited R-R interval (≤220 milliseconds) instead of
the threshold adopted by the 2012 PACES/HRS Guidelines (≤250 mil-
liseconds) for definition of “high-risk” BTs when EP testing is performed
under the influence of isoproterenol.17
In low-risk patients, as determined by noninvasive or invasive testing,
it is appropriate to pursue a strategy of follow-up with ECGs and reevalu-
ation at selected intervals with a high degree of suspicion for new
arrhythmia symptoms. This strategy should incorporate patient educa-
tion about the potential risks associated with preexcitation and the
symptoms of arrhythmias that should prompt them to seek medical
attention. It is also advisable to give the patient a copy of his or her
ECG and a short note about the fact that the WPW pattern is present
to help prevent the misdiagnosis of MI and to explain the basis of
cardiac arrhythmias in case they develop later. Importantly, WPW patients
most susceptible to SCD are symptomatic. Thus the evolution of the
clinical status from an asymptomatic state to symptoms (e.g., syncope
or palpitations) likely portends a higher risk for SCD. Once WPW
patients become symptomatic, catheter ablation may be considered,
regardless of the prior risk assessment.5
In patients with high-risk BT characteristics, prophylactic catheter
ablation is reasonable. A combination of inducible AVRT and short
R-R interval during preexcited AF provides the best indication for abla-
tion. Catheter ablation of the BT, regardless of BT characteristics, is
also reasonable in asymptomatic patients with high-risk occupations
(e.g., school bus drivers, police, and pilots), and is probably reasonable
in: (1) patients involved in moderate- to high-intensity competitive
611
sports; (2) patients with structural heart disease; (3) patients with ven-
tricular dysfunction secondary to dyssynchronous contractions; and
(4) patients with BT locations associated with lower risk of procedural
complications (such as AV block or coronary artery injury), which can
counterbalance the potential benefit of ablation. However, because
knowledge about the success and complication rates plays a major role
in decision-making, the physician must consider his or her own success
and complication rates for ablation of the specific location of the BT
identified, and that information should be made available to the patient.5
It is important to recognize that the majority of adult patients with
asymptomatic preexcitation have a benign course with few clinically
significant arrhythmic events occurring over time; the risk of SCD is
low, is seen mainly in children, and is rarely the initial clinical mani-
festation. Hence, observation without further evaluation or treatment
remains a reasonable option in these patients, even when noninvasive
low-risk markers are not evident. The key is a clear understanding by
the patient of the relative merits of each strategy. The well-informed
patient needs to choose between a very small risk of potentially life-
threatening arrhythmia over a long period of time and a one-time small
procedural risk associated with EP testing and catheter ablation. Certain
patients such as athletes and those in higher risk occupations will gen-
erally choose ablation. Others, especially patients older than 30 years,
may prefer the small risk of a conservative strategy.5,18
It is important to note that both invasive and noninvasive EP markers,
despite their high sensitivity and negative predictive value, lack specific-
ity for identifying patients at risk of life-threatening ventricular arrhyth-
mias, largely due to the very low incidence of SCD.7 The great majority
of individuals with WPW, even with a shortest preexcited R-R interval
less than 250 milliseconds during AF, will not experience SCD; thus
the positive value of predicting SCD remains very low. Therefore the
management of asymptomatic patients with a WPW pattern remains
controversial.7
The ability of noninvasive risk stratification to identify low-risk
patients is low (less than 20%). Hence, according to the 2012 PACES/
HRS Guidelines, invasive EP evaluation would be recommended for
the majority of young asymptomatic WPW patients, and the majority
of those would undergo catheter ablation. A recent report retrospectively
examined the consequences of following the published guidelines in
85 asymptomatic patients (less than 18 years old) with ventricular pre-
excitation ECG pattern persisting at peak exercise, to assess the outcomes
of invasive risk stratification applying current guidelines. Approximately
38% of the patients exhibited adverse BT properties at EP study, fulfill-
ing either the class IIA indication (shortest preexcited R-R interval less
than 250 milliseconds during AF) or class IIB indication (AVRT induc-
ibility) for catheter ablation. The use of isoproterenol infusion during
EP testing shifted an additional 36% of those tested into one of these
two indication classes. About 69% of young patients subjected to risk
stratification underwent BT ablation as a result of the evaluated BT
properties or patient/parental decision.17,19
Although complications of a diagnostic EP study are generally minor
and not life-threatening, the risks associated with an ablation procedure
are likely at least similar to the risk of SCD in asymptomatic WPW
patients. In three large series, procedure-related complications occurred
in 1.8% to 8.2% of cases, and death as a consequence of ablation occurred
in 0.07% to 0.19%.7 If routine EP testing were to be performed in the
majority of asymptomatic WPW patients, many patients would proceed
immediately to catheter ablation and, in others, there would be a strong
temptation to ablate when catheters are in place (regardless of predicted
SCD risk), especially given the fact that the criteria for ablation usually
will not be black or white. This greatly increases the risk to the patient,
which can potentially nullify the benefit of elimination of SCD risk
achieved by BT ablation. A recent study using decision analysis software
612 CHAPTER 18  Typical Atrioventricular Bypass Tracts

to construct a risk-benefit decision tree for a target population of 20- to
40-year-old asymptomatic patients with WPW, found the decision to
ablate resulted in a reduction of 10-year mortality risk of 8.8 patients
for 1000 patients. The study suggested that it is necessary to treat 112
asymptomatic patients with WPW to save one life over 10 years.18
Finally, the physician and the patient must have a shared under-
standing of the value of invasive EP study for risk stratification, rather
than as a therapeutic tool. These issues have to be resolved before pro-
ceeding with invasive measures, and the risks and benefits of proceed-
ing with ablation of BT found not to have high-risk characteristics
should be discussed thoroughly with patients in advance of the EP
procedure.5
Wolff-Parkinson-White Patients and Sports Participation
WPW syndrome accounts for approximately 1% of deaths in athletes.
Although many of the cases of SCD with WPW are associated with
exercise, training does not alter the EP properties in WPW.
Catheter ablation is the treatment of choice for symptomatic WPW
patients (whether or not engaged in athletics). For asymptomatic WPW
patients engaged in moderate- to high-level competitive sports, non-
invasive and, if needed, invasive risk stratification is advisable. For those
with high-risk BT characteristics, ablation of the BT is recommended
before clearance for competitive sports because of risk for life-threatening
arrhythmias.5,20 In low-risk patients, as determined by noninvasive or
invasive testing, BT ablation may still be appropriate, but competitive
sports may be allowed without ablation, especially when BT ablation
confers an unacceptable potential risk (e.g., AV block in the setting of
midseptal or superoparaseptal BTs).5,20
ELECTROCARDIOGRAPHIC FEATURES
Electrocardiography of Preexcitation
Anterogradely conducting AV BTs produce the classic WPW ECG pattern
characterized by a fusion between conduction via the BT and the normal
AVN-HPS: (1) short PR (P-delta) interval (less than 120 milliseconds);
(2) slurred upstroke of the QRS (delta wave); and (3) wide QRS (>120
milliseconds) (see Figs. 18.1 and 18.2).13,14
The degree of preexcitation depends on several factors, including
conduction time over the AVN-HPS, conduction time from the sinus
node to the atrial insertion site of the BT (which depends on the dis-
tance, conduction, and refractoriness of the intervening atrial tissue),
and conduction time through the BT (which depends on the length,
thickness, and conduction properties of the BT).
Pharmacological and/or physiological maneuvers that alter AVN
conduction (e.g., carotid sinus massage, Valsalva maneuvers, adenosine,
beta-blockers) can be used to alter the degree of preexcitation, thereby
confirming the diagnosis of the presence of an anterogradely conduct-
ing AV BT.
The ECG pattern displayed by some patients with WPW syndrome
can simulate the pattern found in other cardiac conditions and can
alter the pattern seen in the presence of other cardiac disease. A negative
delta wave (presenting as a Q wave) can mimic a myocardial infarction
(MI) pattern. Conversely, a positive delta wave can mask the presence
of a previous MI. Intermittent WPW can also be mistaken for frequent
premature ventricular complexes (PVCs) (Fig. 18.10). If the WPW
pattern persists for several beats, the rhythm can be misdiagnosed as
an accelerated idioventricular rhythm or, if sufficiently rapid, VT. The

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

V5

Fig. 18.10  Preexcitation Alternans. Surface electrocardiogram during sinus tachycardia demonstrating inter-
mittent preexcitation in which a QRS complex manifesting a delta wave (red arrow) alternates with a normal
QRS complex (blue arrow) (i.e., preexcitation alternans). Note the intermittent abrupt loss of delta wave
associated with prolongation of the PR interval and the presence of a stable sinus rate, indicating that loss
of preexcitation is secondary to anterograde block in the bypass tract (i.e., intermittent preexcitation) rather
than enhanced atrioventricular nodal conduction.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 613

WPW pattern is occasionally seen on alternate beats and may suggest
ventricular bigeminy. An alternating WPW and normal pattern can
occasionally suggest electrical alternans. On the other hand, late-coupled
PVCs (eFig. 18.2) and ventricular pacing (eFig. 18.3) with inapparent
pacing artifacts can occasionally mimic ventricular preexcitation.
Inapparent Versus Intermittent Preexcitation
Inapparent preexcitation.  With inapparent preexcitation, preex-
citation is absent on the surface ECG despite the presence of an antero-
gradely conducting AV BT because conduction over the AVN-HPS
reaches the ventricle faster than that over the BT. In this setting, the
PR interval is shorter than the P-delta interval would be if preexcitation
were present. Therefore the transition from manifest to inapparent
preexcitation is characterized by normalization of the QRS in conjunc-
tion with shortening of the PR interval, reflecting the now better AVN-HPS
conduction.
Inapparent preexcitation is usually caused by: (1) enhanced AVN
conduction, so that it is faster than conduction over the BT; (2) pro-
longed intraatrial conduction from the site of atrial stimulation to the
atrial insertion site of the BT (most often left lateral), favoring antero-
grade conduction and depolarization of the ventricle over the AVN-HPS;
or (3) prolonged conduction over the BT, so that it is slower than
AVN-HPS conduction.
Intermittent preexcitation.  Intermittent preexcitation is defined
as the presence and absence of preexcitation on serial ECGs or ambula-
tory cardiac monitoring (Fig. 18.11). True intermittent preexcitation
is characterized by an abrupt loss of the delta wave (regardless of how
fast or slow AVN conduction is), with prolongation (normalization) of
the PR interval (reflecting the loss of the faster BT conduction, and the
subsequent conduction over the slower AVN), and normalization of
the QRS in the absence of any significant change in heart rate.13,14
The mechanism of intermittent preexcitation is poorly understood,
but is likely related to the BT refractory period and cellular connectivity
within the BT. Potential mechanisms include (1) phase 3 (i.e., tachycardia-
dependent) or phase 4 (i.e., bradycardia-dependent) block in the BT
(see Chapter 10); (2) anterograde or retrograde concealed conduction
produced by PVCs, premature atrial complexes (PACs), or atrial arrhyth-
mias; (3) BTs with a long ERP and the gap phenomenon in response
to PACs; and (4) BTs with a long ERP and supernormal conduction.
Preexcitation alternans is a form of intermittent preexcitation in
which a QRS complex manifesting a delta wave alternates with a normal
QRS complex (see Fig. 18.10). Concertina preexcitation is another form
of intermittent preexcitation in which the PR intervals and QRS complex
durations show a cyclic pattern; that is, preexcitation becomes progres-
sively more prominent over a number of QRS complex cycles followed
by a gradual diminution in the degree of preexcitation over several
QRS cycles, despite a fairly constant heart rate.
Differentiation between intermittent preexcitation and inapparent
preexcitation on an ECG showing QRS complexes with and without
preexcitation can be achieved by comparing the P-delta interval
during preexcitation and the PR interval when preexcitation is absent.
Loss of preexcitation associated with a PR interval longer than the
P-delta interval is consistent with intermittent preexcitation (see Fig.
18.11), whereas loss of preexcitation associated with a PR interval shorter
than the P-delta interval is consistent with inapparent preexcitation.
Furthermore, maneuvers that slow AVN conduction (e.g., carotid sinus
massage, AVN blockers) would unmask inapparent preexcitation but
would not affect intermittent preexcitation.

II

V1

P-delta interval PR interval

91 msec 167 msec
HRA

H H
His A A

CSprox

CSdist

RVA

Fig. 18.11  Intermittent Preexcitation. Surface electrocardiogram leads II and V1 and intracardiac recordings
in a patient with Wolf-Parkinson-White syndrome and a right anterior bypass tract (BT). Note the intermittent
abrupt loss of delta wave (stars) associated with prolongation of the PR interval and normalization of the His
bundle–ventricular interval, despite the presence of a constant atrial–His bundle (AH) interval (atrioventricular
node [AVN] conduction) and a stable sinus rate, indicating that loss of preexcitation is secondary to antero-
grade block in the BT (i.e., intermittent preexcitation) rather than enhanced AVN conduction. A, Atrial elec-
trogram; CSdist, distal coronary sinus; CSprox, proximal coronary sinus; H, His bundle potential; HRA, high right
atrium; RVA, right ventricular apex.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 613.e1

1000 msec

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

eFig. 18.2  Late-Coupled Premature Ventricular Complexes (PVCs) Mimicking Intermittent Ventricular
Preexcitation. Surface electrocardiogram of normal sinus rhythm with late-coupled PVCs, which are inscribed
shortly after the sinus P waves, resulting in a short PR interval and wide QRS complexes mimicking intermit-
tent ventricular preexcitation. Note that the degree of widening of the QRS and the variability of the QRS
morphology and the varying relationship to the preceding P waves all argue against ventricular preexcitation.

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

II II II II

eFig. 18.3  Ventricular Pacing Mimicking Ventricular Preexcitation. Surface electrocardiogram (ECG) of
normal sinus rhythm with atrial-tracking ventricular pacing. The QRS complexes are the result of fusion from
ventricular pacing and conduction over the normal atrioventricular conduction axis, resulting in a pseudo-delta
wave, mimicking a Wolf-Parkinson-White ECG pattern. The pacing artifacts are very small, but careful inspec-
tion reveals those artifacts most clearly in lead III.
614 CHAPTER 18  Typical Atrioventricular Bypass Tracts
Supraventricular Tachyarrhythmias Associated With
Wolff-Parkinson-White Syndrome
Orthodromic Atrioventricular Reentrant Tachycardia
The ECG during orthodromic AVRT shows retrograde P waves inscribed
within the ST-T wave segment with an RP interval that is usually less
than half of the tachycardia R-R interval (i.e., RP interval <PR interval)
(Fig. 18.12). The RP interval remains constant, regardless of the tachy-
cardia cycle length (TCL), because it reflects nondecremental retrograde
conduction over the BT. QRS morphology during orthodromic AVRT
is generally normal and not preexcited, even when preexcitation is present
during NSR (see Fig. 18.5). Functional bundle branch block (BBB) can
be observed frequently during orthodromic AVRT at fast rates (see Fig.
18.12). The presence of BBB during SVT in a young person (less than
40 years) should raise the suspicion of orthodromic AVRT incorporat-
ing a BT ipsilateral to the blocked bundle, because the longer conduction
time through the involved ventricle engendered by the BBB facilitates
orthodromic reentry by enabling all portions of the circuit enough
time to recover excitability from the prior cycle. This is particularly
true with left bundle branch block (LBBB), which is very uncommon
in younger patients.
Orthodromic AVRT tends to be a rapid tachycardia, with rates ranging
from 150 to more than 250 beats/min, generally faster in younger people.
A beat-to-beat oscillation in QRS amplitude (QRS alternans) is present
in up to 38% of cases and is most commonly seen when the rate is very
rapid (Fig. 18.13). The mechanism for QRS alternans is not clear but
may partly result from oscillations in the relative refractory period of
the distal portions of the HPS.
Ischemic-appearing ST segment depression also can occur during
orthodromic AVRT, even in young individuals who are unlikely to have
coronary artery disease. An association has been observed between repo-
larization changes (ST segment depression or T wave inversion) and the
underlying mechanism of the tachycardia because such changes are more
common in orthodromic AVRT than AVNRT (57% vs. 25%). Several
factors can contribute to ST segment depression in these arrhythmias,
including changes in autonomic tone, intraventricular conduction distur-
bances, a longer VA interval, and a retrograde P wave of longer duration
that overlaps into the ST segment.21 The location of the ST segment
changes can vary with the location of the BT; ST segment depression in
leads V3 to V6 is almost invariably seen with a left lateral BT, whereas
ST segment depression and a negative T wave in the inferior leads is
associated with a posteroseptal or posterior BT. A negative or notched
T wave in leads V2 or V3 with a positive retrograde P wave in at least
two inferior leads suggests an anteroseptal BT. However, ST segment
depression occurring during orthodromic AVRT in an older patient
mandates consideration of possible coexisting ischemic heart disease.
Antidromic Atrioventricular Reentrant Tachycardia
Antidromic AVRT is characterized by a wide (fully preexcited) QRS
complex, usually regular R-R intervals, and ventricular rates of up to
250 beats/min (see Fig. 18.5). The width of the preexcited QRS complex
and the amplitude of the ST-T wave segment usually obscure the ret-
rograde P wave on the surface ECG. When the P waves can be identified,
they are inscribed within the ST-T wave segment with an RP interval
that may be more than half of the tachycardia R-R interval because
retrograde conduction occurs slowly via the AVN-HPS. The PR (P-delta)
interval remains constant, regardless of the TCL, because it represents
nondecremental anterograde conduction over the BT.
Permanent Junctional Reciprocating Tachycardia
PJRT tends to be incessant, stopping and starting spontaneously every
few beats without initiating PACs or PVCs. The heart rate is usually
between 120 and 200 beats/min and the QRS duration is generally
normal. Slow retrograde conduction over the BT causes the RP interval
during PJRT to be long, usually more than half of the tachycardia R-R
interval (Fig. 18.14). The P waves resulting from retrograde conduction
are easily seen on the ECG and are inverted in leads II, III, aVF, and
V3 to V6.
Atrioventricular Nodal Reentrant Tachycardia and
Atrial Tachycardia
Both AVNRT and AT can be associated with partially or fully preexcited
QRS complex secondary to anterograde conduction to the ventricles
over the bystander BT. When AVNRT occurs in the WPW syndrome,
the arrhythmia can be difficult to distinguish from orthodromic AVRT
without EP testing.
Atrial Fibrillation
There are several characteristic findings on the ECG in patients with
AF conducting over a BT, so-called preexcited AF. The rhythm is irregu-
larly irregular, and can be associated with very rapid ventricular response
caused by the nondecremental anterograde AV conduction over the BT
(Fig. 18.15). However, a sustained rapid ventricular rate of more than
180 to 200 beats/min will often create R-R intervals that appear to be
regular when the ECG is recorded at 25 mm/s. Although the QRS com-
plexes are conducted aberrantly, resembling those during preexcited
NSR, their duration can be variable and they can become normalized.
This is not related to the R-R interval (i.e., it is not a rate-related phe-
nomenon), but rather is related to the variable relationship between
conduction over the BT and AVN-HPS. Preexcited and normal QRS
complexes often appear “clumped.” This can result from concealed ret-
rograde conduction into the BT or the AVN (Fig. 18.16).
The QRS complex during preexcitation is a fusion between the
impulse that preexcites the ventricles caused by rapid conduction through
a BT and the impulse that takes the usual route through the AVN. The
number of impulses that can be transmitted through the BT and the
amount of preexcitation depend on the refractoriness of the BT and
AVN. The shorter the anterograde ERP of the BT, the more rapid is the
anterograde impulse conduction over the BT and, because of more
preexcitation, the wider the QRS complexes. Patients who have a BT
with a very short ERP and rapid ventricular rates represent the group
at greatest risk for development of VF.
Anterograde block in the BT during AF abolishes retrograde con-
cealment into the AVN, which in turn allows the AVN to recover
its excitability and conduct anterogradely. In turn, these conducted
impulses through the AVN can result in retrograde concealment into
the BT, causing anterograde block of the BT and, thereby, slowing the
ventricular rate.
Atrial Flutter
AFL, like AF, can conduct anterogradely via a BT resulting in a preexcited
tachycardia. Depending on the various refractory periods of the normal
and pathological AV conduction pathways, AFL can potentially conduct
1:1 to the ventricles during a preexcited tachycardia, making the arrhyth-
mia difficult to distinguish from VT (see Fig. 12.10).
Electrocardiographic Localization of the Bypass Tract
Careful analysis of the preexcitation pattern during NSR can potentially
allow an accurate approximation of the location of the BT. This provides
the electrophysiologist with important information that can guide patient
counseling regarding the risks and benefits of ablation. In particular,
it provides some guidance about the proximity of the BT to the normal
conduction system and the subsequent risk of AV block associated with
an ablation attempt, as well as the need for left heart catheterization
 Orthodromic AVRT

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Fig. 18.12  Orthodromic Atrioventricular Reentrant Tachycardia (AVRT) Using a Concealed Superopara-
septal Bypass Tract (BT). Note the P waves (arrows) inscribed within the ST-T wave segment (short RP
interval). Ischemic-appearing ST segment depression is also observed. Functional right bundle branch block
occurs in the right side of the tracing, with prolongation of the RP (ventriculoatrial [VA]) interval, suggesting
that retrograde VA conduction during the supraventricular tachycardia is mediated by a right-sided BT. The
dashed lines denote the QRS onset and P wave onset.
616 CHAPTER 18  Typical Atrioventricular Bypass Tracts

1 aVR V1 V4

2 aVL V2 V5

3 aVF V3 V6

Fig. 18.13  Electrocardiogram (ECG) of Orthodromic Atrioventricular Reentrant Tachycardia Showing

QRS Alternans in Multiple ECG Leads.

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

II

Fig. 18.14  Surface Electrocardiogram (ECG) of Permanent Junctional Reciprocating Tachycardia (PJRT).
Note the incessant nature of the arrhythmia, stopping and starting spontaneously every few beats without
initiating atrial or ventricular ectopic beats. Slow retrograde conduction over the bypass tract causes the RP
interval during PJRT to be long (long RP tachycardia). The P waves resulting from retrograde conduction are
easily seen on the ECG and are inverted in the inferior leads.

and atrial septal puncture and their potential complications. In addi-
tion, it can help in planning the ablation procedure, such as the use of
cryoablation for septal BTs or the need for special equipment for atrial
septal puncture for left-sided BTs.
Localization Using the Delta Wave
Delta wave morphology reflects the ventricular insertion site of the BT
and, hence, is helpful in approximating the BT location, especially when
maximal preexcitation is present. However, during NSR, only partial
ventricular preexcitation is usually observed, which limits the accuracy
of BT localization based on the surface ECG. In addition, the degree
of preexcitation can vary in an individual, depending on heart rate,
autonomic tone, and AVN function, as well as the location and EP
characteristics of the BT. Therefore it is important first to assess the
degree of preexcitation visible throughout the entire ECG and then use
only delta wave polarity for localization (the first 20 to 60 milliseconds
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 617

Sinus rhythm with ventricular preexcitation

I
II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Preexcitation atrial fibrillation

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Fig. 18.15  Electrocardiogram of Sinus Rhythm Atrial Fibrillation With Ventricular Preexcitation. Ven-
tricular preexcitation by the same right superoparaseptal bypass tract. Note the fast ventricular rate during
preexcited atrial fibrillation (exceeding 100 beats/min).
618 CHAPTER 18  Typical Atrioventricular Bypass Tracts
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Fig. 18.16  Preexcited Atrial Fibrillation. Note the “clumping” of preexcited and normal QRS complexes,
likely due to concealed retrograde conduction into the bypass tract or the atrioventricular node.
of the QRS in most cases, unless fully preexcited) rather than the overall
QRS polarity, which may vary from each other.
Several algorithms have been developed to predict the anatomic
location of manifest BTs based on delta wave polarity on the surface
ECG (Box 18.2; Figs. 18.17–18.20). Although these algorithms facilitate
prediction of the location of a BT, they are inherently limited by bio-
logical variability in anatomy (e.g., rotation of the heart within the
thorax), variable degree of preexcitation and QRS fusion, the presence
of more than one manifest BT, intrinsic ECG abnormalities (such as
prior MI and ventricular hypertrophy), patient body habitus, and tech-
nical variability in ECG acquisition and electrode positioning. The
accuracy of these algorithms in more recent studies has not reached
the accuracy previously reported by their designers.22 Therefore these
algorithms should be regarded as an orientation rather than a precise
localization tool. No single published algorithm offers extremely high
sensitivity and specificity for all BT locations. The algorithms appear
most accurate in predicting left free-wall BT locations and least accurate
in predicting midseptal or right anteroseptal BT locations. Hence, it
may be more realistic to initially identify a general area in which the
BT is located, and then to apply more subtle criteria from one or more
of the algorithms to attempt a more precise localization. This can be
achieved by applying some basic rules while maintaining a mental 3-D
representation of the mitral and tricuspid annuli and their anatomical
relationships to adjacent structures as they lie within the chest (i.e.,
“attitudinally correct orientation”) while analyzing the ECG and pre-
dicting morphology of the preexcited QRS.
Of note, the mere presence and the degree of preexcitation can
sometimes help in predicting the location of the BT. Posteroseptal and
right-sided BTs tend to be associated with a prominent degree of pre-
excitation because of the proximity to the sinus node, whereas left
lateral BTs are often associated with subtle preexcitation. Nevertheless,
when preexcitation is prominent, the accuracy of surface ECG localiza-
tion of manifest BTs tends to be higher for the diagnosis of left free-wall
BTs than for BTs in other locations.
On the surface ECG, analysis of delta wave polarity and amplitude
progression in precordial leads, and frontal plane horizontal and verti-
cal axes, are valuable for predicting the site of origin of manifest BTs
(Fig. 18.21).
Precordial transition.  Lead V1 is a unipolar lead positioned at the
right anterior chest wall. Therefore, as the BT location shifts progres-
sively more to the left or posteriorly, the precordial transition (i.e., the
first precordial lead where the R wave amplitude exceeds the S wave
amplitude) becomes sequentially earlier, thereby transforming the pre-
cordial preexcited QRS morphology from a late transition LBBB pattern
of the preexcited QRS to a positively concordant right bundle branch
block (RBBB) pattern. Hence, left-sided BTs exhibit positive delta waves
in lead V1, while right-sided BTs exhibit negative delta waves. The farther
the BT is to the left or posteriorly on the mitral annulus, the larger the
positive delta wave, and the farther the BT is to the right along the
tricuspid annulus, the deeper the negative delta wave is in lead V1.
Frontal plane horizontal axis.  Lead I primarily reflects the hori-
zontal axis. BTs closer to the left axilla will produce a deeply negative
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 619

BOX 18.2  Delta Wave Characteristics During Preexcitation According to Bypass Tract Locationa
Left Lateral/Left Anterolateral BTs
A. R/S ≥1 in V2 and positive delta in III, or R/S <1 in V2 and positive delta in
III and V1
B. RS transition ≤V1 and >2 positive delta in the inferior leads or S > R in aVL
C. QS or QR morphology in aVL and no negative QRS in III and V1
Left Posterior/Left Posterolateral BTs
A. R/S ≥1 in V1 and V2, no positive delta in III and positive delta in V1
B. R/S transition ≤V1, no ≥2 positive delta in the inferior leads, no S > R in
aVL, in lead I R <(S 0.8 mV), and the sum of the inferior delta is not
negative
C. Positive QRS in aVL and an equiphasic QRS or positive in V1 and no negative
QRS in III
Left Posteroseptal BTs
A. R/S ≥1 in V2, no positive delta in III, and positive delta and R/S <1 in V1
B. R/S transition ≤V1, no ≥2 positive delta in the inferior leads, no S > R in
aVL, in lead I R <(S 0.8 mV), and the sum of the inferior delta is negative
C. Negative QRS in III, V1, and aVF, tallest precordial R wave in V2–V4 and R
wave width in V1 >0.06 msec
Midseptal BTs
A. R/S <1 in V2, no positive delta in III, and negative delta in V1
B. R/S transition between V2 and V3 or between V3 and V4 but the delta
amplitude in lead II ≥1.0 mV (septal location), and the sum of delta polarities
in inferior leads is −1, 0, or +1 mV
C. Negative QRS in leads III, V1, and aVF, tallest precordial R in leads V2–V4
and R wave width in V1 <0.06 msec
a
A, algorithm of Chiang and colleagues; B, algorithm of Fitzpatrick and colleagues; C, algorithm of Xie and colleagues.
BT, Bypass tract; R/S, R-S wave ratio.
From Katsouras CS, Greakas GF, Goudevenos JA, et al. Localization of accessory pathways by the electrogram. Pacing Clin Electrophysiol.
2004;27:189.
Right Posteroseptal BTs
A. R/S ≥1 in V2 and no positive delta in III and V1
B. The sum of delta polarities in inferior leads is less than or equal to −2 mV
C. Negative QRS in leads III, V1, and aVF and tallest precordial R in V5 or V6
Right Posterior/Right Posterolateral BTs
A. R/S <1 in V2, no positive delta in III and no negative delta in V1, and negative
delta polarity in aVF
B. R/S transition between V3 and V4 with delta amplitude in lead II <1.0 mV
or ≥V4 and the delta axis is <0 degrees and the R in lead III is ≤0 mV
C. Positive QRS in III, negative in V1, and RS morphology in aVL
Right Lateral/Right Anterolateral BTs
A. R/S <1 in V2, no positive delta in III and no negative delta in V1 and negative
or biphasic delta in aVF
B. R/S transition between leads V3 and V4 with delta amplitude in lead II
<1.0 mV or >V4 and the delta axis is <0 degrees and the R amplitude in lead
III is <0 mV
C. Positive QRS in leads aVL and III and negative in V1
Right Anterior/Right Superoparaseptal BTs
A. R/S <1 in V2, positive delta in III and no positive delta in V1
B. The sum of delta polarities in inferior leads is ≥2
C. Positive QRS in aVF and negative in leads III and V1

Step 1 Step 2 Step 3 Step 4

Lead I  or  Lead II  V1  or  Remaining
or
V1 R/S1

Left free wall CS/MCV Septal Right free wall

Sens. 95% 100% 97%
Spec. 99% 95% 88%
PPV 99% 62% 94%
aVF   or  aVF    aVF  

QRS 0° 0° QRS   

axis axis
LL LP RA RAP RL RP
LAL LPL AS MS LPS RPS RAL RPL
Sens. 93% 68% 100% 80% 80% 70% 87% 91% 100%
Spec. 68% 93% 96% 90% 84% 100% 95% 97% 96%
PPV 90% 76% 87% 40% 47% 100% 93% 91% 89%

Fig. 18.17  Algorithm for Localization of Bypass Tract Using Delta Wave Morphology on the Surface
Electrocardiogram. +, Positive delta wave; ±, isoelectric delta wave; −, negative delta wave; AS, right
anteroseptal; CS/MCV, coronary sinus/middle cardiac vein; LAL, left anterolateral; LL, left lateral; LP, left
posterior; LPL, left posterolateral; LPS, left posteroseptal; MS, midseptal; PPV, positive predictive value;
RA, right anterior; RAL, right anterolateral; RAP, right anterior paraseptal; RL, right lateral; RP, right posterior;
RPL, right posterolateral; RPS, right posteroseptal; R/S, R-S wave ratio; Sens., sensitivity; Spec., specificity.
(From Arruda M, Wang X, McClelland J. ECG algorithm for predicting sites of successful radiofrequency
ablation of accessory pathways [abstract]. Pacing Clin Electrophysiol. 1993;16:865.)
620 CHAPTER 18  Typical Atrioventricular Bypass Tracts

R/S  1
V2

No Yes

Delta () Delta ()

III

No Yes No Yes

Delta () Delta () Delta () LL/LAL

V1
98.2%

No Yes No Yes No Yes

MS LL/LAL RPS

83.3% 100% 80%

RAS/RA

90.9%
Delta V1
in aVF R/S  1

() () () No Yes

RP/RPL RAL LPS LP/LPL

94.1% 90% 86.7% 96.4%

RL

90%
Fig. 18.18  Stepwise Algorithm for Localization of the Bypass Tract (BT) by Delta Wave Polarity. Numbers
indicate the accuracy of the algorithm for each BT location. LAL, Left anterolateral; LL, left lateral; LP, left
posterior; LPL, left posterolateral; LPS, left posteroseptal; MS, midseptal; RA, right anterior; RAL, right
anterolateral; RAS, right anteroseptal; RL, right lateral; RP, right posterior; RPL, right posterolateral;
RPS, right posteroseptal; R/S, R-S wave ratio. (From Chiang CE, Chen SA, Teo WS, et al. An accurate step-
wise electrocardiographic algorithm for localization of accessory pathways in patients with Wolf-Parkinson-
White syndrome from a comprehensive analysis of delta waves and R/S ratio during sinus rhythm. Am J
Cardiol. 1995;6:40.)

complex in lead I (i.e., rightward axis). Conversely, BTs closer to the
right axilla are strongly positive in lead I (i.e., leftward axis). Leads II/
aVL and III/aVR also have net leftward and rightward vectors, respec-
tively. Hence, as the BT location moves progressively to the left (e.g.,
from anterior to lateral mitral annulus), the delta wave assumes pro-
gressively less positive/more negative deflection in lead I, a taller R wave
in lead III than in lead II, and a larger S wave in lead aVL compared
to lead aVR. Opposite changes are expected as the BT location moves
progressively to the right (from anteromedial to lateral tricuspid annulus).
Frontal plane vertical axis.  The inferior leads (II, III, and aVF)
reflect the vertical axis. Therefore BTs located at the superior aspect of
the tricuspid or mitral annulus exhibit positive deflections in the inferior
leads (i.e., vertical axis). The magnitude of the inferiorly directed vector
diminishes as the site of origin shifts from superior to inferior regions
of either annulus.
Left vs. right free-wall BTs.  Delta wave polarity in right precordial
leads is most helpful in distinguishing between right- and left-sided
free-wall BTs. Ventricular activation originating from the right ventricle
(RV) (as mediated by right-sided BTs) is expected to produce a pre-
dominantly negative deflection in right precordial leads, whereas more
posterior or left-sided sites of origin produce more positive deflections.
Hence, an R/S ratio greater than 1 or a dominant R wave in lead V1 is
consistent with left-sided BTs, whereas R/S transition after lead V2
suggests right-sided BTs. When the R/S transition is at lead V2 or between
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 621

Q or isoelectic delta
in I, aVL, or V6

Yes No

LBBB Q or isoelectic delta

in two of the inferior leads
(II, III, aVF)
Yes No Yes No

RAS LL Rs or RS LBBB
in V1, V2, or V3
Yes No

Yes No

PS RL

QRS axis Rs or RS
> +30° in V1 or V2

Yes No Yes No

RAS RL LL Undetermined
Fig. 18.19  Algorithm of Bypass Tract Localization Based on Delta Wave Morphology on the Surface
Electrocardiogram. LBBB, Left bundle branch block-type pattern (QRS ≥90 milliseconds in lead I with an
rS pattern in leads V1 or V2); LL, left lateral; PS, posteroseptal; RL, right lateral; RAS, right anteroseptal; QRS
> 30°, QRS axis >+30°. (From Fox DJ, Klein GJ, Skanes AC, Gula LJ, Yee R, Krahn AD. How to identify the
location of an accessory pathway by the 12-lead ECG. Heart Rhythm. 2008;5:1763–1766.)

Step 1 R/S ratio in V1 ≥ 0.5 LV, BTs originating from the anterior mitral annulus exhibit larger R
wave amplitudes in the inferior leads. As the BT location shifts pro-
No Yes
gressively more laterally, R wave amplitude becomes progressively larger
in lead III and smaller in lead II. The delta wave amplitude ratio in
Step 3 R/S ratio in V2 ≥ 0.5 Step 2 R/S ratio in aVF ≥ 1 leads III/II is greater than 1 for posterolateral BTs and less than 1 for
anterolateral BTs. BTs located at the inferior aspects of the mitral annulus
No Yes No Yes
exhibit negative delta waves in the inferior leads. Furthermore, BT
locations at the lateral aspect of the mitral annulus produce a more
Step 4 R/S ratio in aVF ≥ 1 Left or right negative delta wave in the left lateral limb leads (aVL and I) than
LPL/LP LA/LL
MS/PS anterior or posterior annular locations. In fact, a negative delta wave
Yes No
in the left lateral leads (aVL, I, and V6) is pathognomonic of a left
lateral BT.
RAS/RA/RL RPL/RP Right-sided BTs.  BTs arising from the tricuspid annulus demon-
Fig. 18.20  Stepwise Electrocardiogram Algorithm for the Determina- strate negative delta wave polarity in the right precordial leads and
tion of Bypass Tract Location. LA, Left anterior; LL, left lateral; LP, positive polarity in leads V5 and V6. As the BT location moves from
left posterior; LPL, left posterolateral; MS, midseptal; PS, posteroseptal; medial/septal to lateral locations along the tricuspid annulus, the pre-
RA, right anterior; RAS, right anteroseptal; RL, right lateral; RP, right cordial transition becomes later (at lead V3 in septal locations, and
posterior; RPL, right posterolateral. (From Taguchi N, Yoshida N, Inden after lead V3 in free-wall locations) and the negative delta wave becomes
Y, et al. A simple algorithm for localizing accessory pathways in patients deeper in anterior precordial leads (V1 to V3). Right-sided BTs typically
with Wolff-Parkinson-White syndrome using only the R/S ratio. J Arrhyth- display a large positive delta wave in the left lateral limb leads (aVL
mia. 2014;30:439–443.)
and I), but a predominantly negative delta wave in lead aVR. Delta
wave polarity in the inferior leads is positive in anterior annular BTs.
leads V1 and V2, the R/S wave in the left lateral limb leads (I and aVL) As the BT location moves laterally and inferiorly, the delta wave becomes
favors right-sided BTs, otherwise left-sided BTs are likely. more negative in the inferior leads. Positive delta waves in leads II and
Left-sided BTs.  All left free-wall BTs exhibit positive delta wave aVF are consistent with anteroseptal locations, whereas negative delta
polarity in the right precordial leads, an R/S ratio greater than 1, or a waves in the inferior leads suggest posteroseptal locations. Flat or biphasic
dominant R wave in lead V1. Because of its superior location in the delta waves suggest midseptal locations.
622 CHAPTER 18  Typical Atrioventricular Bypass Tracts

I I I I I I I I I

II II II II II II II II II

III III III III III III III III III

aVR aVR aVR aVR aVR aVR aVR aVR aVR

aVL aVL aVL aVL aVL aVL aVL aVL aVL

aVF aVF aVF aVF aVF aVF aVF aVF aVF

V1 V1 V1 V1 V1 V1 V1 V1 V1

V2 V2 V2 V2 V2 V2 V2 V2 V2

V3 V3 V3 V3 V3 V3 V3 V3 V3

V4 V4 V4 V4 V4 V4 V4 V4 V4

V5 V5 V5 V5 V5 V5 V5 V5 V5

V6 V6 V6 V6 V6 V6 V6 V6 V6

A B C D E F G H I
(LAL) (LL) (LPL) (LP) (LPS) (RPS) (MS) (RAS) (RL)

H
A
I
G
B
E F
C
D

Fig. 18.21  Delta Wave Morphology on the Surface Electrocardiogram (ECG) During Ventricular Preex-
citation. Representative surface 12-lead ECG of delta wave morphology (top panels) with the corresponding
location of the successful ablation site around the valvular annulus on an anatomic illustration (bottom). (A)
left anterolateral (LAL); (B) left lateral (LL); (C) left posterolateral (LPL); (D) left posterior (LP); (E) left postero-
septal (LPS); (F) right posteroseptal (RPS); (G) midseptal (MS); (H) right anteroseptal (superoparaseptal, RAS);
(I) right lateral (RL). MV, Mitral valve; TV, tricuspid valve. (Anatomic illustration of mitral and tricuspid annuli
is shown at the bottom [from Netter Images {www.netterimages.com} with permission].)
 CHAPTER 18  Typical Atrioventricular Bypass Tracts
Anteroseptal BTs.  Right superoparaseptal (anteroseptal) BTs connect
the RA and RV free walls at the anteromedial aspect of the tricuspid
annulus. Because of its relatively superior and anterior ventricular inser-
tion compared to the rest of the ventricular mass, these BTs exhibit
positive delta waves in the inferior leads (II, III, and aVF). In addition,
delta waves are often negative in leads V1 and V2, but slightly positive
(R/S < 1) delta waves also are observed. Similar to right free-wall BTs,
delta waves are typically positive in leads I and aVL and negative in
lead aVR.
Midseptal BTs.  The delta wave is positive in lead II, predominantly
negative in lead III, and negative or isoelectric in lead aVF. The delta
wave in lead V1 is usually negative and R/S transition occurs after lead
V2 (usually between leads V2 and V3). However, variations are not
infrequent, especially in the inferior leads and in V2. Midseptal BTs can
be differentiated from superoparaseptal and para-Hisian BTs by a nega-
tive delta wave in lead III, a biphasic delta wave in lead aVF, and a larger
R/S ratio in lead V2, likely due to the posterior location of the AV
septum compared to the anterior tricuspid annulus.23
Posteroseptal BTs.  Posteroseptal BTs are characterized by a deeply
negative delta wave in lead III. The delta wave is often negative in lead
aVF, especially for right posteroseptal BT locations. A negative delta
wave in lead II predicts an epicardial location of the posteroseptal BT.
The delta wave in lead V1 can be negative, isoelectric, or positive. Lead
V2 typically displays a positive delta wave, with the R wave larger than
the S wave. A negative delta wave polarity in lead V1 with abrupt transi-
tion to positive polarity (with R/S ratio greater than 1) in lead V2 favors
a right-sided location of the posteroseptal BT, whereas left posteroseptal
BTs are often associated with biphasic or positive delta wave polarity
in leads V1 and V2. An R/S ratio greater than 1 in lead V1 is a more
accurate marker of left posteroseptal BTs. The tallest precordial R wave
is typically recorded in the midprecordial leads (V2 to V4) in left pos-
teroseptal BTs, and in the lateral precordial leads (V5 or V6) in right
posteroseptal BTs.
Localization Using Polarity of the Retrograde
P Wave Morphology
The polarity of the retrograde P waves during orthodromic AVRT is
dependent on the location of the atrial insertion of the BT, and is helpful
in localizing the BT. However, the P wave is usually inscribed within
the ST segment and its morphology may not be easily determined.24,25
In general, P wave morphology in leads I and V1 and in the inferior
leads is most helpful (Fig. 18.22). A negative P wave vector in lead I is
highly suggestive of left free-wall BTs, whereas a positive vector is sug-
gestive of right free-wall BTs. On the other hand, a negative P wave in
lead V1 predicts right-sided BTs. P wave polarity in the inferior leads,
positive or negative, suggests superior or inferior location of the BT,
respectively.24,25
Left free-wall BTs have positive P waves in lead V1 and negative P
waves in leads I and aVL. If the retrograde P wave is negative in all
three inferior leads, the BT is located at the inferoposterior mitral annulus.
As the BT location moves to the lateral mitral annulus, the P wave
becomes isoelectric or biphasic in one of the three inferior leads. The
P wave becomes positive in all inferior leads for left anterior/anterolateral
BTs. Thus, as the BT moves from posterior to anterior locations along
the mitral annulus, the positive P wave is seen initially in lead III, fol-
lowed by lead aVF and lead II.24,25
For right free-wall BTs, the P wave is negative in lead V1 and positive
or isoelectric in lead I. If the P wave is positive in all inferior leads, the
BT is located in the anterior wall. If the P wave is negative in all inferior
leads, the BT is located in the posterior wall. However, moving from
the posterior to the anterior location, the positive P wave is seen initially
in lead II, followed by lead aVF and lead III.24
623
Posteroseptal BTs display positive P waves in leads V1, aVR, and
aVL, and isoelectric or biphasic P waves in lead I. P waves are negative
in all inferior leads (II, III, aVF). Left posterior BTs also have negative
P waves in the inferior leads, but the P waves are more negative in lead
II than in lead III and are more positive in lead aVR than in lead aVL.
Discrimination between left and right posteroseptal BTs based on P
wave morphology is limited. In contrast, anteroseptal BTs display posi-
tive P waves in inferior leads and biphasic P waves in lead V1.24
ELECTROPHYSIOLOGICAL TESTING
EP testing is used to study the features, location, and number of BTs
and the tachycardias, if any, associated with them (Box 18.3). Typically,
three quadripolar catheters are positioned in the high RA, RV apex or
septum, and HB region, and a decapolar catheter is positioned in the
CS (see Fig. 4.4). If a right-sided BT is suspected, a duo-decapolar
(Halo) catheter along the tricuspid annulus can be helpful.
Some investigators have advocated a simplified approach to abla-
tion using only one or two catheters. Although often successful, 10%
of patients with preexcitation have multiple arrhythmias, and 10% to
20% of such patients have multiple BTs that can result in a very complex
procedure. Because it is difficult to know beforehand in any given patient
whether the procedure will be straightforward or complex, the single-
catheter approach to ablation of arrhythmias should be discouraged.26
Baseline Observations During Sinus Rhythm
Ventricular preexcitation is associated with a short His bundle–ventricular
(HV) or H-delta interval during NSR. The HV interval can even be
negative or the His potential can be buried in the local ventricular
electrogram. The QRS is a fusion between conduction over the BT and
that over the AVN-HPS. The site of earliest ventricular activation is
near the ventricular insertion site of the BT (i.e., near the tricuspid
annulus or mitral annulus at the base of the heart). Slowing of conduc-
tion in the AVN by carotid sinus massage, AVN blockers, or rapid atrial
pacing unmasks and increases the degree of preexcitation, because these
maneuvers do not affect the conduction over the BT. Dual AVN pathways
are present in 8% to 40% of patients.
Programmed Atrial Stimulation During Sinus Rhythm
In the presence of a manifest AV BT, atrial stimulation from any atrial
site can help unmask preexcitation if it is not manifest during NSR
because of fast AVN conduction. Incremental rate atrial pacing and
progressively premature AES produce decremental conduction over the
AVN (but not over the BT), increasing the degree of preexcitation and
shortening the HV interval, until the His potential is inscribed within
BOX 18.3  Goals of Electrophysiological
Evaluation in Patients With Wolff-Parkinson-
White Syndrome
• Confirming the presence of an atrioventricular BT
• Evaluation for the presence of multiple BTs
• Localization of the BT(s)
• Evaluation of the refractoriness of the BT and its implications for life-
threatening arrhythmias
• Induction and evaluation of tachycardias
• Demonstration of the BT role in the tachycardia
• Evaluation of other tachycardias not dependent on the presence of the BT
• Termination of the tachycardias
BT, Bypass tract.
624 CHAPTER 18  Typical Atrioventricular Bypass Tracts

V1 pseudo r’ or
II, III, AVF pseudo S

Yes NO

V1
AVNRT
ant.
+ ± –
42/42
(100%)

III INF INF

– ± + 2+ 2– 2+ 2–

I AVF

± – ± +

d-RP

>20 ≤20
msec msec

AVNRT RPS LP LL LA RAS RMS RA RP

post. LPS

3/4 21/24 15/16 25/28 10/12 4/5 3/4 12/14 14/15

(75%) (87.5%) (93.8%) (89.3%) (83.3%) (80%) (75%) (85.7%) (93.3%)
Fig. 18.22  Stepwise Algorithm for Predicting Bypass Tract Location Based on Retrograde P Wave
Morphology During Orthodromic Atrioventricular Reentrant Tachycardia. The accuracy of the algorithm
is indicated based on results of a prospective study in 164 patients. The denominator is the total number of
patients in that group; the numerator is the number of patients with correct predictions. AVNRT, Atrioven-
tricular nodal reentrant tachycardia; INF, inferior leads (II, III, aVF); LA, left anterior; LL, left lateral; LP, left
posterior; LPS, left posteroseptal; RA, right anterior; RAS, right anteroseptal; RMS, right midseptal; RP, right
posterior; RPS, right posteroseptal. (From Tai CT, Chen SA, Chiang CE, et al. A new electrocardiographic
algorithm using retrograde P waves for differentiating atrioventricular node reentrant tachycardia from atrio-
ventricular reciprocating tachycardia mediated by concealed accessory pathway. J Am Coll Cardiol. 1997;29:
394–402.)

the QRS. The His potential remains activated anterogradely over the
AVN until anterograde block in the AVN occurs; the QRS then becomes
fully preexcited, and the His potential becomes retrogradely activated
(Fig. 18.23).
Atrial stimulation close to or at the AV BT insertion site results in
maximal preexcitation and the shortest P-delta interval because of the
lack of intervening atrial tissue whose refractoriness may otherwise
limit the ability of atrial stimulation to activate the AV BT as early (Fig.
18.24). Atrial pacing can reveal the presence of multiple BTs (eFig.
18.4). Rare cases of catecholamine-dependent BTs have been reported
that require isoproterenol infusion to manifest preexcitation that is
absent at baseline.
The failure of atrial stimulation to increase the amount of preex-
citation can be caused by: (1) markedly enhanced AVN conduction;
(2) the presence of another AV BT; (3) pacing-induced block in the
AV BT because of a long ERP of the BT (longer than that of the AVN);
(4) total preexcitation already present at the basal state caused by pro-
longed or absent AVN-HPS conduction; (5) decremental conduction
in the BT; or (6) the presence of a fasciculoventricular BT rather than
an AV BT.
Programmed Ventricular Stimulation During Sinus Rhythm
Retrograde ventriculoatrial conduction.  The normal AVN response
to rate-incremental ventricular pacing or progressively premature single
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 624.e1

II

III

V1

V6

HRA
Hisprox

Hismid
Hisdist
CSprox

S S S S

CSdist

RVA
200 msec
eFig. 18.4  Atrial Pacing in the Presence of Two Bypass Tracts (BTs). Surface electrocardiogram and
intracardiac recordings during coronary sinus pacing (S) in a patient with both right and left lateral BTs. The
first two complexes show a left lateral preexcitation pattern (red arrows), whereas this pathway fails to
conduct on the last two complexes, which show a right lateral preexcitation pattern (blue arrows). CSdist,
Distal coronary sinus; CSprox, proximal coronary sinus; Hisdist, distal His bundle; Hismid, middle His bundle;
Hisprox, proximal His bundle; HRA, high right atrium; RVA, right ventricular apex.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 625

Effect of AES on preexcitation

II

V1
440 msec S2
HRA S1 600 msec S1
A A A H
H H
His

CSprox

CSdist

RVA
A

II

V1
350 msec
HRA S1 600 msec S1 S2

A A H
H A H
His

CSprox

CSdist

RVA
B

II

V1
190 msec
HRA S1 600 msec S1 S2
H’ A
A A A (ECHO)
His H

CSprox

CSdist

RVA
C
Fig. 18.23  Effect of Atrial Extrastimulation (AES) on Preexcitation. (A) Preexcitation is manifest during
normal sinus rhythm and atrial pacing associated with a short His bundle–ventricular (HV) interval (−11 mil-
liseconds). AES produces decremental conduction over the atrioventricular node (AVN) (with prolonged
atrial–His bundle interval) but not over the bypass tract (constant P-delta interval), increasing the degree of
preexcitation with the His potential inscribed within the QRS (HV interval of −64 milliseconds). (B) An earlier
coupled AES produces more pronounced preexcitation and an HV interval of −93 milliseconds. (C) A more
premature AES produces full preexcitation with the His bundle activated retrogradely (H′), followed by ven-
triculoatrial conduction over the AVN and an echo beat (atrioventricular reentry). A, Atrial electrogram; CSdist,
distal coronary sinus; CSprox, proximal coronary sinus; H, His bundle potential; HRA, high right atrium; RVA,
right ventricular apex.
 Effect of site of pacing on preexcitation

II

V1

S1 S1 S1 S2
HRA
600 msec 600 msec 200 msec
His

CSprox

CSdist

RVA

II

V1

HRA

His

CSprox

S1 S1 S1 S2
S2
CSdist
600 msec 600 msec 200 msec
RVA

B
Fig. 18.24  Effect of Site of Pacing on Preexcitation. (A) In the presence of a manifest left lateral bypass
tract (BT), pacing from the high right atrium at a cycle length (CL) of 600 milliseconds produces minimal
preexcitation. The degree of preexcitation increases with premature stimulation because of delay in atrio-
ventricular nodal conduction. (B) In the same patient, pacing at the same CLs from the distal coronary sinus,
close to or at the BT insertion site, results in a larger degree of preexcitation and shorter P-delta interval
because of the lack of intervening atrial tissue whose refractoriness might otherwise limit the ability of atrial
stimulation to activate the BT as early. CSdist, Distal coronary sinus; CSprox, proximal coronary sinus; HRA,
high right atrium; RVA, right ventricular apex.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 627

ventricular extrastimulation (VES) is a gradual delay of VA conduction Ventricular stimulation resulting in eccentric retrograde atrial acti-
(manifest as gradual prolongation of the VA and His bundle–atrial vation sequence not consistent with normal conduction over the AVN
[HA] intervals) as the PCL or VES coupling interval decreases. Con- is consistent with VA conduction over an AV BT (see Fig. 18.25). Ven-
versely, nondecremental VA conduction characterizes BT conduction. tricular pacing can also reveal the presence of multiple BTs (Fig. 18.26).
Nonetheless, some BTs with retrograde decremental conduction proper- However, a concentric retrograde atrial activation sequence does not
ties can also exhibit prolongation of conduction time and VA interval exclude the presence of a septal or paraseptal BT or a free-wall BT when
with ventricular pacing or VES. In addition, at short ventricular PCLs VA conduction is mediated by the AVN. In addition, AVN slow pathway
or VES coupling intervals, intramyocardial conduction delay can occur, conduction can be associated with an eccentric atrial activation sequence
resulting in prolongation in the VA interval; however, the local VA interval in the CS. Accurate analysis of an atrial activation sequence frequently
at the BT location remains unchanged. Furthermore, short ventricular
PCLs or VES coupling intervals can encroach on the BT refractoriness,
causing some decremental conduction, with a consequent increase in
the surface VA interval and the local VA interval.
The absence of VA conduction (at long ventricular PCLs) or the pres-
ence of decremental VA conduction makes the presence of a retrogradely II
conducting BT unlikely, except for the rare catecholamine-dependent V1
BTs that require isoproterenol infusion for demonstration.
Retrograde atrial activation sequence.  In the presence of a ret- HRA
rogradely conducting AV BT (whether manifest or concealed), VES His
during NSR can result in VA conduction over the BT, AVN, both, or CSprox
neither (Fig. 18.25). Conduction over the BT alone is the most common
pattern at short PCLs or short VES coupling intervals. In this setting, CSdist
the VA conduction time is fairly constant over a wide range of PCLs RVA 600 msec 350 msec
S1 S1 S2
and VES coupling intervals (given the absence of intraventricular con- A
duction abnormalities or additional BTs). On the other hand, retrograde
conduction over both the BT and HPS-AVN is especially common
II
when RV pacing is performed at long PCLs or long VES coupling inter-
vals and in the presence of a left-sided BT. This occurs because it is V1
easier to engage the RB and conduct retrogradely through the AVN
than it is to reach a distant left-sided BT. In this setting, the atrial HRA
activation pattern depends on the refractoriness and conduction times His
over both pathways and usually exhibits a variable degree of fusion. In CSprox
addition, VA conduction can proceed over the HPS-AVN alone, result-
ing in a normal pattern of VA conduction, or can be absent because of CSdist
block in both the HPS-AVN and BT, which is especially common with RVA 600 msec 330 msec
S1 S1 S2
short PCLs and very early VES. B

II

V1

Fig. 18.25  Retrograde Conduction During Ventricular Extrastimula-

HRA
tion (VES) in a Patient With a Bidirectional Left Lateral Bypass Tract
(BT). (A) The ventricular pacing drive is conducted retrogradely over the His
atrioventricular node (AVN) with a concentric atrial activation sequence. CSprox
The VES is conducted over both the AVN and BT (atrial fusion). (B) An
earlier VES encounters delay in the His-Purkinje system (HPS)–AVN and CSdist
conducts solely over the BT with an eccentric atrial activation sequence. RVA S1 600 msec 300 msec
S1 S2
(C) An early-coupled VES blocks retrogradely in the BT and conducts
solely over the AVN. (D) The VES conducts only over the HPS-AVN with
C
more pronounced ventriculoatrial (VA) delay, which allows recovery of
the BT and anterograde conduction, initiating antidromic atrioventricular
II
reentrant tachycardia (AVRT). The VA delay is provided by conduction
delay, not only within the AVN but also within the HPS. Note that the V1
VES encounters retrograde block in the right bundle branch, and His
bundle activation is mediated by retrograde conduction over the left
HRA
bundle branch. Consequently, the His potential is visible after the ven- H1 H1
H2 H H
tricular electrogram. Note that despite the fact that the H1-H2 interval His
318 msec 315 msec
following VES approximates the H-H interval during supraventricular CSprox
tachycardia (SVT), the His bundle–atrial interval following the initiating
VES is shorter than that during the SVT, which favors antidromic AVRT CSdist
over preexcited atrioventricular nodal reentrant tachycardia as the mecha- RVA 600 msec 290 msec
S1 S1 S2
nism of the SVT. CSdist, Distal coronary sinus; CSprox, proximal coronary
sinus; HRA, high right atrium; RVA, right ventricular apex. D
628 CHAPTER 18  Typical Atrioventricular Bypass Tracts

II

III

V1

V6

HRA

Hisprox

Hismid

Hisdist

CSprox

CSdist

RVA
S S S S
400 msec
Fig. 18.26  Ventricular Pacing Revealing the Presence of Multiple Bypass Tracts (BTs). The first complex
shows sinus rhythm with preexcitation, showing a left free-wall pattern. Four complexes of right ventricular
apical (RVA) pacing follow, the first two paced complexes (S) show fusion of retrograde activation over both
a left lateral BT (red arrows), which is present in each complex, and a right lateral BT (blue arrows). The last
two paced complexes conduct over the left lateral BT. Dashed lines aid in comparing activation sequences.
CSdist, Distal coronary sinus; CSprox, proximal coronary sinus; Hisdist, distal His bundle; Hismid, middle His bundle;
Hisprox, proximal His bundle; HRA, high right atrium.

requires the use of multielectrode catheters around the tricuspid annulus
and deep in the CS.27
VES during HB refractoriness.  A VES delivered when the HB is
refractory (i.e., when the His potential is already manifest or within 35
to 55 milliseconds before the time of the expected His potential) that
results in atrial activation is diagnostic of the presence of a retrogradely
conducting BT. Because the HPS-AVN is already refractory and cannot
mediate VA conduction, retrograde atrial activation from ventricular
stimulation has to be mediated by a BT.
Furthermore, an early coupled VES that results in an atrial activation
that either precedes HB activation (Fig. 18.27) or is associated with an
apparent HA interval shorter than that during drive complexes indicates
“atrial preexcitation” via an AV BT.
Importantly, if a VES delivered when the HB is refractory does not
result in atrial activation, this does not necessarily exclude the presence
of a retrogradely conducting AV BT, because such a VES can be associ-
ated with retrograde block in the BT itself (see Fig. 18.25). In addition,
the lack of such a response does not exclude the presence of unidirec-
tional (anterograde-only) AV BTs.
Retrograde RBBB during VES.  During the delivery of progressively
premature single VESs, an abrupt increase in the VA conduction interval
is often observed. This can be due to a variety of reasons including: (1)
retrograde block in the AVN fast pathway and subsequent VA conduc-
tion over the slow pathway; (2) retrograde block in the RB and subsequent
retrograde conduction over the left bundle branch (LB); or (3) retrograde
block in the BT and subsequent VA conduction only over the AVN.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 629

I
II
III
V1
V6
HRA
Hisprox
Hismid
Hisdist
CSprox

CSmid

CSdist

RVA
S1 200 msec S1 S2
Fig. 18.27  Ventricular Extrastimulation Revealing the Presence of a Bypass Tract (BT). A retrograde His
potential is present on both drive complexes (S1) and following the extrastimulus (arrows). Although atrial
activation also follows each stimulus, it occurs (dashed line) before the inscription of the His potential on
the ventricular extrastimulus (S2). Thus a BT is present because atrial activation is not dependent on His
bundle–atrioventricular activation. CSdist, Distal coronary sinus; CSmid, middle coronary sinus; CSprox, proximal
coronary sinus; Hisdist, distal His bundle; Hismid, middle His bundle; Hisprox, proximal His bundle; HRA, high
right atrium; RVA, right ventricular apex.

Retrograde RBBB occurs frequently during VES testing, and can be
diagnosed by observing the retrograde His potential during the drive
train and its abrupt delay following the VES. Often, however, it is dif-
ficult to visualize the retrograde His potential during the pacing train;
nevertheless, the sudden appearance of an easily distinguished retrograde
His potential, separate from the ventricular electrogram following the
VES, can be sufficient to recognize retrograde RBBB.
Prolongation of the ventriculo-His (VH) interval is observed on
development of retrograde RBBB because conduction must traverse
the interventricular septum (which requires approximately 60 to 70
milliseconds in normal hearts), enter retrograde via the LB, and ascend
to reach the HB. Although an increase in the VH interval necessarily
occurs with retrograde RBBB, whether a similar increase occurs in the
VA interval depends on the nature of VA conduction (over the AVN
vs. BT).
Measurement of the effect of the development of retrograde RBBB
during VES on the retrograde VH and VA intervals can help distinguish
between retrograde AVN and BT conduction. In the absence of a BT,
the AVN can be activated in a retrograde fashion only after retrograde
activation of the HB; as a consequence, VA activation will necessarily
be delayed with retrograde RBBB, and the increase in the VA interval
will be similar to the increase in the VH interval. On the other hand,
when retrograde conduction is via a BT, there will be no expected
increase in the VA interval when retrograde RBBB is induced. Thus the
increase in the VA interval is minimal and always less than the increase
in the VH interval.28
Differential-site RV pacing.  The response of the VA interval (i.e.,
the stimulus-to-atrial [SA] interval) and atrial activation sequence to
differential-site RV pacing (i.e., RV basal versus RV apical pacing) can
help demonstrate or exclude the presence of a retrogradely conducting
septal AV BT (Fig. 18.28).
The RV apex, although anatomically more distant from the atrium
than the RV base, is nonetheless electrically closer because of the prox-
imity of the distal RB to the pacing site. Consequently, in the absence
of a retrogradely conducting septal AV BT, pacing at the RV apex allows
entry into the rapidly conducting HPS and results in a shorter VA
interval during pacing from the apex than from the base. Pacing from
the RV base requires the paced wavefront to travel a longer distance by
muscle-to-muscle conduction to reach the RV apex and then propagate
retrogradely through the RB and HB. In other words, the VH interval
is shorter with pacing at the RV apex versus the RV base. In the pres-
ence of a retrogradely conducting septal BT, pacing at the RV base
allows the wavefront to access the BT rapidly and activate the atrium
with a shorter VA interval than during RV apical pacing, which is distant
from the ventricular insertion site of the BT (i.e., because the V-BT
interval is shorter with pacing at the RV base versus the RV apex).
In the absence of a retrogradely conducting BT, the atrial activation
sequence will be similar during pacing at the RV apex and at the RV
base because the atrium is activated exclusively over the AVN in both
settings. On the other hand, if a septal AV BT is present, atrial activation
results from VA conduction over the septal BT during pacing at the RV
base, and over the AVN, the BT, or a fusion of both during pacing at
the RV apex. Therefore a change in the retrograde atrial activation
sequence in response to RV base versus RV apex pacing indicates the
presence of an AV BT, but a constant atrial activation sequence is not
helpful in excluding the presence of a BT.
Of note, the exact entrance to the HPS (i.e., the terminus of the
RB) is difficult to identify; the entrance site can be located in the
630 CHAPTER 18  Typical Atrioventricular Bypass Tracts

Preablation

Pacing from RV base Pacing from RV apex

II

V1

HRA

SA  44 msec SA  106 msec

AH AH H A H A
His
SH  60 msec SH  43 msec
CSprox

CSdist

RVA
A

Postablation

Pacing from RV base Pacing from RV apex

II

V1

HRA

SA  188 msec SA  189 msec

H A H A H A H A
His
SH  60 msec SH  43 msec
CSprox

CSdist

B RVA

Fig. 18.28  Differential-Site Right Ventricular (RV) Pacing in a Patient With Concealed Superoparaseptal
Bypass Tract (BT). In each panel, the first two complexes show RV basal-septal pacing, and the last two
complexes show RV apical pacing. (A) RV pacing is performed before ablation of the BT. The stimulus-to-
atrial (SA) (ventriculoatrial [VA]) interval is shorter during pacing at the RV base than during pacing at the RV
apex, suggesting VA conduction occurring over a BT. Note that atrial activation occurs even before His bundle
(HB) activation during pacing from the RV base, suggesting that VA conduction is independent of the atrio-
ventricular node (AVN). (B) RV pacing is performed after successful ablation of the BT. During pacing from
the RV apex, the SA interval is longer than before ablation, and it prolongs further by pacing at the RV base,
consistent with the occurrence of VA conduction exclusively over the AVN. Note that in both panels the
stimulus–His bundle (SH) (ventriculo-His) interval during RV apical pacing is shorter than that during RV basilar
pacing because of the faster access of the paced wavefront to the right bundle branch–His bundle (RB-HB)
during pacing at the RV apex. However, when VA conduction occurs over a BT (A), the SA interval remains
constant; in contrast, in the absence of a BT (B), the SA interval shortens, coinciding with shortening of the
S-H interval during pacing at the RV apex compared with pacing at the RV base. CSdist, Distal coronary sinus;
CSprox, proximal coronary sinus; HRA, high right atrium; RVA, right ventricular apex.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 631

midseptum and not at the RV apex. In such situations, both the RV
base and apex can be equidistant from the entrance to the HPS so that
pacing at either location will produce a constant VA interval during
retrograde conduction over the AVN. Therefore patient-to-patient vari-
ability with regard to the distance of the pacing catheter to the RB
terminus can potentially introduce conflicting results. This problem is
largely resolved by first pacing from the HB region (while avoiding HB
capture) and then moving the pacing catheter in a stepwise fashion
along the septum toward the RV apex. Pacing from sequential sites in
this path brings the catheter closer to the RB terminus (entrance of the
HPS), as reflected by shortening of the VA interval for AVN conduction,
but not for BT conduction. As the pacing catheter is moved farther
apically, the pacing sites become less useful diagnostically because the
relative distance from the RB terminus to the insertion of the BT becomes
less clear.29
This maneuver, however, does not exclude the presence of a distant
right or left free-wall BT because the site of pacing is far from the BT;
as a consequence, pacing from the RV apex or RV base may result in
preferential VA conduction exclusively over the AVN and a constant
atrial activation sequence. This can be avoided by moving the basal
pacing site closer to the putative BT location along the tricuspid or
mitral annulus.29
In addition, this maneuver does not exclude the presence of a slowly
conducting BT. The VA interval criterion identifies the actual route of
VA conduction and therefore the fastest path of this conduction; hence,
a slowly conducting BT would be missed in the presence of fast VA
conduction over the HPS-AVN.
The occurrence of RBBB (but not LBBB) can also alter the sig-
nificance of the VA interval criterion, especially when VA conduction
propagates over the HPS-AVN. In the presence of retrograde RBBB, VA
conduction occurs over the LB-HB; therefore the VA interval depends
on the distance between the pacing site and the LB rather than the
RB, and access of the paced wavefront to the LB can be faster for
RV basilar or septal pacing compared with pacing from the RV apex
(see Fig. 20.6).
Para-Hisian Pacing During Sinus Rhythm
Para-Hisian pacing helps demonstrate or exclude the presence of a
septal AV BT, which can mediate an orthodromic AVRT with a retro-
grade atrial activation sequence similar to that during AVNRT. The
response to para-Hisian pacing can be determined by comparing the
following four variables between HB-RB capture and noncapture while
maintaining local ventricular capture and no atrial capture: (1) atrial
activation sequence, (2) SA interval, (3) local VA interval, and (4) HA
interval (Figs. 18.29 and 18.30). Seven patterns of response to para-
Hisian pacing can be observed (see Box 20.1). Please refer to Chapter
20 for a more detailed discussion of para-Hisian pacing.30
Atrial activation sequence.  An identical retrograde atrial activa-
tion sequence, with and without HB capture, indicates that retrograde
conduction is occurring over the same system during HB-RB capture
and noncapture (either the BT or the AVN) and does not help prove
or exclude the presence of a BT. On the other hand, a retrograde atrial
activation sequence that is different, depending on whether the HB is
captured, indicates the presence of a BT.31
HA and ventriculoatrial intervals.  The HA and VA (SA) intervals
are recorded at multiple sites, including close to the site of earliest atrial
activation during SVT. A VA (SA) interval that is constant regardless
of whether the HB-RB is being captured indicates the presence of a BT,

Para-Hisian pacing

NSR RA  RV  HB RV only RV only RV  HB RV  HB

RBBB capture capture capture capture capture

II

V1

HRA
A SA  67 msec H SA  67 msec H SA  67 msec SA  67 msec
Hisprox H

S1 A S1 A S1 A S1 A S1 A
Hisdist
CSprox

CSdist

RVA

Fig. 18.29  Para-Hisian Pacing in a Patient With Concealed Midseptal Bypass Tract and Right Bundle
Branch Block (RBBB). The first complex is a sinus beat with RBBB. The second complex shows capture of
the atrium, ventricle, and His bundle–right bundle branch (HB-RB). Atrial capture is indicated by immediate
inscription of atrial electrogram following the pacing artifact. It is important to identify this occurrence to
avoid erroneous interpretation of the results of para-Hisian pacing. The third and fourth complexes show
right ventricle (RV)–only capture, and the last two complexes show RV and HB-RB capture but without atrial
capture. Note that the atrial activation sequence and stimulus-atrial (SA) intervals remain unchanged, regard-
less of whether HB-RB capture occurs, because retrograde ventriculoatrial (VA) conduction occurs over the
bypass tract in either case. During RV-only capture, the HB activation occurs after atrial activation, indicating
that VA conduction is independent of the atrioventricular node. Note that para-Hisian pacing could be per-
formed successfully even in the presence of RBBB if capture of the HB-RB is achieved proximal to the site
of block. CSdist, Distal coronary sinus; CSprox, proximal coronary sinus; Hisdist, distal His bundle; Hisprox, proximal
His bundle; HRA, high right atrium; RA, right atrium; NSR, normal sinus rhythm; RVA, right ventricular apex.
632 CHAPTER 18  Typical Atrioventricular Bypass Tracts

Preablation

RV-only capture RV and HB-RB capture

II

V1

HRA
SH  60 msec
AH AH A A
Hisprox

Hisdist S1 S1 S1 S1

SA  44 msec SA  44 msec
CSprox

CSdist

A RVA

Postablation

RV-only capture RV and HB-RB capture

II

V1

HRA
SH  60 msec
H A H A A A
Hisprox

Hisdist S1 S1 S1 S1

SA  194 msec SA  134 msec

CSprox

CSdist

B RVA
Fig. 18.30  Para-Hisian Pacing in a Patient With a Concealed Superoparaseptal Bypass Tract (BT). In
each panel, the first two complexes show right ventricle (RV)-only capture, and the last two complexes
show RV and His bundle–right bundle branch (HB-RB) capture. The loss of HB-RB capture is identified by
delay in the HB activation (stimulus–His bundle [SH] interval = 60 milliseconds) and widening of the QRS.
The His potential is not visible during HB-RB capture. (A) Para-Hisian pacing is performed before ablation of
the BT; the stimulus-atrial (SA) interval remains unchanged regardless of whether HB-RB capture occurs,
because retrograde ventriculoatrial (VA) conduction occurs over the BT in either setting. In fact, during RV-only
capture, the SA interval is shorter than the SH interval, indicating that VA conduction is independent of the
atrioventricular node (AVN). (B) Para-Hisian pacing is performed after successful ablation of the BT; the SA
interval is longer than before ablation, and it prolongs further on loss of HB-RB capture, concomitant with
delay in HB activation (i.e., prolongation in the SH interval) and a constant HA interval, indicating that VA
conduction is mediated only by the AVN. Note that the activation sequence before ablation (VA conduc-
tion occurring over the BT) is slightly different from after ablation (VA conduction occurring over the AVN).
However, in each case (preablation and postablation), the atrial activation sequence occurs over the same
pathway and remains constant, regardless of whether HB-RB occurs. CSdist, Distal coronary sinus; CSprox,
proximal coronary sinus; Hisdist, distal His bundle; Hisprox, proximal His bundle; HRA, high right atrium; RVA, right
ventricular apex.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 633

whereas prolongation of the VA (SA) interval on loss of HB capture,
compared with that during HB capture, excludes the presence of a
retrogradely conducting septal BT, except for slowly conducting and
far free-wall BTs.31
Dual-Chamber Sequential Extrastimulation
During Sinus Rhythm
Although the various ventricular pacing maneuvers described previously
can expose an eccentric or nondecremental atrial activation pattern
that suggests retrograde conduction over a BT rather than the AVN, in
certain circumstances, these maneuvers may not be adequate to confirm
the presence or absence of BT conduction, especially when the BT has
an ERP, retrograde atrial activation pattern, and conduction time similar
to the AVN. In particular, identification, mapping, and verification of
success of ablation of BT function can be challenging in the setting of
septal BTs with a retrograde activation pattern similar to retrograde
AVN conduction, slowly conducting BTs, as well as BTs with decremental
properties.32
Dual-chamber sequential extrastimulation is a useful maneuver for
identifying concealed slowly conducting BTs not revealed with standard
pacing maneuvers. This maneuver relies on concealed AVN conduction
during a critically timed AES to cause transient retrograde AVN blockade
at the time a VES is delivered, thereby allowing the BT to become
manifest with the VES (analogous to delivering a VES during SVT while
the HB is refractory).32
The dual-chamber sequential extrastimulation maneuver consists
of an eight-beat drive train of simultaneous atrial and RV pacing at
600 milliseconds, followed by an AES (A2) delivered at a coupling interval
equal to the AVN ERP, followed by a VES (V2) delivered at a coupling
interval equal to the drive train CL (600 milliseconds). Repeat drives
are then performed with decrements of 10 milliseconds for V2 until
VA block is observed.32
The critically timed A2 prolongs the AVN refractory period via
concealed anterograde conduction, causing V2 to block in the AVN
when it would have conducted had A2 not been delivered. If a BT is
present, V2 conducts back to the atrium while the AVN remains refrac-
tory, resulting in a retrograde atrial activation pattern consistent with
exclusive BT conduction. Although there can also be some degree of
concealed anterograde conduction into the BT during A2 stimulation,
the more pronounced decremental properties of AVN tissue should
prolong AVN refractoriness to a greater degree than that of the BT,
allowing exclusive retrograde conduction over the BT to remain intact
during V2 stimulation.32
This maneuver has several potential limitations. First, atrial ERP
may exceed anterograde AVN ERP. In addition, local atrial ERP at the
site of BT insertion can render the atrium refractory to the wavefront
traveling retrogradely over the BT. Therefore atrial pacing during this
maneuver should ideally be performed at a site in close proximity to
the atrial insertion of the BT if possible. Furthermore, the AES may
cause anterograde concealed conduction in the BT, potentially resulting
in BT conduction block during delivery of V2. The success of this pacing
maneuver relies on the differential effects of concealed conduction into
the AVN and BT, with greater extension of refractoriness in the former
than the latter.32
Induction of Tachycardia
Initiation by Programmed Atrial Stimulation
Orthodromic AVRT: bidirectional AVT BT.  In the presence of a
manifest AV BT, initiation of orthodromic AVRT with an AES requires
the following: (1) anterograde block in the AV BT; (2) anterograde
conduction over the AVN-HPS; and (3) slow conduction over the
AVN-HPS, with adequate delay to allow for the recovery of the atrium
and AV BT and subsequent retrograde conduction over the BT (Fig.
18.31; see Fig. 3.9). The first two requirements are facilitated by the
fact that, while the BT conducts more rapidly than the AVN, it has a
longer ERP, so the early atrial impulse blocks anterogradely in the BT
but conducts over the AVN. For the third condition, the site of AV delay
is not important; it is most commonly in the AVN, but it can also occur
in the HB, bundle branches, or ventricular myocardium. Because the
coupling intervals of the AES required to achieve anterograde block in

II

V1

Atrial pacing with preexcitation Anterograde BT block Orthodromic AVRT

HRA

His

CSprox

CSdist

RVA
Fig. 18.31  Induction of an Orthodromic Atrioventricular Reentrant Tachycardia (AVRT) Using a Bidi-
rectional Bypass Tract (BT) With Atrial Pacing. Rapid atrial pacing is initially associated with ventricular
preexcitation via a left lateral BT. With pacing at a progressively shorter cycle length, anterograde block in
the BT develops, as evident with loss ventricular preexcitation concurrent with prolongation of the PR interval.
Cessation of pacing is followed by initiation of orthodromic AVRT utilizing the same BT as the retrograde
limb of the reentry circuit. CSdist, Distal coronary sinus; CSprox, proximal coronary sinus; HRA, high right atrium;
RVA, right ventricular apex.
634 CHAPTER 18  Typical Atrioventricular Bypass Tracts

the BT are usually short, sufficient AVN delay is usually present so that
orthodromic AVRT is initiated once anterograde BT block occurs. The
presence of dual AVN physiology can facilitate the initiation of ortho-
dromic AVRT by providing adequate AV delay by mediating anterograde
conduction over the slow AVN pathway. BBB ipsilateral to the AV BT
provides an additional AV delay that can facilitate tachycardia
initiation.
Induction of orthodromic AVRT is easier with atrial stimulation at
a site in close proximity to the AV BT insertion site; the closer the
stimulation site is to the BT, the easier it is to encroach on the refrac-
tory period of the BT and achieve block, because it is not limited by
the refractoriness or conduction time of intervening atrial tissue. Fur-
thermore, the earlier the atrial insertion of the BT is activated, the more
likely it will recover before arrival of the retrograde wavefront to the
BT atrial insertion site, thereby facilitating reentry. Thus one may actu-
ally require less anterograde AV delay if recovery of excitability is shifted
earlier in time. In addition, different sites of atrial stimulation can
produce different AVN conduction velocities and refractoriness (even
at the same AES coupling intervals).
If SVT induction fails, the use of multiple AESs, rapid atrial pacing,
and pacing closer to the BT would achieve block in the BT and produce
adequate AV delay.
AES can also result in a 1:2 response caused by conduction over
both the BT and the AVN-HPS (i.e., a single AES resulting in two
ventricular complexes; the first is fully preexcited and the second is
normal). For this response to occur, significant delay in AVN-HPS con-
duction should be present (usually anterograde conduction is mediated
by the slow AVN pathway) to allow for recovery of the ventricle after
its activation via the BT. AES can also produce sinus nodal or AVN
echo beats that in turn may block in the BT and achieve adequate AV
delay to initiate orthodromic AVRT.
Orthodromic AVRT: concealed AV BT.  Orthodromic AVRT in
patients with concealed BTs is identical to that in patients with mani-
fest BTs (Figs. 18.32 and 18.33). The only difference is that in patients
with concealed BTs, anterograde block in the BT is already present.
Consequently, the only condition needed to induce orthodromic
AVRT is adequate AV delay (in the AVN or HPS) to allow for recovery
of the atrium and atrial insertion site of the AV BT. Therefore ortho-
dromic AVRT initiation requires less premature coupling intervals
of the AESs in patients with concealed BTs than in patients with
WPW.
Permanent junctional reciprocating tachycardia.  PJRT is usually
incessant and is initiated by spontaneous shortening of the sinus CL,
without a triggering PAC or PVC. The tachycardia can be transiently
terminated by PACs or PVCs but usually resumes after a few sinus beats
(eFig. 18.5). This phenomenon has three potential mechanisms: a rate-
related decrease in the retrograde ERP of the BT, a rate-related decrease
in atrial refractoriness that allows the impulse to reactivate the atrium
retrogradely over the BT, or a concealed Wenckebach block with block
at the atrial-BT junction terminating the Wenckebach cycle, relieving
any anterograde concealed conduction that may have prevented retro-
grade conduction up the BT. The latter is the most likely mechanism,
because such slow BTs actually demonstrate decremental conduction at
rapid rates and, in most cases, the atrial ERP at the atrial-BT junction
is shorter than the RP (VA) interval. Thus some sort of anterograde
concealment during NSR in the BT must be operative, preventing
tachycardia from always occurring. Late-coupled AESs can also readily
initiate PJRT.
Antidromic AVRT.  The initiation of antidromic AVRT by an AES
requires the following: (1) intact anterograde conduction over the BT;
(2) anterograde block in the AVN or HPS; and (3) intact retrograde
conduction over the HPS-AVN once the AVN resumes excitability

II

S1 S1 S2
HRA
400 msec 230 msec

His

CSprox

CSdist

RVA

Fig. 18.32  Induction of an Orthodromic Atrioventricular Reentrant Tachycardia Using a Concealed

Bypass Tract (BT) With Atrial Extrastimulation (AES). Note that the AES (S2) conducts with atrioventricular
(AV) delay, which allows for recovery of the atrium and atrial insertion site of the AV BT. The atrial activa-
tion sequence during the tachycardia is eccentric in the coronary sinus recording, consistent with left free
lateral BT. CSdist, Distal coronary sinus; CSprox, proximal coronary sinus; HRA, high right atrium; RVA, right
ventricular apex.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 634.e1

Carotid sinus pressure

III

aVF

eFig. 18.5  Permanent Junctional Reciprocating Tachycardia (PJRT). Two surface electrocardiogram leads
are shown during PJRT. Carotid sinus pressure is applied (at left), resulting in termination of the tachycardia
caused by block in the bypass tract (the tachycardia terminates with a QRS). Several escape and sinus
complexes follow, and then the SVT resumes. This phenomenon gives rise to the use of the term permanent
or incessant.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 635

II

HRA

His

S1 S1 S1
CSprox
230 msec 230 msec

CSdist

RVA

Fig. 18.33  Induction of an Orthodromic Atrioventricular Reentrant Tachycardia (AVRT) Using a Con-
cealed Bypass Tract (BT) With Atrial Pacing. The last atrial paced complex conducts anterogradely over
the slow atrioventricular nodal (AVN) pathway and results in an AVN echo beat (blue arrow and shade) and
simultaneous atrial and ventricular activation. The echo beat induces orthodromic AVRT with an eccentric
atrial activation sequence (red arrow and shade), consistent with left free lateral BT. Note that the VA interval
during the AVN echo beat is significantly shorter than that during orthodromic atrioventricular nodal reentrant
tachycardia. CSdist, Distal coronary sinus; CSprox, proximal coronary sinus; HRA, high right atrium; RVA, right
ventricular apex.

following partial anterograde penetration (see Fig. 18.23). The latter is
usually the limiting factor for the initiation of antidromic AVRT. A
delay of more than 150 milliseconds between atrial insertion of the BT
and HB is probably required for the initiation of antidromic AVRT.
Several mechanisms of antidromic AVRT initiation can be operative.
The AES can block in the AVN with anterograde conduction down the
BT and subsequent retrograde conduction over the HPS-AVN. In this
setting, VH interval prolongation is required to allow recovery of the
AVN. Because antidromic AVRTs have relatively short VA intervals, this
mechanism of initiation is probably uncommon, except with left-sided
BTs, which would potentially provide sufficient VH delay to allow ret-
rograde conduction. Tachycardia initiation can be facilitated by a short
retrograde AVN ERP, a common finding in patients with these SVTs.
Alternatively, the AES may block in the AVN, with anterograde conduc-
tion down the BT and subsequent retrograde conduction over a different
BT. Subsequent complexes can conduct retrogradely over the AVN-HPS
or the second BT. Changing TCL (and VA interval) may relate to whether
retrograde conduction proceeds over the AVN-HPS or the second BT.
A third potential mechanism for the initiation of antidromic AVRT
involves AES conduction over the BT and simultaneously over the slow
pathway of a dual AVN pathway situation, with anterograde block in
the fast AVN pathway. Conduction beyond the HB to the ventricle is
not possible because of ventricular refractoriness, yet an AVN echo to
the atrium may occur, which in turn may conduct anterogradely over
the BT, when the ventricle would have recovered excitability, and sub-
sequently back up the now-recovered AVN, initiating antidromic AVRT.
AVN reentry may not persist or may be preempted by retrograde con-
duction up the fast AVN pathway because of the premature ventricular
activation over the BT. In this scenario, the location of the His potential
will depend on whether it was anterograde or retrograde.
In general, if atrial stimulation induces antidromic AVRT, multiple
BTs are often operative. Whether they are operative throughout the
SVT depends on the relative retrograde activation times over the addi-
tional BTs and HPS-AVN and the varying degree of anterograde and
retrograde concealment into the additional BTs and HPS-AVN during
the SVT.
The site of atrial stimulation plays an important role in inducibility
of AVRT, and can also determine the type of AVRT initiated in patients
with bidirectional BTs. The closer the stimulation site to the BT, the
more likely anterograde block in the BT will occur and orthodromic
AVRT will result. Conversely, antidromic AVRT is more likely to occur
with atrial stimulation close to the AVN.
Initiation by Programmed Ventricular Stimulation
Orthodromic AVRT.  Ventricular stimulation can induce orthodromic
AVRT in the majority of patients (inducibility rate of 60% with VES
and 80% with ventricular pacing), regardless of whether the BT is
manifest or concealed (Fig. 18.34). Initiation of orthodromic AVRT by
ventricular stimulation requires the following: (1) retrograde block of
the ventricular impulse in the HPS-AVN; (2) retrograde conduction
only over the BT; and (3) adequate VA conduction delay to allow for
recovery of the AVN-HPS from any concealment produced by ventricular
stimulation, so it can support anterograde conduction of the reentrant
impulse. Because the BT retrograde ERP is usually very short, the prime
636 CHAPTER 18  Typical Atrioventricular Bypass Tracts

II

V1

VA VA
HRA 138 msec 120 msec
176 msec 164 msec 162 msec
A H A H A H
His

CSprox

CSdist

RVA 300 msec 312 msec

S1 S1 S1
Fig. 18.34  Induction of an Orthodromic Atrioventricular Reentrant Tachycardia (AVRT) Using a Con-
cealed Posteroseptal Bypass Tract With Ventricular Pacing. Note that although the ventricular pacing
cycle length (CL) approximates the tachycardia CL, the ventriculoatrial (VA) interval (dashed lines) during
ventricular pacing is only slightly longer than that during supraventricular tachycardia (SVT), which favors
orthodromic AVRT over atrioventricular nodal reentrant tachycardia as the mechanism of the SVT. In addition,
the atrial–His bundle interval of the first SVT complex is longer than that of subsequent beats, indicating
retrograde concealment in the AVN produced by the last ventricular stimulus. CSdist, Distal coronary sinus;
CSprox, proximal coronary sinus; HRA, high right atrium; RVA, right ventricular apex.

determinant of orthodromic AVRT initiation is the extent of retrograde
conduction and/or concealment in the HPS-AVN.
Multiple modes of initiation of orthodromic AVRT can be present,
depending on the PCL or VES coupling interval, conduction velocities,
and refractoriness of the HPS-AVN and BT, as well as the site of ven-
tricular stimulation. Ventricular pacing at a CL or a VES with a coupling
interval that is shorter than the ERP of the AVN but longer than that
of the HPS and BT would block retrogradely in the AVN and conduct
over the BT to initiate orthodromic AVRT. Block in the AVN, which is
more likely to occur with rapid ventricular pacing or VES delivered
after a short pacing drive CL, can cause concealment and subsequent
delay in anterograde conduction of the first SVT impulse over the AVN,
resulting in longer AH and PR intervals of the first SVT beat compared
with subsequent beats (see Fig. 18.34). On the other hand, ventricular
pacing at a CL or a VES with a coupling interval shorter than the ERP
of the HPS, but longer than that of the BT, would block retrogradely
in the HPS and conduct over the AV BT to initiate orthodromic AVRT.
When block occurs in the HPS, which is more likely to occur with a
VES delivered during NSR or after a long pacing drive CL, the first
SVT beat will approach a fully recovered AVN and conduct with short
AH and PR intervals equal to subsequent SVT beats. In this setting,
adequate prolongation of the HV interval may be required to allow for
the recovery of ventricular refractoriness for the ventricle to be activated
and support reentry, because AVN delay may have not been sufficient.
When HV interval prolongation is required to initiate orthodromic
AVRT, it is almost invariably associated with LBBB. A short-coupled
VES, especially following a pacing drive with a long CL, that blocks
retrogradely in both the BT and RB and conducts transseptally and
then retrogradely over the LB, can result in a bundle branch reentrant
(BBR) beat that conducts to the ventricle down the RB, and then ret-
rogradely to the atrium over the AV BT, mediating the initiation of
orthodromic AVRT. The long HV interval often associated with BBR
beats, plus the LBBB pattern, facilitate the induction of orthodromic
AVRT using a left-sided BT (Fig. 18.35).
When induction of the SVT is achieved by ventricular pacing at a
PCL similar to the subsequent TCL or by a VES that activates the HB
at a coupling interval (i.e., H1-H2 interval) similar to the H-H interval
during the SVT (i.e., similar to the TCL), the HA interval following the
initiating ventricular stimulus is then compared with that during the
SVT. During AVNRT, the HA interval of the ventricular stimulus ini-
tiating the SVT is longer than the HA interval during the SVT because
both the HB and atrium are activated in sequence during ventricular
stimulation but in parallel during AVNRT (see Fig. 17.14). This is even
exaggerated by the fact that the AVN usually exhibits greater decremental
conduction with repetitive engagement of impulses than to a single
impulse at a similar coupling interval. Therefore the more prolonged
the HA interval with the initiating ventricular stimulus, the more likely
the SVT is AVNRT. On the other hand, if the SVT uses an AV BT for
retrograde conduction, the HA interval during the initiating ventricular
stimulus (at a coupling interval comparable to the TCL) is shorter than
that during orthodromic AVRT because the HB and atrium are activated
in parallel during ventricular pacing (when atrial activation is mediated
by retrograde BT conduction), but in sequence during SVT.
The intervals immediately following tachycardia initiation with a
VES (delivered from the RV apex) provide data that are essentially
equivalent to those observed with ventricular entrainment (see later).
The interval from the VES to atrial activation (surface VA or “SA” inter-
val) is compared to the surface VA interval during SVT, and the post-
VES return cycle (i.e., the interval from the VES to the subsequent RV
apical depolarization) is compared to the TCL. An SA interval that
exceeds the surface VA interval during SVT by less than 85 milliseconds
is consistent with orthodromic AVRT. Similarly, when the post-VES
return cycle exceeds the TCL by less than 115 milliseconds, orthodromic
AVRT is suggested. The small differences between those intervals are
related to the proximity of the RV apical pacing site to the SVT reentry
circuit. Larger differences in these intervals are observed in the setting
of AVNRT or orthodromic AVRT utilizing a left lateral BT or a septal
BT with decremental conduction. The unique advantage of this tech-
nique is that it does not require a sustained tachycardia that can be
successfully entrained.33
Permanent junctional reciprocating tachycardia. Ventricular
stimulation is less effective in initiating PJRT because of the already
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 637

II
V1
VA VA
BBR 92 msec 92 msec
HRA

His

CSprox

CSdist
RVA 600 msec 280 msec
S1 S1 S2
Fig. 18.35  Induction of an Orthodromic Atrioventricular Reentrant Tachycardia (AVRT) Using a Con-
cealed Left Posteroseptal Bypass Tract (BT) With Ventricular Extrastimulation (VES). The VES conducts
retrogradely over the BT, but also results in a bundle branch reentrant (BBR) beat, which in turn conducts
to the atrium over the BT and initiates orthodromic AVRT. Note that right bundle branch block (RBBB)
develops shortly after initiation of the tachycardia; however, the ventriculoatrial (VA) interval (dashed lines)
remains constant, regardless of the presence or absence of RBBB, because the BT is in the contralateral
ventricle. CSdist, Distal coronary sinus; CSprox, proximal coronary sinus; HRA, high right atrium; RVA, right
ventricular apex.

impaired conduction in the BT, such that an early VES produces block
in the BT. A late-coupled VES (when the HB is refractory) can initiate
SVT in some cases.
Antidromic AVRT.  Initiation of classic antidromic AVRT by ven-
tricular pacing and VES requires the following: (1) retrograde block in
the BT; (2) retrograde conduction over the AVN or HPS; and (3) adequate
VA delay to allow for recovery of the atrium and BT so it can support
subsequent anterograde conduction (see Fig. 18.25).
When induction of the SVT is achieved by ventricular pacing at a
CL similar to the TCL or by a VES that activates the HB at a coupling
interval (i.e., H1-H2 interval) similar to the H-H interval during the
SVT, the HA interval following the initiating ventricular stimulus is
always equal to or shorter than that during the antidromic AVRT. This
is because the HB and atrium are activated in sequence during anti-
dromic AVRT and in parallel during ventricular stimulation (in the
presence of a retrogradely conducting BT). Therefore an HA interval
of the initiating ventricular stimulus longer than the HA interval during
SVT favors preexcited AVNRT and excludes antidromic AVRT (see Fig.
18.25). Moreover, because the AVN usually exhibits greater decremental
conduction with repetitive engagement of impulses than to a single
impulse at a similar coupling interval, the more prolonged the HA
interval with the initiating ventricular stimulus, the more likely that
the SVT is preexcited AVNRT.
Tachycardia Features
Orthodromic Atrioventricular Reentrant Tachycardia
Atrial activation sequence.  The initial site of atrial activation
during orthodromic AVRT depends on the atrial insertion site of the
BT, but is always near the AV groove and without multiple break-
through points. The atrial activation sequence during orthodromic
AVRT should be identical to that during ventricular pacing at com-
parable CLs when VA conduction occurs exclusively over the BT.
However, retrograde conduction during ventricular pacing can proceed
over the AVN or over both the BT and AVN, resulting in fusion of
atrial activation, depending on the site of ventricular stimulation rela-
tive to the BT and HPS, and on retrograde conduction and refractori-
ness of the HPS-AVN.
Atrial-ventricular relationship.  The conduction time over the
typical (fast) AV BT is approximately 30 to 120 milliseconds. Therefore
the RP interval during orthodromic AVRT is short, but longer than
that during typical AVNRT, because in the setting of orthodromic AVRT
the wavefront has to activate the ventricle before it reaches the ventricular
insertion site of the BT at the AV groove and subsequently conduct to
the atrium. Consequently, a very short VA interval (less than 70 mil-
liseconds) or short V–high RA interval (less than 95 milliseconds) largely
excludes orthodromic AVRT, and favors typical AVNRT (see Fig. 18.33).34
However, VA intervals shorter than 70 milliseconds have occasionally
been observed in patients with orthodromic AVRT utilizing left lateral
or left posteroseptal BTs.35 Importantly, the RP and VA intervals during
orthodromic AVRT remain constant regardless of oscillations in the
TCL from whatever cause and regardless of changes in the PR interval
(AH interval); as a consequence, the TCL is most closely associated
with the PR interval (i.e., anterograde AVN conduction) and the RP/
PR ratio may vary (Fig. 18.36).
A 1:1 A-V relationship is a prerequisite for maintenance of AVRT
because parts of both the atrium and the ventricle are essential com-
ponents of the reentrant circuit. If an SVT persists despite the presence
of AV or VA block, orthodromic AVRT is excluded.
When dual AVN pathways are present, the slow AVN pathway func-
tions in most cases as the anterograde limb during orthodromic AVRT.
An AH interval of more than 180 milliseconds during orthodromic
AVRT suggests a slow AVN pathway mediating the anterograde limb
of the reentrant circuit, whereas an AH interval of less than 160 mil-
liseconds suggests anterograde conduction over the fast AVN pathway.
Obviously, orthodromic AVRT using the slow pathway will have a
longer TCL.
Slow-slow AVNRT is associated with an RP interval and P wave
morphology similar to that during orthodromic AVRT using a pos-
teroseptal AV BT. However, although both SVTs have the earliest atrial
activation in the posteroseptal region, conduction time from that site
to the HB region is significantly longer in AVNRT than in orthodromic
AVRT, resulting in a significantly longer RP interval in lead V1 and a
larger difference in the RP interval between lead V1 and the inferior
leads. Therefore a ΔRP interval (V1 to III) longer than 20 milliseconds
638 CHAPTER 18  Typical Atrioventricular Bypass Tracts

Spontaneous termination of orthodromic AVRT

II

V1

A A A A A A
332 msec 374 msec 344 msec 390 msec 370 msec
HRA
H H H H H H
340 msec 368 msec 348 msec 386 msec 374 msec
His

CSprox

CSdist
V V V V V V
RVA 334 msec 372 msec 348 msec 388 msec 372 msec

Fig. 18.36  Spontaneous Termination of Orthodromic Atrioventricular Reentrant Tachycardia (AVRT)

Using a Concealed Superoparaseptal Bypass Tract. Note that the tachycardia terminates with an atrial
complex not followed by a QRS, consistent with anterograde block in the atrioventricular node (AVN). Also,
note the oscillation in the tachycardia cycle length (CL) preceding termination. Changes in H-H and V-V
intervals precede the subsequent changes in A-A intervals, and the ventriculoatrial (VA) interval remains
constant despite oscillation of the CL. This indicates that the variability in the tachycardia CL is secondary
to changes in the anterograde conduction over the AVN, whereas VA conduction over the retrograde limb
of the reentrant circuit (the bypass tract) remains constant. CSdist, Distal coronary sinus; CSprox, proximal coro-
nary sinus; HRA, high right atrium; RVA, right ventricular apex.

suggests slow-slow AVNRT with a sensitivity of 71%, specificity of 87%,
and positive predictive value of 75%.
Effects of BBB.  The presence of BBB during SVT is much more
common in orthodromic AVRT than AVNRT or AT; in fact, the majority
of SVTs with sustained LBBB are orthodromic AVRTs. Two reasons
have been proposed to explain why prolonged aberration occurs less
commonly during AVNRT than orthodromic AVRT. First, the induction
of AVNRT requires significant AVN delay, which makes the H1-H2
interval longer and makes aberration unlikely. Conversely, in ortho-
dromic AVRT, AVN conduction need not be slow, resulting in a shorter
AH interval and an impulse encroaching on HPS refractoriness, in turn
resulting in BBB. Second, LBBB facilitates the induction of orthodromic
AVRT when a left-sided AV BT is present by providing the necessary
AV delay required to maintain the reentry circuit.36
BBB is more common when AVRT is initiated by an AES that is
delivered during NSR or after long pacing drive CLs, during which HPS
refractoriness is longest and AVN conduction and refractoriness are
shortest. When AVRT is induced by atrial stimulation, RBBB is twice
as common as LBBB. In contrast, when AVRT is induced by ventricular
stimulation, LBBB is much more common than RBBB (because of
retrograde concealment of the paced wavefront in the LB). In addition,
the incidence of BBB is more common in AVRTs induced by ventricular
stimulation than those induced by atrial stimulation (75% vs. 50%).
BBB ipsilateral to the BT results in prolongation of the “surface VA
interval.” Block in the ipsilateral bundle branch forces the reentrant
circuit to follow a longer path. Hence, more time is needed for the
tachycardia wavefront to travel from the AVN down the HB and contra-
lateral bundle branch, and then transseptally to the ventricle ipsilat-
eral to the BBB in order to reach the BT and then activate the atrium
(Fig. 18.37). However, the “local VA interval” (measured at the site of
BT insertion) remains constant. On the other hand, the TCL usually
increases in concordance with the increase in the surface VA interval
as a result of ipsilateral BBB because of the now larger tachycardia
circuit. However, because the time the wavefront spends outside the
AVN is now longer because of the larger circuit, AVN conduction may
improve to a small degree, resulting in shortening of the AH interval
(PR interval), which can potentially counterbalance, at least in part,
the effects of prolongation of the VA interval on the total TCL. Thus
the surface VA interval and not the TCL should be used to assess the
effects of BBB on the SVT (see Figs. 18.37 and 18.38).
Prolongation of the surface VA interval during SVT in response to
BBB by more than 35 milliseconds compared to that with normal QRS
or contralateral BBB indicates that an ipsilateral free-wall BT is present
and is participating in the SVT (i.e., diagnostic of orthodromic AVRT)
(see Fig. 18.38). On the other hand, prolongation of the surface VA by
25 to 35 milliseconds suggests a septal or paraseptal BT (posteroseptal
AV BT in association with LBBB, and superoparaseptal AV BT in asso-
ciation with RBBB). In contrast, BBB contralateral to the BT does not
influence the VA interval or TCL because the contralateral ventricle is
not part of the reentrant circuit (see Figs. 18.35 and 18.37). Of note,
prolongation of the VA interval by more than 45 milliseconds in response
to RV pacing entraining the orthodromic AVRT is also diagnostic of a
left-sided BT, whereby RV pacing results in effects analogous to those
created by LBBB and, as a consequence, VA interval prolongation.
Oscillations in the tachycardia cycle length.  Oscillation of the
TCL during orthodromic AVRT can occur and generally is caused by
changes in the anterograde conduction over the AVN (see Fig. 18.36).
Because retrograde conduction through the BT is much less variable,
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 639

Orthodromic AVRT Orthodromic AVRT with RBBB Orthodromic AVRT with LBBB

AVN AVN AVN

HB BT HB BT HB BT

RB RB= LB RB LB
=
Fig. 18.37  Schematic Illustration of the Effect of Bundle Branch Block on the Reentrant Circuit During
Orthodromic Atrioventricular Reentrant Tachycardia (AVRT) Using a Left-Sided Bypass Tract (BT).
Block in the left bundle branch (LB) (ipsilateral to the BT) results in prolongation of the reentrant pathway
and, therefore, prolongation of the ventriculoatrial interval. In contrast, block in the right bundle branch (RB)
(contralateral to the BT) has no effect on the reentrant circuit. AVN, Atrioventricular node; HB, His bundle;
LBBB, left bundle branch block; RBBB, right bundle branch block.

Orthodromic AVRT RBBB LBBB

I
II
III
aVL
V1
HRA
Hisprox
Hismid
Hisdist
VA 110 ms VA 110 ms VA 148 ms
CSprox

CSdist
RVA 290 ms 290 ms 290 ms 290 ms 290 ms 290 ms 315 ms 315 ms 315 ms
A B C
Fig. 18.38  Effect of Bundle Branch Block on Orthodromic Atrioventricular Reentrant Tachycardia (AVRT).
Orthodromic AVRT is recorded in the same patient. (A) Orthodromic AVRT with normal intraventricular con-
duction. (B) Orthodromic AVRT with right bundle branch block (RBBB). (C) Orthodromic AVRT with left bundle
branch block (LBBB). Note that the tachycardia cycle length (TCL) and ventriculoatrial (VA) interval are not
affected by the development of RBBB. In contrast, the development of LBBB during tachycardia is associ-
ated with prolongation of the VA interval (by 38 milliseconds) and a lesser degree of prolongation of the TCL
(by 25 milliseconds), indicating the presence and participation of a left lateral bypass tract in the reentrant
circuit. CSdist, Distal coronary sinus; CSprox, proximal coronary sinus; Hisdist, distal His bundle; Hismid, middle
His bundle; Hisprox, proximal His bundle; HRA, high right atrium; RVA, right ventricular apex.

the changes in ventricular CL that result from variability in the antero-
grade AVN conduction precede the subsequent changes in atrial CL,
and changes in atrial CL do not predict changes in subsequent ventricular
CL (similar to observations during typical AVNRT). In contrast, changes
in atrial CL predict the changes in subsequent ventricular CL during
atypical AVNRT and AT.37
In addition, orthodromic AVRT in the presence of dual AVN physi-
ology can be associated with anterograde conduction alternating over
the slow and fast AVN pathways, resulting in a regular irregularity of
the TCL (alternating long and short cycles). Alternatively, the presence
of dual AVN pathways can lead to two separate stable TCLs. In either
setting, the RP interval during the SVT remains constant.
QRS alternans.  Alternans of the QRS complex amplitude during
a relatively slow SVT is almost always indicative of orthodromic AVRT
(see Fig. 18.13). On the other hand, although QRS alternans during
fast SVTs is most commonly seen in orthodromic AVRT, it can also be
seen with other types of SVT.
Termination and response to physiological and pharmacological
maneuvers.  Spontaneous termination of orthodromic AVRT is usually
caused by gradual slowing and then block in the AVN (see Fig. 18.36),
sometimes causing initial oscillation in the TCL, with alternate com-
plexes demonstrating a Wenckebach periodicity before block. However,
termination with block in the BT without any perturbations of the
TCL can occur during very rapid AVRT or following a sudden shorten-
ing of the TCL (e.g., after resolution of ipsilateral BBB or shift of antero-
grade conduction from the slow to the fast AVN pathway).
Carotid sinus massage can terminate orthodromic AVRT by gradual
slowing and then block in the AVN. Adenosine, digoxin, verapamil,
diltiazem, and beta-blockers terminate orthodromic AVRT by block in
the AVN; therefore the SVT terminates with a P wave that is not fol-
lowed by a QRS. Verapamil rarely produces block in the BT and, when
it does, block is usually preceded by oscillation in the TCL produced
by changes in AVN conduction, leading to long-short sequences. Class
IA and IC antiarrhythmic agents can produce block in the BT with
variable effect on the AVN-HPS. Amiodarone can terminate AVRT by
block in the AVN, HPS, or AV BT. Sotalol affects the AVN with little
or no effect on the AV BT.
Permanent junctional reciprocating tachycardia
Atrial activation sequence.  The initial site of atrial activation
is most often in the posteroseptal part of the triangle of Koch near
the coronary sinus ostium (CS os), similar to that in atypical AVNRT
(Fig. 18.39).3
640 CHAPTER 18  Typical Atrioventricular Bypass Tracts
aVF
V1
HRA
522 ms 522 ms
H H
His
CSprox
CSdist
RVA
S2
Fig. 18.39  Ventricular Extrastimulation (VES) During Permanent Junctional Reciprocating Tachycardia.
The supraventricular tachycardia has a stable baseline cycle length (522 milliseconds). A single VES (S2)
introduced during His bundle refractoriness retards the timing of the next atrial complex (538 milliseconds).
The anticipated timing of the high right atrium electrogram is indicated by the dashed line. CSdist, Distal coro-
nary sinus; CSprox, proximal coronary sinus; HRA, high right atrium; RVA, right ventricular apex.
Atrial-ventricular relationship.  Because the retrograde limb
of the reentry circuit is the slow BT (which conducts more slowly than
the AVN), the RP interval is longer than the PR interval, similar to
fast-slow AVNRT (see Figs. 18.14 and 18.39). In contrast to the typical
(fast) AV BTs, the RP interval during PJRT is not fixed because the BT
serving as the retrograde limb of the reentrant circuit has decremental
properties. Similar to all types of AVRTs, a 1:1 A-V relationship is a
prerequisite to sustenance of the tachycardia.
Oscillations in the TCL.  The tachycardia rate typically fluctuates
(100 to 220 beats/min) in response to autonomic tone and physical
activity, and the rate changes result from modulation of the PR and
RP intervals. Typically, the TCL is often just longer than the shortest
CL at which the BT can conduct retrogradely.
Effects of BBB.  BBB affects PJRT in a manner analogous to that
described for orthodromic AVRT.
Termination and response to physiological and pharmaco-
logical maneuvers.  Carotid sinus massage and AVN blockers (adenos-
ine, digoxin, calcium channel blockers, and beta-blockers) usually
terminate PJRT by block in the AVN (two-thirds) or in the BT (one-
third) (see eFig. 18.5). Although the mode of tachycardia termination
by adenosine has been suggested to distinguish between PJRT and
atypical AVNRT, one report has shown that termination of atypical
AVNRT with adenosine can also result from block in the fast AVN
pathway and, therefore, its value in distinguishing between atypical
AVNRT and PJRT is questionable.
Antidromic AVRT
Atrial activation sequence.  The initial site of atrial activation
in classic antidromic AVRT is consistent with retrograde conduction
over the AVN. If the preexcited AVRT is using a second BT for retro-
grade conduction, then the atrial activation sequence will depend on
the location of that BT (see eFig. 18.1). In addition, ventricular activa-
tion precedes HB activation by more than 10 milliseconds during
classic antidromic AVRT because the ventricle and HB are activated
sequentially by the same reentrant wavefront. On the other hand,
during preexcited AVNRT, the ventricle and HB can be activated in
parallel (the ventricle is activated via the bystander BT and the HB
activated via the AVN). Therefore, during a preexcited SVT, a positive
HV interval (i.e., HB activation preceding ventricular activation) or
538 ms 525 ms
H H
a VH interval not more than 10 milliseconds, especially when the HA
interval is not more than 50 milliseconds, favors preexcited AVNRT
over antidromic AVRT.
Atrial-ventricular relationship.  The conduction time over classic
(fast) AV BTs is approximately 30 to 120 milliseconds. Therefore the
PR is short and fixed, regardless of oscillations in the TCL from whatever
cause. Similar to all types of AVRT, the A/V ratio is always equal to 1.
If the SVT persists in the presence of AV or VA block, antidromic AVRT
is excluded.
Oscillations in the TCL.  Antidromic AVRT can be irregular.
Tachycardia CL changes are usually caused by changes in retrograde
conduction over different fascicles of the HPS with different VA intervals
(regardless of the type and degree of changes in the VH or HA intervals),
retrograde conduction over dual AVN pathways (with different HA
intervals), different routes of anterograde conduction (with different
AV intervals), and/or retrograde conduction over different BTs (with
different VA intervals). When the change in the TCL can be ascribed
to a change in the VH interval or the subsequent HA interval, it sug-
gests that retrograde conduction occurs over the HPS and AVN and
not over a second BT.
The TCL tends to be shorter during classic antidromic AVRT than
orthodromic AVRT when these arrhythmias occur in the same patient.
This may be explained by the fact that antidromic AVRT uses the fast
AVN pathway (of a dual AVN physiology) retrogradely, whereas ortho-
dromic AVRT uses the slow pathway anterogradely or, in the absence
of dual AVN physiology, this may be merely supportive evidence that
retrograde conduction during antidromic AVRT uses another fast BT
instead of the slower AVN. On the other hand, antidromic AVRTs using
two or more BTs may have longer TCLs than orthodromic AVRT or
classic antidromic AVRT because the two BTs are typically in opposite
chambers and are incorporated in a larger reentrant circuit than one
involving a midline AVN.
Effects of BBB.  Retrograde BBB affects antidromic AVRT in a
manner analogous to that described for orthodromic AVRT. Abrupt
prolongation of the VH and VA intervals and TCL when retrograde
BBB occurs is consistent with retrograde HB activation via the ipsilateral
bundle branch, which is typical for antidromic AVRT using an ipsilateral
AV BT, but can also occur in preexcited AVNRT. However, if VH
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 641

prolongation is accompanied by prolongation of the VA interval (without
a change in the activation sequence) and the TCL, true antidromic
tachycardia (using the AV conduction system as the retrograde limb)
can be diagnosed and preexcited AVNRT is excluded. Lack of effects
on the VH interval can occur in: (1) preexcited AVRT (utilizing a second
BT as the retrograde limb); (2) antidromic AVRT utilizing a left-sided
BT; (3) antidromic AVNRT utilizing an atriofascicular BT inserting
into the RB proximal to the site of RBBB; and (4) preexcited AVNRT.
Termination and response to physiological and pharmaco-
logical maneuvers. Various physiological and pharmacological
maneuvers affect the BT and AVN during antidromic AVRT in a fashion
similar to that described for orthodromic AVRT. Carotid sinus massage
and adenosine terminate classic antidromic AVRT after ventricular
activation, secondary to retrograde block up the AVN. In contrast, pre-
excited typical AVNRT terminates after atrial activation, secondary to
anterograde block down the slow AVN pathway.
Tachycardia termination or prolongation of the VA (and VH) interval
and TCL with transient RBBB, caused by mechanical trauma or intro-
duction of VES, is diagnostic of antidromic AVRT using a right-sided
or septal BT and excludes preexcited AVNRT. Continuation of an SVT
at the same TCL, despite anterograde block in the BT (by drugs, mechani-
cal trauma caused by catheter manipulation, or ablation), excludes
antidromic AVRT.
Diagnostic Maneuvers During Tachycardia
Programmed Atrial Stimulation During Tachycardia
Orthodromic AVRT
Resetting.  AES can easily reset orthodromic AVRT. In fact, it is
usual for AES not to affect the SVT because of the large size and large
excitable gap of the reentrant circuit. However, this can be influenced
by the distance between the site of atrial stimulation and the atrial
region incorporated in the AVRT circuit (i.e., atrial myocardium between
the BT and the AVN). Because only parts of the atrium ipsilateral to
the BT are requisite components of the orthodromic AVRT circuit, AES
delivered in the contralateral atrium may not affect the circuit, whereas
AESs delivered at sites in close proximity to the BT or the AVN have
the highest success at resetting the reentrant circuit.
AES over a wide range of coupling intervals can reset orthodromic
AVRT via conduction down the AVN-HPS. In this setting, atrial activa-
tion is a fusion of the AES and the SVT impulse traveling retrogradely
up the BT. The next QRS can be early or late, depending on the degree
of slowing of conduction of the AES anterogradely down the AVN (i.e.,
the degree of prolongation of the A2-H2 interval).
Termination.  An early-coupled AES can terminate the SVT, usually
by block in the AVN-HPS. In this setting, the SVT terminates with an
AES not followed by a QRS (i.e., AV block). Alternatively, the AES can
render the atrium refractory to the SVT impulse traveling retrogradely
up the BT, in which case the SVT terminates with an AES followed by
a QRS (i.e., VA block). The AES can also anterogradely penetrate the
BT and collide with the retrogradely traveling SVT wavefront (VA block).
Lastly, the AES can conduct down the AVN-HPS and advance the next
QRS, which then blocks in the still-refractory BT or atrium (VA block).
Atrial entrainment.  Atrial pacing at a CL approximately 10 to
30 milliseconds shorter than the TCL can generally entrain orthodromic
AVRT (Fig. 18.40).
Resetting and entrainment with manifest atrial fusion.  Reset-
ting and entrainment with manifest atrial fusion can be demonstrated
in AVRT. The morphology of the fusion P wave is hybrid between the
tachycardia P wave morphology and the fully paced P wave morphol-
ogy. This can be difficult to demonstrate if the P waves cannot be
visualized on the surface ECG (due to overlapping ST-T wave), which
is usually the case; however, manifest fusion can be demonstrable on
intracardiac recordings (see Fig. 18.40). Atrial fusion results from
intraatrial collision of the impulse propagating from the paced site with
the tachycardia impulse emerging from the BT. In contrast, manifest
fusion cannot be demonstrated during resetting or entrainment of
AVNRT. For atrial fusion (i.e., fusion of atrial activation from both the
tachycardia wavefront and the AES) to occur, the AES should be able
to enter the reentrant circuit, while at the same time the tachycardia
wavefront should be able to exit the circuit. This requires spatial

II

V1
VA VA
290 msec 300 msec
HRA
S1 S1 S1 S1
His

CSprox

CSdist
RVA
Fig. 18.40  Atrial Entrainment of Orthodromic Atrioventricular Reentrant Tachycardia (AVRT). Overdrive
atrial pacing is from the high right atrium (HRA) during an AVRT using a left lateral bypass tract (BT). Note
that the atrial activation sequence during entrainment (blue shade) is different from the tachycardia atrial
activation sequence (yellow shade), and is also different from the expected purely paced atrial activation
sequence as evidenced by a distal-to-proximal activation sequence in the coronary sinus. This indicates the
presence of atrial fusion (between the paced and tachycardia wavefronts) during entrainment, which is
consistent with AVRT and excludes both focal atrial tachycardia and atrioventricular nodal reentrant tachy-
cardia. Note that the ventriculoatrial (VA) interval (dashed lines) of the return cycle after cessation of atrial
pacing is similar to that of the supraventricular tachycardia (VA linking), because retrograde VA conduction
of the last entrained QRS is mediated by the BT. CSdist, Distal coronary sinus; CSprox, proximal coronary sinus;
RVA, right ventricular apex.
642 CHAPTER 18  Typical Atrioventricular Bypass Tracts
separation between the entry and exit sites to the reentrant circuit, a
condition that seems to be lacking in the setting of AVNRT.38,39
Ventriculoatrial linking.  The initial atrial complex following
cessation of atrial pacing entraining orthodromic AVRT is linked to,
and cannot be dissociated from, the last captured ventricular complex.
As a consequence, the VA intervals of the return cycle after cessation
of atrial pacing are fixed and similar to those during tachycardia
(with less than 10 milliseconds of variation) after different attempts
at SVT entrainment (see Fig. 18.40). The postpacing VA intervals
typically remain constant regardless of the site, duration, or CL of the
entraining atrial pacing drive because the timing of atrial activation
is dependent on retrograde VA conduction of the last entrained QRS
mediated by the BT, which is fixed and constant. VA linking is also
observed after introduction of an AES with a wide range of coupling
intervals during tachycardia. VA linking can also be observed in typical
AVNRT but not AT.34,40
Antidromic AVRT.  AES is of value in distinguishing antidromic
AVRT from preexcited AVNRT. A late-coupled AES, delivered close to
the BT atrial insertion site during SVT when the AV junctional atrium
is refractory (i.e., when the atrial electrogram is already manifest in the
HB recording at the time of AES delivery) that advances (accelerates)
the timing of both the next ventricular activation and the subsequent
atrial activation, proves that the SVT is an antidromic AVRT using an
AV BT anterogradely, and excludes preexcited AVNRT (Fig. 18.41A).
Because the AV junctional atrium is refractory at the time of the AES,
the AES cannot penetrate the AVN; hence, resetting of the SVT by such
an AES is therefore incompatible with AVNRT.
Also, an AES delivered during the SVT that advances ventricular
activation and does not influence the VA interval excludes preexcited
AVNRT and is diagnostic of antidromic AVRT (see Fig. 18.41A). The
VA interval should change in the setting of preexcited AVNRT because
the AES penetrates the AVN, producing slower conduction down the
AVN slow pathway before the reentrant wavefront conducts retrogradely
over the fast pathway and activates the atrium. As a consequence, the
delay in atrial activation is expected to produce a longer VA interval,
given the presence of a fixed AV interval in response to the AES (medi-
ated by anterograde conduction down the bystander BT in the setting
of preexcited AVNRT). In addition, the advanced ventricular activation
(resulting from anterograde conduction of the AES over the bystander
BT) can potentially invade and capture the HB retrogradely and conduct
up the fast AVN pathway and reset the AVNRT circuit. Then the VH
interval of the advanced QRS plus the HA interval in response to this
QRS should add up to the same VA interval on an undisturbed AVNRT,
which is clearly unlikely.
Exact atrial and ventricular capture by an AES delivered when the
AV junction is depolarized excludes AVNRT (see Fig. 18.41A). An AES
that captures the ventricle at the same coupling interval as that of the
AES indicates that the atrial stimulation site is inside the reentrant
circuit, because if there were intervening atrial tissue between the stimu-
lation site and the tachycardia circuit (as is the case during AVNRT),
the AV interval would prolong, and consequently, the V-V interval would
exceed the AES coupling interval.
The presence of a fixed and short VH interval during entrainment
of the SVT with atrial pacing suggests antidromic AVRT, and makes
AVNRT unlikely (but does not exclude AVNRT). Moreover, failure of
entrainment by atrial pacing to influence the VA interval during SVT
excludes preexcited AVNRT.
An early-coupled AES can terminate antidromic AVRT by retrograde
block in the AVN-HPS (the SVT terminates with an AES followed by
a QRS; i.e., VA block; see Fig. 18.41B) or by anterograde block in the
BT (the SVT terminates with an AES not followed by a QRS; i.e., AV
block; see Fig. 18.41C).
Programmed Ventricular Stimulation During Tachycardia
Orthodromic AVRT
Resetting.  VES can easily reset orthodromic AVRT, and is fre-
quently capable of terminating the tachycardia (Fig. 18.42).34 However,
the ability of the VES to affect the SVT depends on the distance between
the site of ventricular stimulation to the ventricular insertion site of
the BT and on the VES coupling interval. Because only parts of the
ventricle ipsilateral to the BT are requisite components of the ortho-
dromic AVRT circuit, a VES delivered in the contralateral ventricle
may not affect the circuit. However, failure to reset (advance or delay)
atrial activation with an early-coupled VES and at different VES cou-
pling intervals, despite advancement of the local ventricular activation
at all sites (including the site of the suspected BT) by more than 30
milliseconds, excludes orthodromic AVRT and the presence of a ret-
rogradely conducting BT.41
Preexcitation index.  The preexcitation index analyzes the degree
of prematurity (coupling interval) of the latest coupled VES (delivered
from the RV apex) that is capable of resetting the tachycardia. Later
coupled VESs with a relative preexcitation index (the ratio of the VES
coupling interval to the TCL) of more than 90% suggests that the BT
is close to the site of ventricular stimulation (i.e., right-sided or septal
BT). An absolute preexcitation index (TCL minus VES coupling interval)
of at least 75 milliseconds suggests a left free-wall BT; an index of less
than 45 milliseconds suggests a septal BT; and an index of 45 to 75
milliseconds is indeterminate. AVNRT would require even earlier coupled
VESs and could be distinguished from AVRT if the absolute preexcita-
tion index was greater than 100 milliseconds.42
VES during HB refractoriness.  A VES delivered when the HB
is refractory (i.e., when the His potential is already manifest or within
35 to 55 milliseconds before the time of the expected His potential)
that advances (accelerates, i.e., makes it activate earlier than expected)
the next atrial activation is diagnostic of the presence of a retrogradely
conducting BT. Such a VES has to conduct and advance atrial activation
via a BT because the HPS-AVN is already refractory and cannot mediate
retrograde conduction of the VES to the atrium (see Fig. 18.42). Although
such an observation excludes AVNRT, it does not exclude AT or prove
orthodromic AVRT, and the preexcited atrial activation can reset or
even terminate an AT, whereby the BT is an innocent bystander. However,
if this VES advances atrial activation with an activation sequence identi-
cal to that during the SVT, this suggests that the SVT is orthodromic
AVRT and the BT is participating in the SVT, although it does not
exclude the rare case of an AT originating at a site close to the atrial
insertion site of a bystander AV BT. Furthermore, a VES delivered when
the HB is refractory may not affect the next atrial activation if the
ventricular stimulation site is far from the BT. Conduction from the
ventricular stimulation site to the BT, local ventricular refractoriness,
and the TCL all determine the ability of a VES to reach the reentrant
circuit before ventricular activation over the normal AVN-HPS.
Although such a VES can advance atrial activation during AT through
fast retrograde conduction over a bystander BT, it should not be able
to delay an AT beat by conduction over the AV BT. Thus a VES delivered
when the HB is refractory that delays the next atrial activation indicates
that the VES was conducted with some delay over the BT and that the
next atrial activation was dependent on this slower conduction; hence,
the BT is participating in the SVT, proving orthodromic AVRT as the
mechanism of the SVT. Similarly, a VES delivered when the HB is refrac-
tory that terminates the SVT without atrial activation is diagnostic
of AVRT.
Exact and paradoxical capture.  Exact and paradoxical capture
phenomena are diagnostic of AVRT. A VES that captures the atrium
at the same coupling interval as that of the VES (exact capture phe-
nomenon) indicates that the ventricular stimulation site is inside the
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 643

AES during antidromic AVRT

II

HRA
340 340 330
His msec msec msec

CSprox
Fig. 18.41  Atrial Extrastimulation (AES)
During Antidromic Atrioventricular Reen-
trant Tachycardia (AVRT) Using a Left
CSdist 326
msec S2 Lateral Bypass Tract (BT). (A) A late-
coupled AES delivered when the atrioven-
326
RVA tricular (AV) junction is refractory (as
msec
indicated by lack of advancement of the
A timing of the local atrial electrogram record-
ing by the His bundle catheter) resets both
the next ventricular activation and the
I
subsequent atrial activation. This proves
that the supraventricular tachycardia (SVT)
II is an antidromic AVRT using an AV BT
anterogradely, and excludes preexcited
atrioventricular nodal reentrant tachycardia
HRA (AVNRT). In addition, the reset ventricular
340 340 activation occurs at a coupling interval
His msec msec identical to the AES coupling interval (i.e.,
exact coupling phenomenon), and the
CSprox
ventriculoatrial (VA) interval following the
AES remains similar to that during SVT,
which is consistent with antidromic
CSdist AVNRT. (B) Late-coupled AES delivered
S2 when the AV junction is refractory advances
RVA the subsequent QRS and terminates the
SVT by retrograde block in the His-Purkinje
B system–atrioventricular node. (C) An earlier
AES terminates the SVT without conduc-
tion to the ventricle (i.e., anterograde block
I in the BT). The AES advances the timing
of AV junctional atrial activation. CSdist,
II Distal coronary sinus; CSprox, proximal coro-
nary sinus; HRA, high right atrium; RVA,
right ventricular apex.
HRA
340 322
His msec msec

CSprox

CSdist
S2

RVA

reentrant circuit, because if there were intervening tissue involved, the
VA interval would increase and, subsequently, the A-A interval would
exceed the VES coupling interval. Similarly, a VES that captures the
atrium at a shorter coupling interval than that of the VES (paradoxical
capture phenomenon) indicates that the ventricular stimulation site is
not only inside the reentrant circuit but also closer to the ventricular
insertion site of the BT than the initial site of ventricular activation
over the AVN-HPS during the SVT, so that the VA interval following
the VES is shorter than that during the SVT. This is easier to demon-
strate with RV apical pacing during orthodromic AVRT mediated by
a right-sided BT.
Termination.  Termination of orthodromic AVRT by VES can occur
secondary to block of the VES retrogradely in the BT, conduction of
the VES retrogradely over the AVN-HPS with or without conduction
644 CHAPTER 18  Typical Atrioventricular Bypass Tracts

VES during orthodromic AVRT

II

V1

HRA 432 msec 432 msec 432 msec 432 msec

H H H
His
432 432
CSprox msec msec

CSdist
RVA S2

II
Fig. 18.42  Ventricular Extrastimulation (VES)
During Orthodromic Atrioventricular Reentrant V1
Tachycardia (AVRT) Using a Left Lateral Bypass
Tract (BT). (A) A late-coupled VES delivered when
the His bundle (HB) is refractory (as indicated by 434 msec 432 msec 370 msec 518 msec 414 msec
HRA
lack of advancement of the timing of the His poten- H H H
tial) fails to reset the supraventricular tachycardia His
(SVT). (B) An earlier VES fails to advance the timing 434 434
CSprox msec msec
of the HB but advances the subsequent atrial acti-
vation, indicating the presence of a retrogradely
conducting BT, and suggests orthodromic AVRT. CSdist
Note that the reset atrial impulse is followed by S2
RVA
a prolonged atrial–His bundle (AH) interval caused
by decremental anterograde conduction in the B
atrioventricular node (AVN). However, the local
ventriculoatrial (VA) interval (retrograde BT conduc- II
tion) remains constant. (C) An earlier VES delivered
before the HB is refractory resets the subsequent
V1
atrial activation and terminates the SVT by antero-
grade atrioventricular block in the AVN. (D) A more
430 msec 430 msec 350 msec
premature VES terminates the SVT by retrograde HRA
VA block in the BT, excluding atrial tachycardia, but H H H
can still occur in atrioventricular nodal reentrant His
tachycardia because the VES is delivered before CSprox
anterograde activation of the HB and could poten-
tially penetrate the AVN. CSdist, Distal coronary
sinus; CSprox, proximal coronary sinus; HRA, high CSdist
right atrium; RVA, right ventricular apex. S2
RVA
C

II

V1

430 msec 430 msec

HRA
H H H
His
CSprox

CSdist
RVA S2

D
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 645

up the BT, or retrograde conduction of the VES up the BT and preex-
citation of the atrium and subsequent anterograde block in the AVN-HPS
(the most common mechanism) (see Fig. 18.42). Termination of SVT
with a single VES strongly suggests orthodromic AVRT as the mechanism
of SVT in three settings: (1) when the VES is late-coupled (greater than
80% of TCL); (2) when the TCL is less than 300 milliseconds; and (3)
when the VES is delivered during HB refractoriness and is associated
with no atrial activation.
Ventricular entrainment.  Ventricular pacing at a CL approxi-
mately 10 to 30 milliseconds shorter than the TCL can easily entrain
AVRT. Although the mere demonstration of the tachycardia does not
help discrimination between the different SVT mechanisms, several
parameters during ventricular entrainment can help establish the lower
portion of the tachycardia circuit as macroreentrant involving the HPS/
ventricle (AVRT) or not (AVNRT), including the presence of manifest
fusion, VA interval during ventricular pacing as compared with that
during SVT, the postpacing interval (PPI), and differential-site ventricular
entrainment.43
Manifest ventricular fusion.  A requirement for the presence of
fusion is spatial separation between the sites of entrance to and exit
from the reentrant circuit. In orthodromic AVRT, the entrance and exit
of the reentrant circuit (to and from ventricular tissue) are separated
from each other, the entrance being from the HPS and the exit being
at the BT ventricular insertion site. In this setting, the paced wavefront
can activate a portion of the ventricles and enter the AVRT circuit and
at the same time the tachycardia wavefront emerge from the reentry
circuit at a distant exit site and activate another part of the ventricles.
Also, the relative proximity of the pacing site to the entry and exit sites
of the reentry circuit, is a critical determinant for the occurrence of
fusion during resetting and entrainment. Pacing at a site closer to the
BT ventricular insertion site (e.g., LV pacing in the setting of left free-
wall BTs, and RV basal pacing in the setting of right-sided or septal
BTs) than the entrance of the reentrant circuit to ventricular tissue (i.e.,
the HPS) would result in a larger degree of fusion of QRS morphology
between baseline morphology during orthodromic AVRT and that of
fully paced QRS (Fig. 18.43).44
Manifest ventricular fusion during SVT entrainment is proof that
the ventricle is part of the SVT circuit (i.e., diagnostic of AVRT). On
the other hand, such phenomena cannot occur during AVNRT and AT
because of the lack of spatial separation of the entrance and exit of the
AVNRT or AT circuit to the ventricles and because the ventricles are
not an obligatory part of that circuit.
ΔVA interval.  Entrainment of the SVT by RV pacing can help
differentiate orthodromic AVRT from AVNRT by evaluating the VA
interval during SVT (measured from the onset of surface QRS to high
RA electrogram) versus the VA interval during pacing (i.e., the SA
interval, measured from the ventricular pacing stimulus to the high RA
electrogram). The ventricle and atrium are activated in sequence during
orthodromic AVRT and during ventricular pacing, but in parallel during
AVNRT. Therefore the VA interval during orthodromic AVRT approxi-
mates that during ventricular pacing (see Fig. 18.43). In contrast, the
VA interval during AVNRT would be much shorter than that during
ventricular pacing (see Fig. 17.19). In general, a difference in the VA
interval (ΔVA [VApacing − VASVT]) greater than 85 milliseconds is con-
sistent with AVNRT, whereas a ΔVA of less than 85 milliseconds is
consistent with orthodromic AVRT (see Fig. 20.14).45,46

Ventricular entrainment of orthodromic AVRT Ventricular

pacing

II

V1
VA VA HA
138 msec 90 msec 137 msec
HRA HA
H H A A A A A 94 msec A
His H H H H H H

CSprox

CSdist
300 msec PPI = 340 msec 308 msec 310 msec
RVA

Fig. 18.43  Ventricular Entrainment of Orthodromic Atrioventricular Reentrant Tachycardia (AVRT) Using
a Concealed Superoparaseptal Bypass Tract. Note that the ΔVA interval (VApacing − VASVT) is less than 85
milliseconds and the (PPI − TCL) is less than 115 milliseconds, both of which favor orthodromic AVRT over
atrioventricular nodal reentrant tachycardia (AVNRT). In addition, ventricular fusion (between the paced and
tachycardia wavefronts) is observed during entrainment (right, pure paced QRS morphology), which is con-
sistent with AVRT and excludes AVNRT. Comparing the HA interval during the tachycardia (left) with that
during ventricular pacing during normal sinus rhythm at the TCL (right) demonstrates that the ΔHA interval
(HApacing − HASVT) is −43 milliseconds, which favors orthodromic AVRT over AVNRT; the HA interval is mea-
sured from the end of the His potential to the atrial electrogram in the high right atrium (HRA). CSdist, Distal
coronary sinus; CSprox, proximal coronary sinus; HA, His bundle–atrial; PPI, postpacing interval; RVA, right
ventricular apex; SVT, supraventricular tachycardia; TCL, tachycardia cycle length; VA, ventriculoatrial.
646 CHAPTER 18  Typical Atrioventricular Bypass Tracts
Postpacing interval.  The PPI reflects conduction time from the
ventricular pacing site to the SVT circuit, once around the reentry
circuit, and then back to the pacing site. The difference between the
PPI and TCL (PPI − TCL) represents the conduction time from the
pacing site to the reentry circuit and back. Thus the (PPI − TCL) dif-
ference can qualitatively estimate how far the reentrant circuit is from
the pacing site; the greater the (PPI − TCL) difference, the longer the
conduction time between the pacing site and reentry circuit, and the
greater the “electrical” distance is between the pacing site and the circuit.
The reentry circuit in AVRT involves the BT, ipsilateral atrium,
AVN-HB, and ipsilateral bundle branch and ventricle. On the other
hand, the circuit of AVNRT (typical or atypical) is confined above the
HB. Because the RV is closer to the AVRT circuit as compared to the
AVNRT circuit, the (PPI − TCL) difference following entrainment from
the RV apex is smaller in the setting of AVRT than during AVNRT (see
Fig. 18.43). In fact, a (PPI − TCL) difference of more than 115 milli-
seconds was found to identify AVNRT, whereas a (PPI − TCL) difference
of less than 115 milliseconds was consistent with orthodromic AVRT.
For borderline values, ventricular pacing at the RV base can help exag-
gerate the (PPI − TCL) difference in the setting of AVNRT, but without
significant changes in the setting of orthodromic AVRT (see differential-
site RV entrainment later).47,48
A relatively common phenomenon encountered during entrainment
of orthodromic AVRT by ventricular pacing is the prolongation of the
AH interval because of either decremental conduction properties of
the AVN or (in the presence of dual AVN physiology) a jump of antero-
grade conduction from the fast pathway to the slow pathway. The pro-
longed AH interval on the last entrained beat will contribute to
prolongation of the PPI that is not reflective of the distance of the
pacing site from the circuit. Thus the (PPI − TCL) differences obtained
after entrainment of orthodromic AVRT employing a septal BT can
actually overlap with those observed after entrainment of AVNRT. “Cor-
rection” of the PPI by subtracting the increment in AVN conduction
time in the first PPI (postpacing AH interval minus prepacing AH
interval) from the (PPI − TCL) difference (“corrected” [PPI − TCL])
has been found to improve the accuracy of this criterion. The difference
between AV intervals (postpacing AV interval minus prepacing AV
interval) can be taken for the latter adjustment when a His deflection
is not clearly visible (assuming the HV interval remains constant). A
corrected (PPI − TCL) difference of less than 110 milliseconds was
found to be more accurate in distinguishing orthodromic AVRT from
AVNRT than the uncorrected (PPI − TCL) difference.49,50
Furthermore, during orthodromic AVRT, the corrected (PPI − TCL)
difference can help localize the BT used for retrograde conduction. The
RV apical pacing site is closer to the reentrant circuit of orthodromic
AVRT utilizing a right-sided BT than orthodromic AVRT utilizing a
left-sided BT. Hence, as expected, the corrected (PPI − TCL) difference
is shorter (less than 55 milliseconds) in patients with orthodromic
AVRT with a right-sided BT when pacing the RV apex. Patients with
left-sided BTs typically have a corrected (PPI − TCL) difference of more
than 55 milliseconds.51
Of note, determinations of the corrected (PPI − TCL) and ΔVA
(VApacing − VASVT) after resetting with single or double VESs from the
RV apex, is of similar value for discrimination between AVNRT and
orthodromic AVRT, even when the SVT is interrupted by ventricular
pacing. Corrected (PPI − TCL) of more than 110 milliseconds and ΔVA
of more than 110 milliseconds after resetting identify AVNRT.52
Importantly, there are several potential pitfalls of the ΔVA interval
and the PPI criteria discussed previously. The TCL and VA interval are
often perturbed for a few cycles after entrainment. For this reason, care
should be taken not to measure unstable intervals immediately after
ventricular pacing. In addition, oscillations in the TCL and VA intervals
can occur spontaneously during the SVT. The discriminant points chosen
may not apply when the spontaneous variability is greater than 30
milliseconds. Also, it is possible to mistake isorhythmic VA dissociation
for entrainment if the pacing train is not long enough or the PCL is
too close to the TCL. Furthermore, this test is less reliable and should
be used with caution in patients with left lateral BTs.
In addition, these criteria may not apply to BTs with significant
decremental properties, although small decremental intervals are unlikely
to provide a false result. A higher cutoff value of 125 milliseconds was
found to increase the sensitivity for orthodromic AVNRT while main-
taining high specificity. Slow, decremental BT conduction can also affect
the sensitivity of the ΔVA criteria for orthodromic AVRT, but the speci-
ficity remains high. Therefore, if any standard criteria positive for
orthodromic AVRT (PPI − TCL <115 milliseconds, corrected [PPI −
TCL] <110 milliseconds, and ΔVA < 85 milliseconds) is diagnostic of
orthodromic AVRT, despite discordance among each other (which can
occur about 50% of the time).43
Differential-site RV entrainment.  Differential-site RV entrain-
ment (from RV apex vs. RV base) can help distinguish AVNRT from
orthodromic AVRT. Because the reentrant circuit in AVNRT is confined
above the HB and does not involve the ventricle, the base of the RV is
electrically more distant (although anatomically closer) to the tachycardia
circuit than the RV apex, given that the His-Purkinje network directly
inserts near the RV apex. Consequently, the PPI after entrainment of
AVNRT from the RV base is longer than that following entrainment
from the RV apex. The difference in PPI from the RV base versus the
RV apex is largely composed of the extra time required to reach the
circuit from the base versus the apex (approximately 30 milliseconds).
Conversely, in orthodromic AVRT, in which the ventricles are an obliga-
tory part of the circuit, the basal pacing site relative to the RV apex is
variably related to the circuit, closer than the RV apex with septal BTs
and equidistant with free-wall BTs, but the paced wavefront from either
the RV apex or RV base tends to have, on average, approximately equal
access and proximity to the reentrant circuit involved in orthodromic
AVRT. Therefore the time taken to reach the circuit (and hence the PPI)
tends to be similar, irrespective of the location of the BT.
Correction of the PPI (to avoid potential error introduced by dec-
remental conduction within the AVN during ventricular pacing) increases
the accuracy of this method, although the degree of decrement is not
expected to be materially different from basal rather than apical pacing
as long as the pacing rates are the same or similar. The “corrected PPI”
is obtained by subtracting any increase in the AV interval of the return
cycle beat (as compared with the AV interval during SVT). A differential
corrected (PPI − TCL) difference of more than 30 milliseconds after
transient entrainment was found to be consistent with AVNRT (i.e.,
corrected [PPI − TCL] difference following pacing from the RV base
was consistently at least 30 milliseconds longer than that following
pacing from the RV apex). In contrast, a corrected (PPI − TCL) differ-
ence of less than 30 milliseconds was observed in all cases of orthodromic
AVRT. In addition, a differential VA interval (VA interval during entrain-
ment from RV base versus RV septum) of more than 20 milliseconds
was consistent with AVNRT, whereas a differential VA interval of less
than 20 milliseconds was consistent with orthodromic AVRT.53,54
The main advantage of this technique is that the differential VA
interval can be calculated from the last paced beat if the tachycardia is
terminated after transient entrainment.
Length of pacing drive required for entrainment.  Assessing
timing and type of response of SVT to RV pacing can also help dif-
ferentiate orthodromic AVRT from AVNRT. In the setting of orthodromic
AVRT, ventricular tissue is the only intervening tissue between the pacing
wavefront and the ventricular insertion site of the BT. Therefore once
ventricular capture is achieved during RV pacing, the paced wavefront
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 647

propagates to the ventricular insertion site of the BT quickly and resets
the tachycardia. Consequently, RV pacing results in a faster response
of resetting the tachycardia. In the setting of AVNRT, the pacing site is
distant from the SVT circuit, and the paced wavefront has to propagate
though ventricular tissue, then through the HPS followed by AVN tissue
prior to resetting the tachycardia. As a consequence, resetting of AVNRT
is delayed for several captured paced beats as compared with ortho-
dromic AVRT.
After initiation of synchronized RV pacing during SVT at a CL that
is 10 to 40 milliseconds shorter than the TCL, once constant-appearing
QRS complexes (as evidenced by fixed pacing morphology of the surface
ECG, either pure paced morphology or fixed QRS fusion) are observed,
the number of RV paced beats required to accelerate the SVT to the
PCL is determined. The first atrial capture beat accelerated to the PCL
is identified by demonstrating a fixed ventricular SA capture interval.
One report demonstrated that using a cutoff of one beat to accelerate
the SVT to the PCL could identify all orthodromic AVRT cases and
essentially exclude all cases of AVNRT with high accuracy. On the con-
trary, if two or more beats are required to accelerate SVT to the PCL,
this can distinguish AVNRT from orthodromic AVRT with very high
confidence as well (see Fig. 20.13).
The major advantage of this method is its independence of tachy-
cardia continuation after cessation of pacing. However, it is likely that
these criteria may not be applicable at PCLs more than 40 milliseconds
shorter than the TCL or prematurity of more than 80% of the TCL
because resetting of the tachycardia can occur earlier in AVNRT in
response to a greater degree of penetration into the tachycardia circuit.
In addition, these findings may not apply in cases in which AVNRT
occurs in the setting of a bystander BT because SVT may be reset using
the bystander BT. In addition, although this technique is effective for
differentiating septal pathways from atypical AVNRT, it may be less
useful in patients with BTs remote from the pacing stimulus (e.g., left
free-wall BTs) (see Fig. 20.15).55
Atrial resetting during the transition zone.  On initiation of
RV pacing trains during SVT at a rate slightly faster than the TCL, there
is a transition zone during which the pacing train fuses with anterograde
ventricular activation (i.e., the zone in which the paced QRS complexes
show progressive fusion with the SVT complexes) until stable QRS
morphology is observed (either completely paced or constantly fused).
The transitional zone begins with progressive fusion beats between the
paced and tachycardia wavefronts and ends with the first beat of stable
QRS morphology, the latter representing constant fusion in the case of
orthodromic AVRT and a fully paced QRS morphology in patients with
AVNRT. In patients with AVNRT or AT, acceleration of the timing of
atrial activation cannot occur through the AVN during the transition
zone. The reason is that the HB is expected to be refractory, as indicated
by at least some ventricular activation still occurring by anterograde
conduction over the HPS. If perturbation of atrial timing occurs during
the transition zone, it indicates the presence of a retrogradely conduct-
ing BT, which can be an integral part of the SVT circuit (i.e., orthodromic
AVRT) or a bystander (Fig. 18.44). In one report, these criteria showed
excellent diagnostic accuracy and could be applied regardless of whether
entrainment was achieved or whether the SVT terminated during pacing.
Perturbation of atrial timing of at least 15 milliseconds or a fixed SA
interval measured from the last beat of the transition zone was seen in
all the patients with orthodromic AVRT and in none of the patients
with AVNRT or AT (unless a bystander retrogradely conducting BT is
present).54,56
Of note, the number of reset beats (defined as fixed SA interval)
in the transitional zone (during ventricular overdrive pacing from
the RV apex during orthodromic AVRT) depends on the proximity
of the BT to the pacing site; hence, it can predict BT location. Right-
sided BTs produce reset earlier than left-sided BTs, and a cut-off of
more than two beats with a fixed SA interval within the transitional
zone was found to successfully discriminate between left-sided and
right-sided BTs.57

Transition zone

I
Resetting
II

V1

442 msec 442 msec 442 msec 442 msec 428 msec 420 msec 420 msec 420 msec 420 msec 420 msec 420 msec
HRA

His

CSprox

CSdist

442 msec 442 msec 420 msec 420 msec 420 msec 420 msec 420 msec 420 msec 420 msec
RVA
S1 S1 S1 S1 S1 S1 S1 S1
Fig. 18.44  Resetting of Supraventricular Tachycardia (SVT) During the Transition Zone. Overdrive ven-
tricular pacing is started from the RVA at a cycle length (CL) of 420 milliseconds, slightly shorter than the
SVT CL (442 milliseconds). On initiation of right ventricular pacing, there is a transition zone during which
the paced wavefronts fuse with anterograde ventricular activation, before stable QRS morphology ensues.
Note that advancement of atrial activation (resetting) initially occurred during the transition zone, indicating
orthodromic atrioventricular reentrant tachycardia as the mechanism of the SVT. CSdist, Distal coronary sinus;
CSprox, proximal coronary sinus; HRA, high right atrium; RVA, right ventricular apex.
648 CHAPTER 18  Typical Atrioventricular Bypass Tracts
Permanent junctional reciprocating tachycardia.  A VES delivered
during PJRT can produce decremental conduction in the BT and pro-
longation of the VA interval, resulting in possible delay of the next
atrial activation (i.e., post excitation or delay of excitation; see Fig.
18.39). Such a response excludes AT, and when this occurs in response
to a VES delivered when the HB is refractory, it is diagnostic of ortho-
dromic AVRT, and excludes both AT and AVNRT. In addition, a late-
coupled VES introduced when the HB is refractory frequently blocks
retrogradely in the BT and reproducibly terminates the tachycardia
without reaching the atrium, again excluding both AT and AVNRT.43
The ability to preexcite the atrium with a VES introduced when the
HB is refractory is difficult to demonstrate in PJRT because of the long
conduction time over the BT, the decremental conduction properties
of the BT, and the fact that the TCL is just longer than the shortest
length at which the BT is capable of retrograde conduction. This can
be facilitated by introduction of the PVC at a site closer to the BT
ventricular insertion.
Antidromic AVRT.  Similar to orthodromic AVRT, ven-
tricular pacing and VES can easily entrain or reset anti-
dromic AVRT because the ventricle is part of the reentrant
circuit. Because both orthodromic and antidromic AVRTs use
similar reentry circuits, the concepts of resetting and entrainment
discussed for orthodromic AVRT also apply, to a large degree, to anti-
dromic AVRT.
Of note, the development of retrograde RBBB following a VES
introduced during the SVT can help distinguish antidromic AVRT from
AVNRT. When the VES results in retrograde RBBB (i.e., blocks retro-
gradely in the RB), such RBBB will not change the timing of the next
atrial activation in the setting of AVNRT. In contrast, in antidromic
AVRT using a right-sided BT, such RBBB will increase the size of the
reentrant circuit, because the impulse cannot reach the HB through
the RB and has to travel transseptally and then retrogradely over the
LB. This results in prolongation in the VA interval and delay in the
timing of the next atrial activation. The increment in the VA interval
is caused by prolongation of the VH interval and, if RBBB persists, the
SVT will have a long VH interval.
Antidromic AVRT can usually be terminated by ventricular pacing.
Termination occurs by retrograde invasion and concealment in the BT,
resulting in anterograde block over the BT following conduction to the
atrium through the AVN.
Para-Hisian Pacing During Tachycardia
Para-Hisian pacing during tachycardia can help discriminate between
AVRT and AVNRT. This pacing maneuver is discussed in detail in Chapter
20. Briefly, entrainment of the SVT is performed by pacing at the para-
Hisian region using the HB catheter at a PCL that is 10 to 30 milliseconds
shorter than the TCL. Entrainment is confirmed when the atrial CL
accelerates to the PCL, without a change in the atrial activation sequence,
and the tachycardia continues after pacing is discontinued.58
Para-Hisian entrainment is performed by alternately pacing at high-
energy output for HB-RB capture or lower energy output for HB-RB
noncapture. Entrainment with HB-RB capture is recorded separately
from that without HB-RB capture. The SA and local VA intervals during
HB-RB capture and noncapture are then examined.
If para-Hisian entrainment cannot be performed because of repetitive
termination of the tachycardia during entrainment attempts, isopro-
terenol infusion may be used to help sustain the rhythm. Alternatively,
single or double VESs can be given to reset the tachycardia (para-Hisian
resetting). These VESs are delivered at progressively shorter coupling
intervals until the first VES that reliably advances or resets the tachycar-
dia. This is performed alternately with high- or low-energy outputs to
achieve HB-RB capture and noncapture, respectively. As with para-Hisian
entrainment, the retrograde atrial activation sequence and timing are
compared during para-Hisian resetting to characterize the response.
In AVNRT (typical or atypical), the AVN-AVN pattern is observed
in response to para-Hisian entrainment or resetting; that is, both the
SA and the local VA intervals increase during HB-RB noncapture com-
pared with HB-RB capture.
In orthodromic AVRT, the BT-BT pattern or BT-BTL pattern is
observed. In the setting of a BT-BT pattern, the SA and local VA intervals
are usually not significantly different between HB-RB capture and non-
capture. Conversely, in the case of a BT-BTL pattern, the SA interval
increases on HB-RB noncapture, but without significant change in the
local VA interval.
A ΔSA interval of less than 40 milliseconds was found to be a rea-
sonable guide to separating the AVN-AVN from the BT-BT response.
Patients with AVNRT uniformly have a ΔSA interval of greater than 40
milliseconds, whereas those with AVRT have a ΔSA interval of less than
40 milliseconds (except for rare patients with a left lateral BT). Using
the Δ local VA interval (instead of the ΔSA interval) provide a more
accurate parameter for discrimination between AVNRT and AVRT.
An AVN-AVN or fusion pattern during para-Hisian entrainment
or resetting has not been observed in patients with AVNRT. This is a
potential advantage over para-Hisian pacing during NSR in identifying
the presence of a BT. Because retrograde VA conduction can only proceed
over a single route during entrainment of the SVT (assuming that
a complex scenario such as multiple BTs is not present), the various
forms of retrograde fusion that might be seen during para-Hisian
pacing during NSR cannot occur during para-Hisian entrainment or
resetting.
Diagnostic Maneuvers During Sinus Rhythm After
Tachycardia Termination
Atrial Pacing at the Tachycardia Cycle Length
Under comparable autonomic tone, the PR and AH intervals during
atrial pacing at a CL similar to the TCL should be comparable to those
during orthodromic AVRT. These findings are also observed in the
setting of AT. In contrast, the AH and PR intervals during atrial pacing
would be longer than those during tachycardia in the setting of AVNRT,
assuming the slow pathway has been engaged. A ΔAH (AHpacing − AHSVT)
of more than 40 milliseconds has been reported to favor AVNRT.48
A major limitation of ΔAH criteria, however, is the sensitivity of
the AVN to rapid fluctuations in autonomic tone so that comparison
of AH intervals between tachycardia and pacing should be done close
in time, allowing for minimal change in the autonomic state of the
patient.43
Ventricular Pacing at the Tachycardia Cycle Length
Under comparable autonomic tone status, 1:1 VA conduction over the
AVN should be maintained during ventricular pacing at a CL similar
to the TCL. If VA block develops during ventricular pacing, orthodromic
AVRT is unlikely, and AT and AVNRT are favored.
In addition, ventricular pacing during NSR at a PCL similar to the
TCL results in HA and VA intervals that are shorter than those during
orthodromic AVRT because the HB and atrium are activated sequentially
during orthodromic AVRT but in parallel during ventricular pacing
whereby the atrium is activated via the BT (see Fig. 18.43). To help
distinguish between orthodromic AVRT and AVNRT, the HA interval
is measured from the end of the His potential (where the impulse leaves
the HB to enter the AVN) to the atrial electrogram in the high RA
recording and the ΔHA interval (HApacing − HASVT) is calculated. In the
setting of orthodromic AVRT the ΔHA interval is typically less than
−10 milliseconds. In contrast, in the setting of AVNRT the ΔHA interval
is typically more than −10 milliseconds because the HA interval during
 CHAPTER 18  Typical Atrioventricular Bypass Tracts
AVNRT is shortened by parallel activation of both the HB and the
atrium during the tachycardia (i.e., the HA interval is a “pseudo-interval”
that represents activation times of the HB and atrium), whereas the
HB and atrium are activated sequentially during ventricular pacing in
the absence of a BT (i.e., the HA interval represents a true conduction
time interval from the HB to the atrium). The ΔHA interval is even
more pronounced in atypical AVNRT, which has a lower common
pathway that is longer than that in typical AVNRT. In focal junctional
tachycardia, the ΔHA interval is typically close to 0.30
The ΔHA interval criterion has high specificity, sensitivity, and posi-
tive predictive accuracy for differentiation between AVNRT and ortho-
dromic AVRT, but it has certain limitations. The main limitation of the
ΔHA interval criterion is the ability to record the retrograde His potential
during ventricular pacing. The retrograde His potential generally appears
before the local ventricular electrogram in the HB tracing, and can be
verified by the introduction of a VES that causes the His potential to
occur after the local ventricular electrogram. Moreover, pacing from
different sites (e.g., midseptum) may allow earlier penetration into the
HPS and facilitate observation of a retrograde His potential. When the
retrograde His potential is not visualized, using the ΔVA interval instead
of the ΔHA interval is not as accurate in discriminating orthodromic
AVRT from AVNRT. Another limitation is that VA conduction during
ventricular pacing may not occur over the BT but propagates prefer-
entially over the HPS-AVN, leading to earlier atrial activation over
this pathway than over the BT. If this were the case, the HA interval
during ventricular pacing would be shorter than that observed if the
atrium were activated via the BT. This would yield a more negative
ΔHA interval.
It is important to recognize that the atrial activation sequence during
ventricular pacing can be mediated by retrograde conduction over the
BT, over the AVN, or a fusion of both, and consequently it can be similar
to or different from that during orthodromic AVRT.
Exclusion of Other Arrhythmia Mechanisms
AVNRT and AT arising near the AV groove can mimic orthodromic
AVRT and, in the presence of a manifest BT, those tachycardias can be
associated with ventricular preexcitation mimicking antidromic AVRT,
whereby the BT is functioning as an innocent bystander. Therefore EP
testing is required, not just to identify the presence of a BT, but also to
define its role in any clinical or inducible arrhythmia. Boxes 18.4 and
18.5 summarize the EP findings indicative of the presence of a BT and
its potential participation in an inducible SVT. Exclusion of other SVT
mechanisms is necessary because the mere presence of a BT is not
adequate to make a diagnosis and a treatment strategy (Boxes 18.6–18.8).
Furthermore, the presence of multiple BTs is not infrequent, and
careful EP testing is required to evaluate this possibility. Several clinical
BOX 18.4  Electrophysiological Findings
Indicating Presence of Retrograde
Atrioventricular Bypass Tract Function
• Eccentric atrial activation sequence during ventricular pacing
• RV apical pacing producing longer VA interval and/or different atrial activa-
tion sequence compared with that during RV basilar pacing
• Para-Hisian pacing producing similar VA interval with and without HB capture
or producing different atrial activation sequence depending on whether the
HB is captured
• VES delivered when the HB is refractory advances the next atrial activation
during SVT
HB, His bundle; RV, right ventricular; SVT, supraventricular
tachycardia; VA, ventriculoatrial; VES, ventricular extrastimulus.
649
and EP findings are indicative of the presence of multiple BTs (Box
18.9; Figs. 18.45 and 18.46; see eFig. 18.1). However, despite these various
methods, many BTs are not identified until after catheter ablation of
the first BT. Failure to detect the presence of multiple BTs during EP
testing has been reported in as many as 5% to 15% of patients. This
may be explained by the fact that changes in the preexcitation pattern
can be subtle in shifting from one BT to another. Furthermore, one BT
can preferentially conduct during atrial pacing or participate in preex-
cited tachycardias while another BT can be responsible for the retrograde
limb during orthodromic AVRT or ventricular pacing. In addition,
there may be fusion of BT conduction, anterograde or retrograde. Repeti-
tive concealed conduction into the BT during AVRT may also preclude
identification of that BT before ablation of the first BT.
LOCALIZATION OF THE BYPASS TRACT
Several EP techniques can help map the location of the AV BT and
guide catheter ablation (Box 18.10). Those techniques are best used in
combination to improve mapping accuracy and ablation outcome.
Pacing From Multiple Atrial Sites
The closer the pacing site to the BT atrial insertion, the more rapidly
the impulse reaches the BT relative to the AVN and, thus, the greater
the degree of preexcitation and the shorter the P-delta interval. This
method is especially helpful when the BT cannot conduct retrogradely,
prohibiting localization with atrial mapping during SVT or ventricular
pacing.
Preexcitation Index
The preexcitation index analyzes the coupling interval of the VES
(delivered from the RV) that resets orthodromic AVRT as a percent-
age of the TCL. A relative preexcitation index (the ratio of the coupling
interval to the TCL) of more than 90% of a VES that advances atrial
activation during orthodromic AVRT suggests that the BT is close to
the site of ventricular stimulation (i.e., RV or septal BT). An absolute
preexcitation index (TCL minus VES coupling interval) of at least 75
milliseconds suggests a left free-wall BT, an index of less than 45 mil-
liseconds suggests a septal BT, and an index of 45 to 75 milliseconds is
indeterminate.
BOX 18.5  Electrophysiological Findings
Indicating Presence and Participation
of Atrioventricular Bypass Tract in
Supraventricular Tachycardia
• VES delivered during SVT when the HB is refractory terminates the SVT
without atrial activation.
• VES delivered during SVT when the HB is refractory delays the next atrial
activation.
• VES during SVT captures the atrium at the same coupling interval as that
of the VES (exact capture phenomenon).
• VES delivered during SVT captures the atrium at a shorter coupling interval
than that of the VES (paradoxical capture phenomenon).
• VA interval (with or without concomitant prolongation in TCL) prolonged
during the SVT secondary to the development of BBB.
• Entrainment of the SVT by ventricular pacing results in prolongation of the
VA interval (VApacing > VASVT).
BBB, Bundle branch block; HB, His bundle; SVT, supraventricular
tachycardia; TCL, tachycardia cycle length; VA, ventriculoatrial;
VES, ventricular extrastimulus.
650 CHAPTER 18  Typical Atrioventricular Bypass Tracts
BOX 18.6  Exclusion of Atrial Tachycardia
Effects of BBB
• Prolongation of surface VA interval during SVT (with or without TCL prolonga-
tion) on development of BBB excludes AT.
Oscillations in TCL
• Spontaneous changes in TCL accompanied by constant VA interval (VA linking)
exclude AT.
• Changes in atrial CL that are predicted by the change in the preceding ven-
tricular CL argue against AT.
VES During SVT
• VES that terminates the SVT without atrial activation excludes AT.
• VES that delays the next atrial activation excludes AT.
• VES during SVT that captures the atrium at the same coupling interval as that
of the VES (exact capture phenomenon) excludes AT.
• VES delivered during SVT that captures the atrium at a shorter coupling interval
than that of the VES (paradoxical capture phenomenon) excludes AT.
• When a VES delivered during HB refractoriness advances the next atrial
activation with an atrial activation sequence similar to that during SVT, AT
is unlikely.
• Manifest ventricular fusion during resetting excludes AT.
Overdrive Ventricular Pacing During SVT
• If atrial activation sequence during ventricular entrainment is similar to that
during the SVT, AT is less likely.
AT, Atrial tachycardia; AVRT, atrioventricular reentrant tachycardia; BBB, bundle branch block; CL, cycle length; HB, His bundle; NSR, normal
sinus rhythm; SVT, supraventricular tachycardia; TCL, tachycardia cycle length; VA, ventriculoatrial; VES, ventricular extrastimulus.
BOX 18.7  Exclusion of Atrioventricular Nodal Reentrant Tachycardia
SVT Induction by VES
• ΔVA (VAVES − VASVT) <85 msec favors orthodromic AVRT over AVNRT.
• (PPIVES − TCL) <115 msec favors orthodromic AVRT over AVNRT.
Atrial Activation Sequence
• Eccentric atrial activation sequence during the SVT excludes AVNRT (with
the exception of left variant AVNRT).
Effects of BBB
• Prolongation of VA interval or TCL on development of BBB excludes AVNRT.
Oscillations in TCL
• Spontaneous changes in TCL accompanied by constant VA interval (VA linking)
make AVNRT unlikely.
Differential RV Pacing
• If the atrial activation sequence changes during pacing at the RV apex versus
pacing at the RV base, AVNRT is less likely.
• If the SA interval is shorter with pacing from the base than from the apex at
the same PCL, AVNRT is less likely.
VES During SVT
• VES delivered during SVT when the HB is refractory that resets (advances or
delays) or terminates the SVT excludes AVNRT.
• VES during SVT that conducts to the atrium at the same coupling interval as
that of the VES (exact capture phenomenon) excludes AVNRT.
• VES delivered during SVT that conducts to the atrium at a shorter coupling
interval than that of the VES (paradoxical capture phenomenon) excludes
AVNRT.
• Presence of A-V electrogram sequence at cessation of ventricular pacing
generally excludes AT.
• Manifest ventricular fusion during entrainment indicates AVRT and
excludes AT.
Overdrive Atrial Pacing During SVT
• If the VA interval following the last entrained QRS is reproducibly constant
(with <10 msec variation), despite pacing at different CLs or for different
durations (VA linking) and similar to that during TCL, AT is unlikely.
• If the VA interval following the last entrained QRS is reproducibly constant
(with <14-msec variation), despite pacing at different atrial sites (VA linking),
AT is unlikely.
• Demonstration of entrainment with manifest atrial fusion excludes focal AT.
Atrial Pacing During NSR at Tachycardia CL
• If the VA interval following the last entrained QRS is reproducibly constant
(with <10-msec variation), despite pacing at different CLs or for different
durations (VA linking) and similar to that during TCL, AT is unlikely.
• If the VA interval following the last entrained QRS is reproducibly constant
(with <14-msec variation), despite pacing at different atrial sites (VA linking),
AT is unlikely.
Ventricular Pacing During NSR at Tachycardia CL
• If retrograde atrial activation sequence during ventricular pacing is similar to
that during SVT, AT is less likely.
• Manifest ventricular fusion during resetting excludes AVNRT.
• Preexcitation index (the difference between the TCL and the longest VES
coupling interval at which atrial capture occurs during tachycardia) ≥100 msec
characterizes AVNRT, whereas an index <45 msec is consistent with AVRT
with a septal BT.
• Corrected (PPI − TCL) <110 msec (after resetting with single or double VESs
from the RV apex) argues against AVNRT.
Overdrive Ventricular Pacing During SVT
• ΔVA interval (VApacing − VASVT) <85 msec argues against AVNRT.
• PPI − TCL <115 msec argues against AVNRT.
• Corrected PPI − TCL <110 msec argues against AVNRT.
• Manifest ventricular fusion during entrainment indicates AVRT and excludes
AVNRT.
• Acceleration of the SVT to the PCL occurring after a single captured paced
RV complex is consistent with orthodromic AVRT and essentially excludes
AVNRT.
• Differential corrected PPI − TCL of <30 msec after transient entrainment from
the RV apex versus the RV base is consistent with orthodromic AVRT and
excludes AVNRT.
• Differential VA interval (ventricular stimulus-to-atrial interval during entrain-
ment from RV base vs. RV septum) of <20 msec is consistent with orthodromic
AVRT and excludes AVNRT.
• Atrial resetting (perturbation of atrial timing by >15 msec) during the transition
zone is consistent with orthodromic AVRT and excludes AVNRT or AT (unless
a bystander retrogradely conducting BT is present).
• Acceleration of the SVT to the PCL occurring by the first beat with stable
paced QRS morphology is consistent with orthodromic AVRT and essentially
excludes AVNRT.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 651

BOX 18.7  Exclusion of Atrioventricular Nodal Reentrant Tachycardia—cont’d

AES During SVT
• Demonstration of resetting with manifest atrial fusion excludes AVNRT.
Overdrive Atrial Pacing During SVT
• ΔAH interval (AHpacing − AHSVT) <20 msec excludes AVNRT.
• Demonstration of entrainment with manifest atrial fusion excludes AVNRT.
• Entry into the tachycardia circuit within 1 beat indicates AVRT, whereas
entry into the circuit occurring only after 3 or more beats is consistent with
AVNRT.
Atrial Pacing During NSR at Tachycardia CL
• ΔAH interval (AHpacing − AHSVT) <20 msec excludes AVNRT.

Para-Hisian Pacing During SVT Ventricular Pacing During NSR at Tachycardia CL

• SA and the local VA intervals that remain constant regardless of whether the
HB-RB is being captured indicate orthodromic AVRT and exclude AVNRT.
• SA interval prolongation on HB-RB noncapture, but without significant change
in the local VA interval, indicates orthodromic AVRT and excludes AVNRT.
• ΔSA interval <40 msec indicates AVRT (except for rare patients with a left
lateral BT) and argue against AVNRT.
• ΔHA interval of less than −10 msec makes AVNRT unlikely.
Para-Hisian Pacing During NSR
• Para-Hisian pacing producing similar VA interval, regardless of whether HB
capture occurs, and/or different atrial activation sequence, depending on
whether HB capture occurs, makes AVNRT unlikely.

AES, Atrial extrastimulation; AH, atrial–His bundle; AVNRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reentrant
tachycardia; BBB, bundle branch block; BT, bypass tract; CL, cycle length; HA, His bundle–atrial interval; HB, His bundle; NSR, normal sinus
rhythm; PCL, pacing cycle length; PPI, postpacing interval; RB, right bundle branch; RV, right ventricle; SA, stimulus-to-atrial; SVT,
supraventricular tachycardia; TCL, tachycardia cycle length; VA, ventriculoatrial; VES, ventricular extrastimulus.

BOX 18.8  Differentiation Between Antidromic Atrioventricular Reentrant Tachycardia and

Preexcited Atrioventricular Nodal Reentrant Tachycardia
SVT Features
• HASVT <70 msec excludes antidromic AVRT.
• Positive HV or VH interval ≤10 msec (especially when HA interval is ≤50 msec)
suggests AVNRT.
Termination of SVT
• Continuation of the SVT at the same TCL, despite anterograde block in the
BT (by drugs, mechanical trauma, or ablation), is diagnostic of AVNRT and
excludes antidromic AVRT.
• Block of the BT by drugs and subsequent induction of narrow-complex SVT
with the same TCL, HA interval, and retrograde atrial activation sequence as
that of the preexcited SVT induced before the BT block is diagnostic of pre-
excited AVNRT and excludes antidromic AVRT.
• Termination of SVT in response to carotid sinus massage or adenosine:
• AVNRT terminates after atrial activation (secondary to anterograde block
down the slow pathway).
• Classic antidromic AVRT terminates after ventricular activation (secondary
to retrograde block up the AVN).
Effects of BBB
• Prolongation of surface ECG VA interval (often with prolonged TCL) on develop-
ment of BBB excludes AVNRT.
SVT Induction With Ventricular Stimulation
• Induction of the SVT by ventricular pacing at a PCL similar to the TCL or by
a VES that advances the timing of the His potential by a coupling interval
(i.e., H1-H2 interval) similar to the H-H during the SVT, the HA interval fol-
lowing such a VES is compared with that during the SVT:
• HAVES or HApacing > HASVT is diagnostic of AVNRT and excludes antidromic
AVRT.
• HAVES or HApacing ≤ HASVT is diagnostic of antidromic AVRT and excludes
AVNRT.
AES Delivered During SVT
• Late-coupled AES is delivered close to the BT atrial insertion site during SVT
when the AV junctional atrium is refractory. If it advances the timing of both
the next ventricular activation and the subsequent atrial activation, it proves
that the SVT is antidromic AVRT using an AV BT anterogradely, and excludes
preexcited AVNRT.
• AES during the SVT that advances ventricular activation and does not affect
VA interval excludes AVNRT and is diagnostic of antidromic AVRT.
• Exact atrial and ventricular capture by AES delivered when the AV junction
is depolarized excludes AVNRT.
Entrainment of SVT by Atrial Pacing
• Failure of entrainment by atrial pacing to influence the VA interval during SVT
excludes AVNRT.
• The presence of a fixed short VH interval during entrainment of the SVT with
atrial pacing suggests antidromic AVRT, and makes AVNRT unlikely (but does
not exclude AVNRT).
Entrainment of SVT by Ventricular Pacing
• Failure of entrainment by ventricular pacing to influence the VA interval during
SVT excludes AVNRT.
Ventricular Pacing During NSR at the Tachycardia CL
• Pacing at the RV apex at TCL is performed, and the HA interval during RV
pacing is compared with the HA interval during SVT. (It is important to verify
that VA conduction occurred only over the same pathway as during SVT for
this analysis to be valid.)
• HApacing > HASVT is diagnostic of AVNRT and excludes AVRT.
• HApacing ≤ HASVT is diagnostic of AVRT and excludes AVNRT.
• VA block during RV apical pacing excludes AVRT.

AES, Atrial extrastimulus; AV, atrioventricular; AVNRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reentrant tachycardia;
BBB, bundle branch block; BT, bypass tract; CL, cycle length; HA, His bundle–atrial; ECG, electrocardiogram; HV, His bundle–ventricular;
NSR, normal sinus rhythm; PCL, pacing cycle length; RV, right ventricle; SVT, supraventricular tachycardia; TCL, tachycardia cycle length;
VA, ventriculoatrial; VES, ventricular extrastimulus; VH, ventricular–His bundle.
652 CHAPTER 18  Typical Atrioventricular Bypass Tracts
BOX 18.9  Electrophysiological Findings
Indicating Presence of Multiple
Atrioventricular Bypass Tracts
During Preexcited Rhythms (NSR, PACs, Spontaneous or
Induced AF, RA, and LA Pacing)
• Changing anterograde delta wave (i.e., variations in preexcited QRS mor-
phology). Atrial pacing from different sites (high RA and CS) may accentuate
preexcitation over one BT and not the other, and help unmask the changes
in the delta wave.
• Atypical pattern of preexcitation (i.e., does not conform to an expected QRS
morphology for a given location)
• Changing anterograde delta wave following antiarrhythmic agents (e.g.,
amiodarone or class I agents) that may block one BT and not the other or
following ablation of one BT
During Ventricular Pacing at Different CLs and From
Multiple Pacing Sites
• Evidence of multiple routes of retrograde atrial activation:
• Changing P wave morphology or atrial activation sequence
• Multiple atrial breakthrough sites
• Changing VA interval
• Evidence of mismatch of site of anterograde preexcitation and site of ret-
rograde atrial activation observed during ventricular pacing
During Orthodromic AVRT
• Evidence of multiple routes of retrograde atrial activation:
• Changing P wave morphology or atrial activation sequence
• Multiple atrial breakthrough sites
• Changing VA interval
• Failure to delay atrial activation at all sites with the development of BBB
ipsilateral to the BT
• Evidence of multiple routes of anterograde ventricular activation:
• Intermittent anterograde fusion (preexcited) complexes
• Evidence of mismatch of site of anterograde preexcitation and site of ret-
rograde atrial activation observed during orthodromic AVRT
During Antidromic AVRT
• Eccentric atrial activation sequence
• Varying degrees of anterograde fusion
• Changing VH interval without any change in the TCL or atrial activation
sequence (suggesting that the HPS is not part of the reentrant circuit)
• Tachycardia CL during antidromic AVRT slower than orthodromic AVRT in
the same patient (in absence of dual AVN pathways)
• Anterograde ventricular activation over posteroseptal BT
• The mere presence of antidromic AVRT
AF, Atrial fibrillation; AVN, atrioventricular node; AVRT, atrioventricular
reentrant tachycardia; BBB, bundle branch block; BT, bypass tract;
CL, cycle length; CS, coronary sinus; HPS, His-Purkinje system;
LA, left atrium; NSR, normal sinus rhythm; PAC, premature atrial
complex; RA, right atrium; TCL, tachycardia cycle length;
VA, ventriculoatrial; VH, ventriculo-His.
Effects of Bundle Branch Block During Orthodromic
Atrioventricular Reentrant Tachycardia
Prolongation of the TCL and, more importantly, the surface VA interval
by more than 35 milliseconds following the development of BBB is
diagnostic of AVRT using a free-wall BT ipsilateral to the BBB (LBBB
with left-sided BT, and RBBB with right-sided BT). Superoparaseptal
and posteroseptal BTs are associated with a lesser degree of prolonga-
tion of the VA interval (approximately 5 to 25 milliseconds) on the
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
HRA
His
CSprox
CSdist
RVA S1 S1 S1 S1
500 msec
Fig. 18.45  Identifying Multiple Bypass Tracts (BTs) in the Same
Patient. The presence of multiple BTs is indicated by the mismatch of
sites of anterograde preexcitation during normal sinus rhythm (the delta
wave morphology is consistent with anterograde conduction over a right
anterior BT) and site of retrograde atrial activation observed during ven-
tricular pacing (the atrial activation sequence is consistent with ventricu-
loatrial conduction over a left lateral BT). CSdist, Distal coronary sinus;
CSprox, proximal coronary sinus; HRA, high right atrium; RVA, right ven-
tricular apex.
development of BBB (RBBB with superoparaseptal BT, and LBBB with
posteroseptal BT). In an analogous fashion, entrainment of the SVT
by ventricular pacing that results in prolongation of the VA interval
(VApacing > VASVT) suggests that the SVT is orthodromic AVRT mediated
by an AV BT in the ventricle contralateral to the site of ventricular
pacing.
Ventricular Entrainment During Orthodromic
Atrioventricular Reentrant Tachycardia
During orthodromic AVRT, the corrected (PPI − TCL) difference fol-
lowing entrainment from the RV apex can help localize the BT used
for retrograde conduction. The RV apical pacing site is closer to the
reentrant circuit of orthodromic AVRT utilizing a right-sided BT than
orthodromic AVRT utilizing a left-sided BT. Hence, as expected, the
corrected (PPI − TCL) difference is shorter (less than 55 milliseconds)
in patients with orthodromic AVRT with a right-sided BT when pacing
the RV apex. Patients with left-sided BTs typically have a corrected (PPI
− TCL) difference of more than 55 milliseconds.51
Furthermore, upon initiation of ventricular overdrive pacing from
the RV apex during orthodromic AVRT, there is a “transitional zone”
during which the paced QRS complexes show progressive fusion with
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 653

II

V1

HRA

His

CSprox

CSdist

RVA
Fig. 18.46  Orthodromic Atrioventricular Reentrant Tachycardia With Multiple Routes of Retrograde
Atrial Activation. The presence of multiple bypass tracts is indicated by the shift in retrograde atrial activa-
tion sequence (indicated by the red and blue arrows) during tachycardia. CSdist, Distal coronary sinus; CSprox,
proximal coronary sinus; HRA, high right atrium; RVA, right ventricular apex.

BOX 18.10  Electrophysiological Maneuvers for Localization of the Bypass Tract

Pacing From Multiple Atrial Sites
• Proximity to the BT atrial insertion is indicating by shortening of the P-delta
interval during atrial pacing.
Preexcitation Index of VES From the RV
• A relative preexcitation index >90% suggests right-sided or septal BT.
• An absolute preexcitation index ≥75 msec suggests a left free-wall BT.
• An absolute preexcitation index <45 msec suggests a septal BT.
• An absolute preexcitation index of 45–75 msec is indeterminate.
Effects of BBB During Orthodromic AVRT
• Prolongation of the TCL and, more importantly, the surface VA interval by
>35 msec following the development of BBB is diagnostic of AVRT using a
free-wall BT ipsilateral to the BBB (LBBB with left-sided BT, and RBBB with
right-sided BT)
• Superoparaseptal and posteroseptal BTs are associated with a lesser degree
of prolongation of the VA interval (approximately 5–25 ms) on the development
of BBB (RBBB with superoparaseptal BT, and LBBB with posteroseptal BT)
Ventricular Entrainment During Orthodromic AVRT From
the RV Apex
• Corrected (PPI − TCL) difference <55 msec is consistent with a right-
sided BT.
• Corrected (PPI − TCL) difference >55 msec is consistent with a left-sided BT.
• Resetting of ≥3 atrial beats (with fixed SA intervals) within the transitional
zone suggests a right-sided BT.
• Resetting of only 1 or 2 atrial beats during the transitional zone suggests a
left-sided BT.
Mapping Ventricular Activation During Preexcited Rhythm
• The site of earliest local ventricular activation (preceding the onset of the
delta wave) along the tricuspid and mitral annuli identifies the BT ventricular
insertion site.
Mapping Atrial Activation During Retrograde Bypass Tract
Conduction
• The site of earliest local atrial activation along the tricuspid and mitral annuli
during orthodromic AVRT or during ventricular pacing with retrograde conduc-
tion over the BT, identifies the BT atrial insertion site.
• The site of polarity reversal of the atrial unfiltered bipolar electrogram (with
the electrodes oriented parallel to the axis of the annulus) during orthodromic
AVRT or during ventricular pacing with retrograde conduction over the BT,
identifies the BT atrial insertion site.
Mapping Bypass Tract Potential
• Recording a BT potential 10–30 ms before the onset of the delta wave (during
anterograde preexcitation) or between the ventricular and atrial electrograms
at the earliest site of retrograde atrial activation (during orthodromic AVRT
or ventricular pacing) identifies the BT location.
Local AV or VA Interval
• When the BT crosses the AV groove perpendicularly, the site of the shortest
local VA interval (during retrograde BT conduction) and the site of the shortest
local AV interval (during anterograde BT conduction) can indicate the BT loca-
tion and is often considered the optimal target for BT ablation.

AV, Atrioventricular; AVRT, atrioventricular reentrant tachycardia; BBB, bundle branch block; BT, bypass tract; LBBB, left bundle branch block;
PPI, postpacing interval; RBBB, right bundle branch block; RV, right ventricle; SA, stimulus-to-atrial; TCL, tachycardia cycle length;
VA, ventriculoatrial; VES, ventricular extrastimulus.

the SVT complexes, until stable QRS morphology is observed (either
completely paced or constantly fused). The closer the BT location is to
the RV apical pacing site, the earlier atrial resetting will occur during
the transition zone, and the greater the number of complexes that show
advancement of atrial activation (as defined by acceleration of atrial
activation to the ventricular pacing rate with fixed SA intervals) during
the transitional zone (Fig. 18.47). Right-sided BTs produce reset earlier
than left-sided BTs, and resetting of at least three atrial beats (with fixed
SA intervals) within the transitional zone was found to successfully
identify right-sided BTs. Left-sided BTs allow atrial resetting later after
 Fixed SA
TZ

l------------l
200 msec

II
*

V1

V6

SA = 114 SA = 142 SA = 144 SA = 144 SA = 142 SA = 144 SA = 144

l-------l l-------l l-------l l-------l l-------l l-------l l-------l

HRA

His p

His d
TCL = 339
l-------------------l
320 320 320 320 320 320
RVA

S S S S S S S
A
Fixed SA
TZ

l-----------l
200 msec
II *

aVR

V2

HRA

SA = 168 SA = 186 SA = 208 SA = 226 SA = 254 SA = 252 SA = 254

l---------l l----------l l-----------l l-------------l l--------------l l--------------l l--------------l

His p

His d

300 300 300 300 300 300 300

RVA

TCL = 316
l------------------l
S S S S S S S S
B
Fig. 18.47  Ventricular Entrainment During Orthodromic Atrioventricular Reentrant Tachycardia (AVRT) for Bypass Tract (BT) Localization.
(A) Orthodromic AVRT over a right lateral BT with a tachycardia cycle length (TCL) of 339 milliseconds. Right ventricular apical (RVA) overdrive
pacing is delivered at 320 milliseconds and the number of beats with a fixed stimulus-atrial (SA) interval within the transition zone (TZ) is 4 (the 4
last beats of the TZ). (B) Orthodromic AVRT using a right posteroseptal BT with a TCL of 316 milliseconds. RVA overdrive pacing is delivered at
300 milliseconds and the number of beats with a fixed SA interval within the TZ is two (the last two beats of the TZ). The star indicates the first
paced beat with a fixed QRS-morphology, representing the last beat of the TZ. His d, Distal His bundle; His p, proximal His bundle; HRA, high right
atrium. (From Akerström F, Pachón M, García-Fernández FJ, et al. Number of beats in the transition zone with fixed SA interval during right ven-
tricular overdrive pacing determines accessory pathway location in orthodromic reentrant tachycardia. Pacing Clin Electrophysiol. 2015;39:21–27.)
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 655

starting ventricular overdrive pacing (due to the larger distance between
the BT and the pacing site) and, hence, only one or two reset beats
during the transitional zone would reveal atrial resetting. Septal BTs
had numbers of reset complexes that overlapped with right- and left-
sided BTs.57
Earliest Ventricular Activation Site During Anterograde
Bypass Tract Conduction
During ventricular preexcitation (preexcited sinus or atrial paced rhythm,
or antidromic AVRT), the surface ECG lead with the earliest onset of
the delta wave, preferably with a relatively sharp delineation of its onset,
should be selected and used as the timing reference during mapping
(eFig. 18.6). The site of earliest local ventricular activation (preceding
the onset of the delta wave) along the tricuspid and mitral annuli identi-
fies the BT ventricular insertion site.
Both bipolar and unipolar recordings on the ablation catheter should
be used for mapping (Fig. 18.48). Bipolar electrograms display electro-
gram components and timing and may demonstrate a BT potential.
The unfiltered (0.05 to 300 Hz) unipolar signal morphology should
show a monophasic QS complex with a rapid negative deflection if the
site was at the origin of impulse formation in the ventricle (i.e., BT
insertion site). Concordance of the timing of the onset of the bipolar
electrogram with that of the unipolar electrogram (with the rapid
downslope of the S wave of the unipolar QS complex coinciding with
the initial peak of the bipolar signal) helps ensure that the tip electrode,
which is the ablation electrode, is responsible for the early component
of the bipolar electrogram. If only bipolar recordings are used, one
does not know which of the two poles is responsible for the earliest
component of the bipolar electrogram.
Earliest Atrial Activation Site During Retrograde
Bypass Tract Conduction
During orthodromic AVRT or during ventricular pacing with retrograde
conduction over the BT, the site of earliest atrial activation along the
tricuspid and mitral annuli identifies the BT atrial insertion site. When
mapping is performed during ventricular pacing, fusion of atrial activa-
tion, caused by simultaneous retrograde conduction over both the AVN
and the BT, has to be considered because it can affect the accuracy of
mapping. This can be an issue in the setting of septal BTs whereby the
retrograde atrial activation sequence over the BT may not be very dif-
ferent from that over the AVN. Dissociation of retrograde conduction
over the BT from that over the AVN is required in these situations, and

Ablation of BT ventricular insertion

II

V1

HRA

His

CSprox

CSdist

RVA

ABLbipolar

ABLunipolar

Fig. 18.48  Catheter Ablation (ABL) of a Left Anterolateral Bypass Tract (BT) During Anterograde Con-
duction. ABL is performed during preexcited atrial pacing. Preexcitation is observed during the first three
complexes. The dashed line indicates the onset of the delta wave. Note the sharp negative deflection (QS
morphology) in the unipolar recording. Also, note the concordance of the timing of the unipolar and bipolar
electrograms (blue arrows), which precedes the onset of the delta wave by 10 to 15 milliseconds. A sharp
potential (possible BT potential, red arrow) is recorded between the atrial and ventricular electrograms. RF
application at this site successfully eliminated preexcitation (last two complexes). CSdist, Distal coronary sinus;
CSprox, proximal coronary sinus; HRA, high right atrium; RVA, right ventricular apex.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 655.e1

Standard ECG High ECG gain + V3

II

III

V1 V3

V6

HRA

Hisprox

Hismid

Hisdist

CSprox

CSmid

CSdist

RVA

Abldist

Abluni

Ablprox
200 msec
eFig. 18.6  Surface Electrocardiogram (ECG) and Intracardiac Recordings of Possible Ablation Site. On
the left, with standard ECG recordings, the features of the ablation site electrograms suggest this would be
a good ablation site (green arrow) because they occur well before the onset of the delta wave (dashed line).
However, on the right, the very same complex is shown, but with increased gain on surface ECG leads as
well as an addition of lead of V3 (showing sharp delineation of delta wave onset, blue arrow). Now, the
dashed line that denotes the true onset of surface preexcitation reveals that the putative ablation site is not
attractive (red arrow). Abldist, Ablation distal bipolar electrodes; Ablprox, ablation proximal bipolar electrodes;
Abluni, ablation distal unipolar electrode; CSdist, distal coronary sinus; CSmid, middle coronary sinus; CSprox,
proximal coronary sinus; Hisdist, distal His bundle; Hismid, middle His bundle; Hisprox, proximal His bundle; HRA,
high right atrium; RVA, right ventricular apex.
656 CHAPTER 18  Typical Atrioventricular Bypass Tracts

can usually be achieved with ventricular stimulation from sites closer
to the BT and with the use of AVN blockers (e.g., adenosine) to ensure
preferential retrograde conduction over the BT.
As with ventricular mapping, both bipolar and unipolar recordings
on the distal ablation electrode should be used for atrial mapping (Fig.
18.49). Determining what components of a complex ablation electrode
recording is atrial versus ventricular can be facilitated by rapid burst
ventricular pacing that does not conduct 1:1 retrogradely (Fig. 18.50)
or by introduction of a VES that does not conduct retrogradely during
fixed-rate ventricular pacing (Fig. 18.51). In either case, the principle
is to compare the electrogram that is known to have no atrial component
with the electrogram in question (with some atrial component), any
difference being due to the contribution of the atrial electrogram.
Atrial Electrogram Polarity Reversal During Retrograde
Bypass Tract Conduction
The morphology and amplitude of the bipolar electrograms are influ-
enced by the orientation of the bipolar recording axis to the direction
of propagation of the activation wavefront. Although the direction of
wavefront propagation cannot be reliably inferred from the morphology
of the bipolar signal, a change in morphology can be a useful finding,
and the unfiltered bipolar electrogram with the electrodes oriented
parallel to the axis of the annulus can be used to localize the atrial
insertion site of the BT.
During retrograde BT conduction (orthodromic AVRT or ventricular
pacing), BT atrial insertion is identified as the site where the polarity
of the atrial potential reverses. Because the site of BT atrial insertion
is usually discrete, atrial activation propagates in two opposite directions
along the annulus from the insertion site. As a result, an RS configura-
tion electrogram will be present on one side of the BT, where the wave-
front is propagating from the distal electrode toward the proximal
electrode, and a QR morphology electrogram on the other side, where
the wavefront is propagating from the proximal electrode toward the
distal electrode.
This technique is typically used for localization of left free-wall
BTs via the transseptal approach, which allows an electrode orienta-
tion parallel with atrial activation along the mitral annulus. As the
ablation catheter is moved along the mitral annulus during retrograde
BT conduction, the amplitude and polarity of the atrial electrogram
are examined. With the tip electrode negative, and the catheter lying
on the mitral annulus from anterior to posterior, an upright atrial
electrogram indicates a catheter position anterior to the insertion site,

Ablation of BT atrial insertion

II

V1

HRA

His

CSprox

CSdist

RVA

ABLbipolar

ABLunipolar

Fig. 18.49  Catheter Ablation (ABL) of a Left Lateral Bypass Tract (BT) During Retrograde Conduction.
ABL is performed during ventricular pacing with atrial fusion (ventriculoatrial conduction occurring over both
the BT and atrioventricular node [AVN]). The dashed line indicates the onset of the earliest atrial activation.
Note the sharp negative deflection (QS morphology) in the unipolar recording. The timing of the unipolar
electrogram coincides with the bipolar electrogram (blue arrows) and precedes the delta wave by 5 to 10
milliseconds. The atrial and ventricular electrograms merge, and the true morphology of the ventricular
electrogram is unmasked after successful ablation (last two complexes). A sharp potential (possible BT
potential, red arrow) is recorded between the two electrograms. After successful elimination of the BT func-
tion, atrial activation occurs exclusively over the AVN (last two complexes, green arrows). CSdist, Distal coronary
sinus; CSprox, proximal coronary sinus; HRA, high right atrium; RVA, right ventricular apex.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 657

I
II

III

V1

V6

HRA
Hisprox
Hismid
Hisdist
CSprox

CSdist

Abldist

Abluni
V V V V
A A
Ablprox

RVA
S S S 200 msec

Fig. 18.50  Using Ventricular Pacing to Evaluate Ablation Site Electrogram Components. Burst ventricular
pacing is shown at a rate that produces 2:1 retrograde conduction over the bypass tract (BT). This facilitates
determination of what portion of the ablation site recording is atrial versus ventricular, because whatever is
present in recordings on cycles during which retrograde conduction is present, but absent when retrograde
conduction fails, is the atrial (or BT plus atrial) recording (red arrows). Abldist, Ablation distal bipolar electrodes;
Ablprox, ablation proximal bipolar electrodes; Abluni, ablation distal unipolar electrode; CSdist, distal coronary
sinus; CSprox, proximal coronary sinus; Hisdist, distal His bundle; Hismid, middle His bundle; Hisprox, proximal His
bundle; HRA, high right atrium; RVA, right ventricular apex.

whereas a negative electrogram indicates positions posterior to the
insertion site. When the bipole approaches and then passes directly
over the atrial insertion site, the atrial electrogram becomes diminished
in amplitude, isoelectric, and fractionated. As the catheter moves from
one side of the insertion site to the other side, reversal of the atrial
electrogram polarity is observed. This maneuver has a sensitivity of
97%, specificity of 46%, and positive predictive value of 75%. For BTs
at other locations, mapping can be facilitated by using a multipolar
catheter positioned in the CS or around the tricuspid annulus (e.g.,
Halo catheter); the site of the BT atrial insertion is enclosed between
the two adjacent bipoles, demonstrating atrial electrogram polarity
reversal.
Direct Recording of Bypass Tract Potential
The BT potential manifests as a sharp narrow spike on both unipolar
and bipolar recordings 10 to 30 milliseconds before the onset of the
delta wave during anterograde preexcitation or between the ventricular
and atrial electrograms at the earliest site of retrograde atrial activation
during orthodromic AVRT or ventricular pacing. The BT potential
amplitude averages 0.5 to 1 mV at successful ablation sites (see Figs.
18.48 and 18.49). Similar electrical signals, however, can be a component
of the atrial or ventricular electrogram, and proof that an electrical
signal is actually a BT potential can be difficult, because it needs to be
dissociated from the local atrial and ventricular electrograms.
During anterograde BT conduction (NSR or atrial pacing), dissocia-
tion of the anterograde BT potential from the ventricular potentials
can be achieved by introduction of VES with progressively shorter
coupling intervals. Dissociation of the BT potential from the local ven-
tricular potential is confirmed when a late-coupled VES (occurring at
the time of the anterograde BT potential) advances the ventricular
electrogram without affecting the timing or morphology of the BT
potential. Furthermore, dissociation of the BT potential from the local
atrial potential is confirmed when an earlier VES advances the BT
potential without affecting the timing or morphology of the atrial elec-
trogram (Fig. 18.52).
A retrograde BT potential (during ventricular pacing or orthodromic
AVRT) can be validated by introduction of progressively premature
AES. A late-coupled AES can advance the timing of the local atrial
potential without affecting the retrograde BT potential, providing evi-
dence that the BT potential is not related to atrial activation. In addition,
dissociation of the BT potential from the local ventricular potential is
confirmed when an earlier AES advances the BT potential (i.e., antero-
gradely activate the BT) without affecting the timing or morphology
of the local ventricular electrogram (Fig. 18.53).
However, these criteria for validation of BT potentials are often
difficult to achieve. Therefore validation of BT potentials by programmed
electrical stimulation is often not practical in clinical settings; instead,
such a potential is called possible or probable BT potential.
658 CHAPTER 18  Typical Atrioventricular Bypass Tracts

I
II
III
V1

V6

HRA
Hisprox
Hismid
Hisdist

CSprox

CSdist
S1 S1 S2 S1 S1
RVA
Abluni

Abldist
Ablprox
200 msec

Fig. 18.51  Using Ventricular Extrastimuli to Evaluate Ablation Site Electrogram Components. Determin-
ing what part of a complex ablation site recording is atrial or bypass tract (BT) is aided by introducing an
extrastimulus (S2) during a fixed-rate drive, which fails to conduct retrogradely while drive complexes do
conduct. The portion of the electrogram that is absent on this complex (green arrow), but present on others
(red arrows), is the atrial (±BT) component. Abldist, Ablation distal bipolar electrodes; Ablprox, ablation proximal
bipolar electrodes; Abluni, ablation distal unipolar electrode; CSdist, distal coronary sinus; CSprox, proximal coro-
nary sinus; Hisdist, distal His bundle; Hismid, middle His bundle; Hisprox, proximal His bundle; HRA, high right
atrium; RVA, right ventricular apex.

Targeting an isolated BT potential has been associated with the highest
rate of ablation success. The usefulness of this criterion, however, has
been limited by difficulty in locating or validating a BT potential in
clinical practice. The difficulty in identifying the BT potential is often
related to the oblique course of the BT. A ventricular or atrial wavefront
propagating concurrently with the BT can overlap and mask the BT
potential. Pacing from the site producing the shorter local VA or local
AV intervals helps identify the BT potential in most of these cases.
Local Atrioventricular (or Ventriculoatrial) Interval
When the BT crosses the AV groove perpendicularly, the site of the
shortest local VA interval (during retrograde BT conduction) and the
site of the shortest local AV interval (during anterograde BT conduc-
tion) can indicate the BT location and is often considered the optimal
target for BT ablation. However, the reliability of this criterion has been
debated and can be misleading in the setting of oblique BTs. Short local
VA intervals can occur at sites along the valve annulus distant from the
BT because atrial and ventricular activation wavefronts can propagate
circumferentially along the annulus, and the timing of local atrial and
ventricular activation can be close to one another at multiple sites along
the annulus (Fig. 18.54). Furthermore, with oblique BTs, the shortest
local VA interval can be shifted away from the BT in the direction of
the ventricular wavefront if the velocity of the ventricular wavefront
along the annulus is less than the velocity of the atrial wavefront.
Similarly, the site of the shortest local AV interval can be shifted away
from the BT in the direction of the atrial wavefront if the atrial wave-
front is slower than the ventricular wavefront.
With an oblique course, the local VA and AV intervals vary by revers-
ing the direction of the paced ventricular and atrial wavefronts, respec-
tively. During ventricular pacing, a ventricular wavefront propagating
from the direction of the ventricular end (concurrently with BT activa-
tion) produces an artificially short local VA interval (measured at the
site of earliest retrograde atrial activation), because activation along
the BT proceeds to the earliest atrial activation site simultaneously and
in the same direction as the ventricular wavefront at the ventricular
aspect of the AV groove. Contrariwise, a ventricular wavefront propa-
gating in the opposite (countercurrent) direction produces a longer
local VA interval because the ventricular wavefront must pass the site
of earliest atrial activation before reaching the ventricular end of the
BT (Fig. 18.55). This has important implications for localizing oblique
AV BTs. With a concurrent wavefront, the ventricular potential can
overlap the BT potential and atrial electrogram, masking the site of
earliest atrial activation and BT potential. If the velocity of the ventricular
wavefront along the annulus were slower than the BT and atrial wave-
fronts, the shortest local VA interval would be shifted away from the
BT. A countercurrent wavefront should expose the atrial activation
sequence and BT potential, but would result in a longer VA interval
measured at the site of earliest retrograde atrial activation.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 659

I
II
III
V1
V2
V6
HRA
S S S
Hisprox
Hismid
Hisdist
CSprox

CSdist
RVA A A A
S
V V V
Abldist

Ablunid

Ablprox
200 msec

Ablunip

Fig. 18.52  Dissociation of Bypass Tract (BT) Potential From Local Atrial Potential. Surface electrocar-
diogram and intracardiac recordings evaluate possible BT potential. Fixed-rate atrial pacing is present on all
three complexes shown. On the first complex, a blue arrow points to a possible BT potential following the
sharp atrial potential (A). This same sharp atrial potential is seen at the same rate as atrial pacing on all three
complexes. On the middle complex, a single ventricular extrastimulus is delivered almost simultaneously
with the atrial drive stimulus (S). Here, the blue arrow shows that the putative BT potential does not follow
the sharp atrial recording (red arrow indicates its absence), and thus is not part of the atrial electrogram.
Abldist, Ablation distal bipolar electrodes; Ablprox, ablation proximal bipolar electrodes; Abluni, ablation distal
unipolar electrode; CSdist, distal coronary sinus; CSprox, proximal coronary sinus; Hisdist, distal His bundle; Hismid,
middle His bundle; Hisprox, proximal His bundle; HRA, high right atrium; RVA, right ventricular apex.

Similarly, during atrial pacing, a concurrent atrial wavefront would
shorten the local AV interval (measured at the site of earliest ventricular
activation) and could mask the BT potential and site of earliest ven-
tricular activation. A countercurrent atrial wavefront should lengthen
the local AV and expose the BT potential and ventricular activation
sequence (see Fig. 18.55).
Reversing the paced ventricular or atrial wavefronts can increase
the local VA or local AV interval, respectively, by at least 15 milliseconds
in more than 85% of patients, which suggests that most BTs have an
oblique course. The increase in the local VA or local AV intervals can
facilitate identification of the BT potential. An anterograde or retrograde
BT potential can be recorded in more than 85% of patients with oblique
BTs, which is much more frequent than that with nonoblique BTs,
because fusion of the atrial, BT, and ventricular potentials may be
expected with nonoblique BTs.
During retrograde BT conduction, the earliest atrial activation can
be recorded 3 to 5 mm (or possibly more) from the actual BT inser-
tion. Ablation is likely to be successful if the electrode is located 3
to 5 mm from the atrial insertion in the direction of the ventricular
insertion and unsuccessful if located in the opposite direction. During
anterograde BT conduction, ablation at a site recording earliest ven-
tricular activation is likely to be successful, even if the electrode is
located 3 to 5 mm from the ventricular end but in the direction of the
atrial insertion and unsuccessful if located in the opposite direction.
This explains the 40% ablation success for the criterion of local ven-
tricular activation preceding the onset of the delta wave by less than
660 CHAPTER 18  Typical Atrioventricular Bypass Tracts

I
II

III

V1

V2
V6
HRA
S
Hisprox
Hismid
Hisdist
CSprox

CSdist
RVA
S S S
A
A V A
Abldist
V V

Ablunid

Ablprox

200 msec

Ablunip

Fig. 18.53  Dissociation of Bypass Tract (BT) Potential From Local Ventricular Potential. Surface elec-
trocardiogram and intracardiac recordings evaluate possible BT potential in the same patient as in Fig. 18.35.
Fixed-rate ventricular pacing is shown in all three complexes, with a single atrial extrastimulus (AES) introduced
during the middle complex. The blue arrow in the first complex points to a putative BT potential between
ventricular (V) and atrial (A) electrograms. In the middle complex, the AES is timed such that the BT potential
follows the atrial electrogram (blue arrow), and not the ventricular recording (red arrow). Thus it is not part
of the ventricular electrogram. Abldist, Ablation distal bipolar electrodes; Ablprox, ablation proximal bipolar
electrodes; Abluni, ablation distal unipolar electrode; CSdist, distal coronary sinus; CSprox, proximal coronary
sinus; Hisdist, distal His bundle; Hismid, middle His bundle; Hisprox, proximal His bundle; HRA, high right atrium;
RVA, right ventricular apex.

0 milliseconds during anterograde BT conduction, even though ven-
tricular activation can usually be recorded as much as 30 milliseconds
before the delta wave in right-sided BTs and 15 to 20 milliseconds in
left-sided BTs.
ABLATION
Target of Ablation
The BT is the target of ablation. Although BT conduction can be elimi-
nated by ablation anywhere between the atrial and ventricular ends,
radiofrequency (RF) applications targeted to the atrial end (site of earliest
atrial activation during retrograde BT conduction) or ventricular end
(site of earliest ventricular activation during anterograde BT conduc-
tion) occasionally fail, likely because of the broader dimension of BT
at the insertion site compared to the annular aspect.
The best site of ablation of an AV BT is where it crosses the mitral
or tricuspid annulus. Localization of the BT can be achieved with dif-
ferent mapping methods, as described earlier. Ablation should be per-
formed at the same side of the annulus to the one being mapped (i.e.,
ablation on the atrial side during mapping of the atrial insertion site
during retrograde BT conduction, and ablation on the ventricular side
during mapping of the earliest ventricular activation during anterograde
BT conduction). This is especially important for oblique BTs, whereby
the earliest ventricular activation site during anterograde BT conduction
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 661

I
II
III
V1

V6
HRA
Hisprox
Hismid
Hisdist

CSprox

A
V

CSdist

RV
S S

Abldist

Abluni

Ablprox

Fig. 18.54  Local Ventriculoatrial Interval for Bypass Tract Localization. Two ventricular paced complexes
with retrograde conduction are shown. Ventricular (V) and atrial (A) recordings are as designated by lines.
Of the recordings indicated, the earliest atrial electrogram is at the proximal coronary sinus (CSprox), whereas
the shortest local ventriculoatrial (VA) interval is far more distal in the coronary sinus recordings; in fact, in
the distal coronary sinus (CSdist), the VA interval is negative. Abldist, Ablation distal bipolar electrodes; Ablprox,
ablation proximal bipolar electrodes; Abluni, ablation distal unipolar electrode; Hisdist, distal His bundle; Hismid,
middle His bundle; Hisprox, proximal His bundle; HRA, high right atrium; RVA, right ventricular apex.

from the atrial aspect of the annulus can be distant from the atrial
insertion site of the BT; hence, ablation at the atrial aspect would not
be successful.
Criteria of successful ablation sites during anterograde or retrograde
activation mapping of BTs are presented in Box 18.11 (see Figs. 18.48
and 18.49). The predictive accuracy of any single criterion is limited.
Therefore selection of the optimal ablation target site should be guided
by multiple criteria.
Ablation Technique: General Considerations
When preexcitation is present, ablation can be performed during NSR
or, preferably, atrial pacing. For concealed BTs, RF energy is delivered
during ventricular pacing, which usually allows for detection of an
altered retrograde atrial activation sequence. RF energy delivery during
AVRT is avoided if possible because of potential catheter dislodgment
from its critical position upon interruption of BT conduction (and
thus abrupt tachycardia termination). This event can be associated with
transient loss of conduction over the BT for a variable period of time
without resulting in permanent damage to the BT due to premature
interruption of the RF application. Occasionally, BT conduction can
resume hours to days after the procedure; therefore one may not find
a suitable target to complete the RF lesion if not addressed adequately
during the initial attempt. Ablation during continuous pacing prevents
this problem. For incessant orthodromic AVRT (e.g., PJRT), or when
retrograde mapping during orthodromic AVRT is used to determine
the optimal atrial ablation site, it is preferable to entrain the AVRT with
ventricular pacing at a slightly shorter PCL so that block in the BT and
termination of the SVT during RF energy delivery will be followed by
ventricular pacing at a rate similar to that of the SVT, minimizing
catheter movement. Also, the use of an electroanatomic mapping system
can obviate this problem by tagging the initial site of ablation, allowing
precise return to that site.
662 CHAPTER 18  Typical Atrioventricular Bypass Tracts

when ablating in small branches of the CS because power delivery with

LA a standard 4-mm electrode is limited because of less passive cooling in
small vessels.
CS
P 4 3 2 d P 4 3 2 d An electrode temperature of 55°C to 60°C should be sought. Tran-
LV sient loss of BT function is seen at roughly 50°C, and permanent loss
of function occurs at 60°C. Therefore sites with favorable electrogram
A1 A2 B1 B2
characteristics should not be abandoned until a temperature higher
V1 than 50°C to 55°C is reached. Conversely, repeated energy applications
at the same location after achieving a temperature of 55°C or higher
A A A A
V V V V
are unlikely to succeed.
CSp
AP AP
Loss of BT conduction is expected within 1 to 6 seconds of RF
CS4 application (once the target temperature and power delivery have been
AP AP reached) for most successful lesions. If no effect is seen after 15 seconds
CS3 of RF delivery, energy delivery should be discontinued because it is
unlikely to be beneficial, and mapping criteria and catheter contact
CS2
should be reexamined. If BT conduction is eliminated during the appli-
CSd cation, RF delivery should be continued for up to 60 seconds. Occasion-
ally, BT conduction can be eliminated in one direction only (most
typically loss of anterograde conduction with persistence of retrograde
conduction). Thus testing for conduction in each direction is manda-
A B
tory after what appears to be a successful RF application.
Transient interruption of BT conduction during RF delivery, with
LA subsequent reappearance of conduction within seconds or minutes after
energy delivery is completed, may be observed, and is more common
CS with right than left free-wall BTs. In this setting, the use of multisite
P 4 3 2 d P 4 3 2 d

LV
C1 C2 D1
V1
CSp
CS4
CS3
CS2
AP
CSd AP AP
A A A A
V V V V
C D
Fig. 18.55  Schematic Representation of Anterograde and Retrograde
Activation of a Left Free-Wall Bypass Tract. The oblique course illus-
trates a change in electrogram timing with the reversal of the paced
ventricular wavefront (A and B) and reversal of the paced atrial wavefront
(C and D). AP, Accessory pathway potential; CS, coronary sinus;
d, distal; LA, left atrium; LV, left ventricular; p, proximal. (From Otomo
K, Gonzalez MD, Beckman KJ, 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;104:550.)
For most free-wall BTs, complete bidirectional block can be achieved
with a conventional 4-mm-tip ablation catheter, using a power setting
of 50 W and targeting a temperature of 60°C. If BT conduction block
is transient, permanent BT block can usually be obtained with better
and more consistent contact at the same site. It is rare that an 8-mm
or irrigated-tip ablation catheter is necessary; failure of BT ablation is
almost always a result of inadequate mapping or poor tissue contact
and not inadequacy of the lesion size created by a 4-mm-tip standard
ablation catheter. Nevertheless, irrigated-tip catheters can be helpful
“insurance lesions” is discouraged, and the use of one or two ablation
sites should be the goal, which requires careful mapping to achieve.
D2 If BT function is not eliminated at a site with apparent favorable
electrographic features, catheter contact with the tissue may be inad-
equate. Adequacy of catheter contact can be verified by evaluating the
electrode temperature, catheter stability on fluoroscopy, electrogram
stability, and ST elevation on the unipolar electrogram (Fig. 18.56). If
the electrode temperature is consistently higher than 50°C with more
than 25 W of energy delivered to the tissue during the RF application,
good catheter contact is likely; however, if electrode temperature reaches
more than 50°C but with very low power (less than 10 W), coagulum
may have formed at the catheter tip. Also, catheter “shimmering” on
AP fluoroscopy suggests poor contact. Similarly, changing electrographic
amplitudes before or during ablation suggest inadequate catheter contact.
Furthermore, ablation-related injury usually yields ST elevation on the
unipolar electrogram; if absent, inadequate tissue heating is likely.
Endpoints of Ablation
Bypass Tract Bidirection Conduction Block
Confirmation of complete loss of BT function, and not just noninduc-
ibility of tachycardias, is essential. Confirmation of loss of anterograde
BT function using AES and atrial pacing is achieved by demonstrating
lack of preexcitation and marked prolongation of the local AV interval
at the ablation site. Atrial stimulation should be performed at sites and
rates that were associated with preexcitation before ablation. As noted,
it is possible to have loss of anterograde conduction with persistence
of retrograde conduction (less commonly the opposite). Therefore care
must be taken to ensure bidirectional conduction block.
Confirmation of complete loss of retrograde BT function using VES
and ventricular pacing is achieved by demonstrating concentric and
decremental retrograde atrial activation, consistent with VA conduc-
tion over the AVN, VA dissociation, and/or marked prolongation of the
local VA interval at the ablation site. Ventricular stimulation should be
performed at sites and rates that were associated with retrograde VA
conduction over the BT before ablation. Para-Hisian pacing and RV
apical versus RV basilar pacing can also help confirm the absence of
septal and paraseptal BTs (Figs. 18.28 and 18.30). Occasionally, AVN
 CHAPTER 18  Typical Atrioventricular Bypass Tracts
BOX 18.11  Electrophysiological Criteria of Successful Bypass Tract Ablation Sites
Criteria of Successful Ablation Sites During Anterograde
Activation Mapping
• Stable catheter position, as confirmed fluoroscopically and by observing a
stable electrogram (<10% change in amplitude in atrial and ventricular elec-
trograms over 5–10 beats).
• Atrial electrogram amplitude >0.4 mV, or A/V ratio >0. Both atrial and ven-
tricular electrogram components should be recorded from the ablation (tip)
electrode. When ablating from the atrial aspect of the annulus, the atrial
electrogram is usually equal to or larger than the ventricular electrogram.
Sometimes, the two can merge and it may be difficult to determine whether
both components are present. Rapid atrial or ventricular pacing resulting in
block in the BT can help eliminate ventricular or atrial electrogram (respectively)
so that the exact morphology of the other component can be visualized.
• Local AV interval on the ablation catheter is usually short (25–50 msec, except
for previously damaged, slowly conducting, oblique, or epicardial BTs).
• The local ventricular electrogram on the ablation catheter should precede the
onset of the delta wave on the ECG by a mean of 0–10 msec for left-sided
BTs and 10–30 msec for right-sided BTs (the local ventricular electrogram is
measured from the peak of the bipolar electrogram or the maximal dV/dt in
the unipolar electrogram).
• QS (or, less preferably, rS) morphology of the unipolar electrogram. Right-sided
BTs usually have unipolar recordings that show more pronounced (rapid and
deeper) QS configuration than left-sided BTs.
• Continuous electrical activity (defined as isoelectric interval of <5 msec between
ventricular and atrial electrograms).
• Presence of BT potential.
A/V, Atrium to ventricle; AVRT, atrioventricular reentrant tachycardia; BT, bypass tract; ECG, electrocardiogram; VA, ventriculoatrial.
conduction is so brisk that it is difficult to determine if a left-sided BT
has been eliminated; in this case, pacing from the LV (either passing the
ablation catheter through the mitral orifice and pacing LV endocardium,
or advancing the CS catheter into a ventricular branch to pace) gives
an advantage to conduction over a left-sided BT compared to the AVN.
Adenosine Testing
Administration of adenosine (starting dose 12 mg, 15 to 30 minutes
after successful BT ablation) has been proposed to help unmask dormant
BT conduction. Doses of adenosine are increased (in 6- to 12-mg incre-
ments) as needed to ensure adequate response in the form of AV block
or sinus slowing. Then, atrial and ventricular programmed stimulation
is performed to evaluate the presence of BT conduction. In a recent
study, adenosine could induce transient anterograde and retrograde
BT conduction (dormant conduction) after apparently successful BT
ablation in 12% of patients. The mechanism of this phenomenon is
thought to be secondary to membrane hyperpolarization of partially
depolarized cardiac tissue after ablation. Dormant conduction was
manifest during the bradycardia phase of adenosine effect. The presence
of dormant BT conduction was associated with higher rates of repeat
BT ablation, particularly in patients in whom dormant BT conduction
was not successfully abolished during the initial procedure.59
Ablation of Left Free-Wall Bypass Tracts
Anatomical Considerations
The mitral annulus is an anatomically ill-defined structure that demar-
cates the hinge line of the mitral leaflets at the junctional zone that
separates the LA and LV. The mitral annulus is not a rigid fibrous ring
but pliable and dynamic, changing shape during the cardiac cycle. En
663
Criteria of Successful Ablation Sites During Retrograde
Activation Mapping
• Stable catheter position, as confirmed fluoroscopically and by observing a
stable electrogram (<10% change in amplitude in atrial and ventricular elec-
trograms over 5–10 beats).
• Earliest local atrial activation timing.
• Local VA interval during retrograde activation of the BT is short (25–50 msec,
except for previously damaged, slowly conducting, oblique, or epicardial BTs),
usually resulting in inscription of the atrial electrogram on the ascending
portion of the terminal ventricular electrogram. The “pseudo-disappearance”
of the atrial electrogram within the terminal portion of the ventricular elec-
trogram (forming a W sign) during orthodromic AVRT is a manifestation of an
extremely short local VA interval, which correlates with successful ablation
sites.
• Surface QRS to local atrial electrogram interval ≤70 msec (during orthodromic
AVRT).
• The local VA interval remains constant regardless of the direction in which
the ventricular wavefront engaging the BT is traveling (i.e., despite pacing
from different ventricular sites). If one uses the ventricular approach to ablate
a concealed BT, the ventricular insertion site can be identified as one that
maintains a constant local VA interval, despite differences in direction of
activation to the ventricular site.
• Continuous electrical activity (defined as isoelectric interval <5 msec between
ventricular and atrial electrograms).
• Presence of BT potential.
face, the mitral annulus resembles a kidney bean. When viewed in a
3-D perspective, the annulus has a nonplanar saddle shape, with elevated
septal and lateral segments. The anterior flatter portion of the mitral
annulus is continuous with the noncoronary and left coronary aortic
cusps (the aortomitral continuity). Both annuli are anchored at two
junctions: the left fibrous trigone (anchoring the anteromedial aspect
of the mitral annulus to the base of the left coronary cusp) and the
right fibrous trigone (formed by the triangular formation between the
aortic valve and the medial parts of the tricuspid and mitral valves).
Between the two trigones, a rigid and broad fibrous curtain (often
referred to as the aortic curtain) extends across the anterior leaflet of
the mitral valve and supports the aortic valve leaflets. The posterior
part of the mitral annulus runs distal to the left and right fibrous trigones
and includes the low points of the saddle close to the lateral and medial
commissures and the posterior saddle horn. Compared to the anterior
portion, the posterior mitral annulus is more loosely anchored to the
surrounding tissue, allowing it to move freely with myocardial contrac-
tion and relaxation. The commissural diameter being larger than the
anteroposterior diameter.60
The aortic and mitral valvular orifices are fitted alongside each other
(at the aortomitral continuity) within the elliptical ostium of the LV,
with no ventricular muscle between. As a result, BTs are rarely found
in the region of the aortomitral continuity. Left-sided BTs predominantly
cross the free-wall portion of the mitral annulus.
Although the atrial insertion of the BT is typically discrete in size
(1 to 3 mm) and close to the mitral annulus, the ventricular insertion
site tends to ramify over the region of tissue and can be displaced a
small distance away from the mitral annulus, toward the ventricular
apex. The BT crosses the annulus on its epicardial aspect and may cross
664 CHAPTER 18  Typical Atrioventricular Bypass Tracts

Failed site Successful site

I
II

III

V1

V2

V6

HRA

Hisprox

Hismid

Hisdist

CSprox

CSdist

RVA

Abldist

Ablunid

Ablprox

Ablunip

200 msec

Fig. 18.56  Effect of Ablation on Unipolar ST Segment. On the left (“Failed Site”), recordings during
orthodromic atrioventricular reentrant tachycardia are shown following an unsuccessful ablation attempt. The
distal ablation unipolar (Ablunid) recording shows minimal, if any, ST segment shift in the ventricular recording
(red arrow). On the right (“Successful Site”), a single complex of sinus rhythm is shown with significant ST
elevation (blue arrow), indicating injury has occurred at that site. Abldist, Ablation distal bipolar electrodes;
Ablprox, ablation proximal bipolar electrodes; Ablunip, ablation proximal unipolar electrode; CSdist, distal coronary
sinus; CSprox, proximal coronary sinus; Hisdist, distal His bundle; Hismid, middle His bundle; Hisprox, proximal His
bundle; HRA, high right atrium; RVA, right ventricular apex.

at variable depths within the epicardial fat pad. Most left free-wall BTs
cross the mitral annulus obliquely, with the atrial insertion typically 4
to 30 mm proximal (posterior) to the more distal (anterior) ventricular
insertion site (as mapped from within the CS).
Conduction at the insertion sites of the BT is markedly anisotropic
because of almost horizontal orientation of the atrial and ventricular
fibers as they insert into the mitral annulus. In addition, the atrial fibers
run parallel to the annulus, giving rise to rapid conduction away from
the insertion site, parallel to the annulus, and slow conduction to the
free-wall of the atrium, perpendicular to the annulus.
Importantly, while the CS is useful as a guide for mapping the mitral
annulus in the left anterior oblique (LAO) fluoroscopy view, it has a
 CHAPTER 18  Typical Atrioventricular Bypass Tracts
variable relationship to the mitral annulus (eFig. 18.7). The CS lies
2 cm superior to the mitral annulus as it empties into the RA. Antero-
laterally, the CS frequently overrides the LV. Thus, depending on the
distance from the ostium, the CS can lie above the mitral annulus and
be associated with the LA, or can cross over the LV side of the mitral
annulus. Furthermore, the CS is located more inferior to the mitral
annulus on fluoroscopy in most patents. Therefore electrograms recorded
from the CS can only provide gross estimates of the true atrial and
ventricular insertion sites of the BT and can only be used to guide the
ablation catheter to areas in which more detailed mapping needs to be
performed.61
Technical Considerations
Transaortic (retrograde) approach.  The right femoral artery is
the most commonly used access for the transaortic approach. A long
vascular sheath can provide added catheter stability, although with a
possibly increased risk of thromboembolism. Anticoagulation is started
before the LV is accessed to maintain the activated clotting time (ACT)
between 250 and 300 seconds. The ablation catheter is advanced to the
descending aorta and, in this position, a tight J curve is formed with
the catheter tip before passage to the aortic root to minimize catheter
manipulation in the arch. In the right anterior oblique (RAO) fluoros-
copy view, the curved catheter is advanced through the aortic valve
with the J curve opening to the right, so the catheter passes into the
LV, oriented anterolaterally. The straight catheter tip must never be
used to cross the aortic valve because of the risk of leaflet perforation.
Once in the LV, and while maintaining a tight curve, the catheter is
rotated counterclockwise and withdrawn in the LA as the tip turns
posteriorly. By opening the J curve slightly, the tip can easily map the
mitral annulus; clockwise torque moves the tip anteriorly (distally along
the CS), and counterclockwise torque returns the tip posteriorly (proxi-
mally along the CS). Alternatively, after crossing the aortic valve, the
catheter can be straightened and steered directly under the mitral annulus
to the BT location or withdrawn in the LV outflow tract, rotated pos-
teriorly with a slight curve, and then advanced under the posterior
mitral annulus for left paraseptal or posterior BTs. When the ablation
catheter is approximated along the mitral annulus, the catheter tip is
simultaneously withdrawn and straightened slightly to slip under the
annulus for fine manipulation. For left lateral and anterior BTs, extended-
reach catheters may be required.
Catheter positions beneath the annulus between the ventricular
myocardium and mitral leaflet are most stable for ablation of the BT
ventricular insertion, but manipulation can be constrained by the chordae.
Catheter positions above or along the annulus provide more freedom
to map along the mitral annulus but are sometimes too unstable for
successful energy delivery. Initial mapping is performed with the abla-
tion electrode on the annulus. From this general area, the catheter is
then positioned beneath the mitral annulus for more precise mapping.
Catheter tip positions beneath the mitral annulus are suggested by
proximity to the CS catheter, motion concomitant with the CS catheter,
and an A/V electrogram ratio of less than 1.
Because the transaortic approach targets the ventricular insertion
site of the BT, it is best suited for mapping anterograde BT activation
(i.e., preexcitation). Mapping retrograde activation from the subannular
position is more difficult than for anterograde mapping because of
obscuration of the low-amplitude atrial electrogram following the large
ventricular electrogram.
Although BT locations are commonly defined by mapping along the
CS catheter, this only approximates localization of the subannular abla-
tion site because of the oblique course of left free-wall BTs, displacement
of the CS above the mitral annulus, variable basilar-apical ventricular
insertion of the BT, and BT location beyond the distal CS electrode.
665
Transseptal approach.  Transseptal and transaortic approaches are
equally effective for ablation of left free-wall BTs. The transseptal approach
is primarily used for mapping of the BT atrial insertion site during
retrograde BT conduction (orthodromic AVRT or ventricular pacing),
while ventricular mapping of manifest BTs (during preexcitation) using
the transseptal approach is limited.
The transseptal approach has several advantages over the transaortic
approach. The transseptal approach provides better access to far lateral
and anterolateral BT locations, easier catheter maneuverability in the
LA, and less risk of coronary injury. In addition, no arterial access is
required with the transseptal approach, and vascular recovery is therefore
shorter. However, the transseptal approach provides less catheter stability
and is associated with a higher risk of cardiac perforation and air embo-
lism. Furthermore, the transseptal approach entails higher cost if intra-
cardiac echocardiography is used.
While mapping using the standard transseptal sheath, the ablation
catheter’s curvature can be modified according to BT location. For
left posterior BTs, the catheter typically reaches the annulus without
modifying the sheath position. The sheath is progressively withdrawn
toward the RA for optimal catheter apposition at lateral BT locations,
and it is almost entirely withdrawn toward the RA for anterior BTs.
Alternatively, preformed or deflectable sheaths may be used. Ablation
catheters with bidirectional asymmetric deflections can also be of value in
some cases.
Once the ablation catheter is positioned on the mitral annulus in a
30-degree RAO view, mapping is performed in the LAO view. In the
absence of preformed septal sheaths, gentle clockwise torque is needed
to maintain the catheter on the posterior mitral annulus. No torque is
needed for lateral positions. As the catheter is moved anteriorly, coun-
terclockwise torque is necessary to keep the catheter tip on the annulus.
In the anterior positions, the catheter tip can dislodge into the LA
appendage or LV, and attention to intracardiac electrograms is necessary
when mapping anterior regions, because the CS catheter rarely provides
an accurate fluoroscopic reference in this setting. The goal is to maintain
the catheter tip on the atrial aspect of the mitral annulus, so that the
mitral annulus can be easily mapped by advancing and withdrawing
the catheter, causing it to slide along the mitral annulus freely in parallel
to the CS catheter. Advancing the catheter moves the tip posteriorly;
withdrawing it moves the tip anteriorly. The ventricular aspect of the
mitral annulus can be mapped by passing the catheter tip across the
mitral valve and deflecting the tip toward the annulus.
The transseptal approach facilitates mapping of the atrial aspect of
the mitral annulus. Catheter position on the atrial aspect of the annulus
can be verified by recording a bipolar A/V electrogram amplitude ratio
greater than 1, and a unipolar electrogram PR segment displacement
from baseline without ST segment displacement. The stability of the
catheter can be assessed by PR segment elevation (confirming good
atrial tissue contact), consistent local electrographic amplitudes, and
concordant motion of the CS and ablation catheters.
Because of the mobility of the ablation catheter and the electrode
orientation parallel with atrial activation along the mitral annulus, a
unique vectorial mapping technique is possible with the transseptal
approach. As noted, using the unfiltered bipolar electrogram with the
electrodes oriented parallel to the axis of the mitral annulus, the BT
atrial insertion can be identified as the site at which the polarity of the
atrial potential reverses.
Occasionally, ablation of far-left lateral BTs can result in apparent
successful elimination of BT conduction, but shift to another, more
septal pathway. Although the latter can happen, this finding is com-
monly due to ablation of tissue proximal to the BT insertion, such that
CS activation must proceed from the (unablated) BT more distally and
then activate the rest of the CS in a proximal-distal direction. Clues
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 665.e1

7.07 mm
MA
5.63 mm
MA

12.57 mm CS
3.2 mm
CS
11.23 mm

A B
eFig. 18.7  Anatomical Relationship Between the Coronary Sinus (CS) and Mitral Annulus. The distances
between the CS and mitral annulus (MA) in the right anterior oblique projection (A) are 12.57 and 5.63 mm
during systole at the proximal and distal CS, respectively. The distances between the CS and MA in the left
anterior oblique projection (B) are 11.23 and 7.07 mm during systole at the proximal, middle, and distal CS,
respectively. (From Kim J, Hwang G, Seo K, et al. Anatomical discrepancy between the coronary sinus and
the mitral annulus by fluoroscopy. Int J Arrhythm. 2016;17:14–19.)
666 CHAPTER 18  Typical Atrioventricular Bypass Tracts
that this is the case include: (1) no change in the SVT CL (if ablation
has been attempted in SVT; (2) no change in the ablation electrogram
(because the BT has not been ablated); and (3) the earliest atrial activa-
tion was at the distal CS recordings, where ablation was attempted
(eFig. 18.8). This can be prevented by mapping more distally than the
site of earliest activation in CS recordings, and making certain the
“earliest” site is surrounded by later ones.
Ablation of Right Free-Wall Bypass Tracts
Anatomical Considerations
Unique features of the tricuspid annulus and important anatomic dif-
ferences as compared with the mitral annulus have often rendered abla-
tion of right-sided BTs more challenging than that of left free-wall BTs.
In addition, transient interruption of BT conduction during RF delivery,
with subsequent resumption of conduction within seconds or minutes,
and recurrence rates over the first few weeks after initially successful
BT ablation, are more common with right-sided BTs compared with
left-sided BTs.
A significantly larger endocardial area is present along the tricuspid
ring because of the larger circumference compared with the mitral
ring (approximately 12 vs. 10 cm). In addition, BTs can exist anywhere
around the tricuspid annulus, whereas the mitral ring has an area of
fibrous continuity with the noncoronary and left coronary aortic cusps
(the aortomitral continuity) where BTs are rarely found. Despite these
facts, right-sided BTs are much less common than left-sided BTs (12%
vs. 59%).
In contrast to the mitral annulus, the tricuspid valve annulus is less
well developed and frequently discontinuous. The tricuspid fibrous
ring is often incomplete and has several gaps at which atrial and ven-
tricular muscle fibers nearly abut. Right free-wall BTs can consist of
thin strands crossing the epicardial aspect of the annulus (similar to
left free-wall BTs) or pass subendocardially as relatively broad bands
of tissue through the fibrous discontinuities. Furthermore, right free-
wall BTs can insert into the myocardium (typically on the atrial side)
several millimeters away from the fibrous annulus and have been associ-
ated with a higher prevalence of branching pathways.62
Unlike the mitral valve, which attaches to its fibrous annulus at a
right angle, the tricuspid valve attaches to its annulus at an acute angle
oriented toward the RV, making it more difficult to wedge an ablation
catheter underneath the tricuspid valve. In addition, unlike left free-wall
AV BTs, which tend to pass close to the hinge line of the mitral valve,
the AV groove between the RA and RV is much deeper than on the left
side. The deep groove can allow the RA wall to fold over onto the RV
wall, and the BT muscle bundles can cross at any depth. Hence, the
right-sided BTs can be somewhat removed from the tricuspid annulus.
In fact, atrial insertion of the BT can be as far as 1 cm away from the
annulus in the folded-over atrial sac. The folded-over atrium and the
bizarre angle required for mapping of the inferior and posterolateral
aspect of the RA by a catheter passed through the RA from the inferior
vena cava (IVC) can make it difficult to achieve a stable catheter posi-
tion at the tricuspid annulus because of a tendency of the catheter to
fall into the folded-over sac. Thus sometimes the superior vena cava
(SVC) approach is required to allow full exploration of the folded-over
atrial sac and the inferior-inferolateral positions around the tricuspid
annulus. The standard IVC approach, however, is usually adequate to
map the superior aspects of the tricuspid annulus. If the IVC approach
is used, a guiding sheath can be especially helpful for better catheter
stability and tissue contact. The use of a multipolar (Halo) catheter
positioned around the tricuspid annulus can provide good regional
localization to guide the ablation catheter.63
Furthermore, closely adjacent but anatomically discrete sites of
catheter ablation can be necessary to eliminate anterograde and retro-
grade BT conduction in up to 10% of patients—the incidence is highest
(18.6%) with right free-wall BTs. The explanation for this phenomenon
is not clear but probably relates to the complexity of fiber orientation,
possibly branching over 1 to 2 cm along the annulus. This factor empha-
sizes the importance of identifying and targeting both the atrial and
the ventricular BT insertion sites.
Right-sided AV BTs are associated with higher incidences of anatomic
variations and congenital abnormalities along the tricuspid annulus.
Ebstein anomaly is an abnormality of the tricuspid valve in which the
septal and often the posterior leaflets are displaced a variable distance
into the RV and the anterior leaflet is usually malformed, excessively
large, and abnormally attached or adherent to the RV free wall. The true
tricuspid annulus, on the other hand, is not anatomically displaced, but
can be poorly developed, with extensive discontinuities of the fibrous
architecture. Thus a portion of the RV is “atrialized” in that it is located
on the atrial side of the tricuspid valve, and the remaining functional
RV is small. The atrialized portion of the RV is morphologically and
electrically ventricular but functionally atrial. Ebstein anomaly can be
associated with other cardiac anomalies, including a patent foramen ovale,
atrial and ventricular septal defects, and RV outflow tract obstruction.
Right-sided BTs have been reported in 10% to 30% of patients with
Ebstein anomaly, and they are multiple in up to 50% of patients. The
BTs bridge the true anatomical tricuspid annulus, regardless of where
the valve is located. Ablation of these BTs can be challenging because
the electrical signals recorded from the atrialized portion of the RV
can be complex and fractionated. Furthermore, identification of the
true AV groove, along which BTs are targeted, can be difficult. Coronary
angiography or insertion of a thin multielectrode catheter in the right
coronary artery can be necessary to help identify the true AV groove
and guide ablation catheter positioning. In addition, electroanatomic
activation mapping during NSR can help define the electrical AV junc-
tion (true tricuspid annulus), where annular atrial and ventricular
electrograms are recorded. Ablation is usually accomplished at the true
tricuspid annulus, above the displaced valve leaflet, although some
patients may undergo successful ablation from the ventricular side of
the tricuspid annulus (but still above the valve leaflet).
Technical Considerations
Characteristically, successful ablation sites for right-sided BTs display
local AV intervals that are shorter than those for BTs elsewhere, local
ventricular electrograms preceding the onset of the delta wave by an
interval longer than that for BTs elsewhere (18 ± 10 milliseconds for
right-sided BTs versus 0 ± 5 milliseconds for left-sided BTs), and the
unipolar recording showing more pronounced (rapid and deeper) QS
configurations (Fig. 18.57).
Most commonly, ablation of right-sided BTs is approached from
the atrial aspect. The optimal site of ablation is the earliest atrial activa-
tion site during retrograde BT conduction (during orthodromic AVRT
or ventricular pacing), preferably with a BT potential present. The earliest
site of atrial activation is identified using a roving catheter or a multi-
polar (Halo) catheter along the tricuspid annulus. If mapping is per-
formed during ventricular pacing, conduction over both the BT and
AVN can occur, resulting in atrial fusion, which can interfere with
localization of the BT. Ventricular pacing performed close to the BT
ventricular insertion site can accentuate atrial activation over the BT.
Occasionally, the BT can be better approached from the ventricular
side. Ventricular activation mapping is performed during preexcited
NSR, atrial pacing, preexcited SVT, or antidromic AVRT. The site of
the earliest ventricular activation during preexcitation, preferably with
a BT potential present, would be the optimal site. The earliest onset of
ventricular activation recorded on the ablation catheter (using unipolar
or bipolar electrograms) should precede the onset of the delta wave by
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 666.e1

I
II
III
V1
V6
Abldist
HRA
Hisprox
Hismid
Hisdist
CSprox

CSmid

CSdist
RVA
Time
l–– 200 msec––l

eFig. 18.8  Apparent Shift of Atrial Activation During Ablation for Orthodromic Atrioventricular Reentrant
Tachycardia (AVRT) Using a Left Lateral Bypass Tract (BT). On the first three cycles, the atrial activation
sequence is distal-to-proximal in the coronary sinus (CS). In the middle, atrial activation sequence suddenly
shifts to proximal-to-distal in the CS due to ablation near the distal CS recording, but proximal to the actual
BT insertion site. Left atrial/CS conduction is interrupted along the CS. AVRT does not terminate and is in
fact the same arrhythmia (tachycardia cycle length remains unchanged, and the interval from QRS onset
[dashed line] to ablation recording [arrow] also remains unchanged). CS propagation continues distally from
the ablation site to the septum (not illustrated), activating the CS between the ostium and BT location in the
proximal-distal direction. Abldist, Ablation distal bipolar electrodes; CSdist, distal coronary sinus; CSmid, middle
coronary sinus; CSprox, proximal coronary sinus; Hisdist, distal His bundle; Hismid, middle His bundle; Hisprox,
proximal His bundle; HRA, high right atrium; RVA, right ventricular apex.
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 667

Right lateral pathway Left lateral pathway not always in the same plane, the CS catheter is only a rough guide to
the location of the tricuspid annulus in the RAO view. Attempts at
I I providing an endocardial reference catheter along the tricuspid annulus
II II have been made using a 20-pole Halo catheter. This approach has had
III III limited success because the catheter often does not position directly on
V1 V1
the AV groove. Introducing the Halo catheter through a preformed
V6 V6 sheath can provide better catheter stability along the tricuspid annulus.
HRAp HRAp Occasionally, a fine angioplasty wire can be passed into the right coro-
HIS P HIS P
nary artery to delineate the location of the tricuspid annulus. The latter
HIS M HIS M approach, however, has not been widely adopted, possibly in part because
HIS D HIS D of concerns of prolonged instrumentation of the right coronary artery
CS 9-10 CS 9-10
CS 8-9 CS 8-9
during the procedure. Another approach is to create a three-dimensional
CS 7-8 CS 7-8 electroanatomic map (EnSite-NavX; St. Jude Medical, St. Paul, MN,
CS 6-7 CS 6-7 United States) of the right coronary artery. After right coronary artery
CS 5-6 CS 5-6 angiography, a 2.3-Fr octapolar microcatheter (Cardima Inc., Fresno,
CS 4-5 CS 4-5
CS 3-4 CS 3-4 CA, United States) is inserted in the right coronary artery. Mapping
CS 2-3 CS 2-3 and acquisition of the bipolar electrograms recorded by the microcath-
CS 1-2 CS 1-2 eter are performed during anterograde or retrograde BT conduction.
RVA p RVA p
A A This map allows for early removal of the catheter from the coronary
Abl D Abl D
V artery while continuously displaying electroanatomic information to
Abl uni-d Abl uni-d V assist with mapping of the BT.64
Abl P Abl P To target the ventricular aspect of the tricuspid annulus, the catheter
Abl uni-p Abl uni-p is introduced across the tricuspid valve and looped back on itself in
l–200 msec–l the RV underneath the valve until a small atrial electrogram and a
larger ventricular electrogram are recorded, confirming adequate prox-
Fig. 18.57  Differences in Mapping Site Electrogram Characteristics imity to the tricuspid annulus. A long sheath may be used to stabilize
With Right Versus Left Lateral Anterogradely Conducting Bypass the body of the catheter and direct the catheter to several different
Tracts (BTs). Dotted lines denote delta wave onset in each panel; A locations along the tricuspid annulus.
and V are atrial and ventricular components of the ablation recording. Three-dimensional electroanatomic mapping can help ablation of
At left is a right lateral BT; note the ventricular electrogram precedes
right-sided BTs, and is especially useful in the presence of multiple BTs
the delta wave onset and the unipolar recording has a deep negative
or complicated anatomy. An electroanatomic color-coded activation
deflection, also before the delta wave. In contrast, with a left lateral BT
(right panel), the ventricular recording in the distal bipole begins coinci- map along the tricuspid annulus can be constructed, either along the
dent with the delta wave onset and the unipolar recording is not as atrial side, during orthodromic AVRT or ventricular pacing, or along
sharp and occurs after the delta wave onset. Abl D, Ablation distal the ventricular side, during anterograde preexcitation. Sites of interest
bipolar electrodes; Abl P, ablation proximal bipolar electrodes; Abl uni-d, can be tagged for further reference, so that the ablation catheter can
ablation distal unipolar electrode; Abl uni-p, ablation proximal unipolar be returned to any of them with precision. Information with regard to
electrode; CS, coronary sinus; His D, distal His bundle; His M, middle catheter stability and movement can also be provided.62
His bundle; His P, proximal His bundle; HRA, high right atrium; RVA,
right ventricular apex. Ablation of Anteroseptal (Superoparaseptal) and
Midseptal Bypass Tracts
Anatomical Considerations
at least 10 to 25 milliseconds. For concealed BTs, the ventricular inser- The midseptum is the only true muscular septal area between the offset
tion site cannot be determined by ventricular activation mapping because attachments of the mitral and tricuspid valves, and it corresponds roughly
of the lack of preexcitation. In this setting, recording of a BT potential to the location of the triangle of Koch. The triangle of Koch constitutes
can be especially useful in guiding ablation. the endocardial surface of the region of the lower RA septum. It is
The tricuspid annulus is usually mapped in the LAO fluoroscopy bordered anteriorly by the insertion of the septal leaflet of the tricuspid
view. The right posterior, posterolateral, and lateral regions are usually valve and posteriorly by the fibrous tendon of Todaro. The apex of the
best mapped from the IVC approach. The right anterior and anterolateral triangle is formed by the junction of these two boundaries. The base
regions can also often be ablated using the IVC approach, but the SVC of the triangle is formed by the anteromedial edge of the CS os and is
approach can offer more stable and better catheter-tissue contact in continuous with the sub-eustachian pouch (see Figs. 17.1 and 9.2).65,66
these areas. The catheter can be prolapsed across the tricuspid valve to Of note, the interatrial sulcus is displaced to the far left of the inter-
help stabilize the tip on the tricuspid annulus. In the LAO view, the ventricular sulcus, and because the AV valves are not isoplanar (the
HB is located at about 1 o’clock and the CS at 5 o’clock; right free-wall attachment of the septal leaflet of the tricuspid valve into the most
BTs span from approximately 6 to 12 o’clock. Right anterior BTs are at anterior part of the central fibrous body is displaced a few millimeters
the most superior aspect of the tricuspid annulus, right superoparaseptal apically relative to the attachment of the septal leaflet of the mitral
BTs are located near the HB catheter, and right posterior free-wall BTs valve), the true septal part of the AV junction (the RA-LV sulcus) actu-
are located at the most posterior aspect of the tricuspid annulus, whereas ally separates the inferomedial RA from the posterior superior process
right posteroseptal BTs are located near the CS. of the LV (the right side above the tricuspid valve while the left side is
Although the location of the mitral annulus is reasonably indicated below the mitral valve). Hence, the triangle of Koch can be considered
by the CS catheter, the location of the tricuspid annulus is not as easily the RA side of the AV muscular septum.
discerned because there is no analogous venous structure to mark with The compact AVN is located beneath the RA endocardium at the
a catheter. Furthermore, because the mitral and tricuspid annuli are apex of the triangle of Koch, anterior to the CS os and directly above
668 CHAPTER 18  Typical Atrioventricular Bypass Tracts
the insertion of the septal leaflet of the tricuspid valve, where the tendon
of Todaro merges with the central fibrous body. Slightly more anteriorly
and superiorly is where the HB penetrates the AV junction through the
central fibrous body and the posterior aspect of the membranous AV
septum.65,66
BTs with an atrial insertion in the floor of the triangle of Koch,
posteroinferior to the compact AVN and HB and above the anterior
portion of the CS os, have been labeled as midseptal; these BTs are the
only truly septal BTs; hence, they can be referred to simply as septal BTs.
The previously named anteroseptal and posteroseptal areas are not
truly “septal” but are parts of the parietal AV junction that are anterior
and posterior to the true septum, respectively. Anterosuperior to the
AV septum and compact AVN and HB, the tricuspid annulus diverges
laterally away from the membranous part of the septum to course along
the supraventricular crest of the RV (crista supraventricularis). This
muscular structure interposes between the attachments of the leaflets
of the tricuspid and pulmonic valves in the roof of the RV. BTs in this
area (at the apex of the triangle of Koch) are labeled anteroseptal, but
they must be considered “superoparaseptal” right free-wall BTs because
anatomically they do not belong to the septum. There is no atrial septum
in the region anterior to the HB recording site; the aortic root separates
the right and left atrial walls here.
BTs are classified as “superoparaseptal” if the BT potential and His
potential are simultaneously recorded from the mapping catheter placed
at the HB region. A “para-Hisian” BT (which accounts for only 1% to
2% of all BTs) is a superoparaseptal BT with intimate proximity to the
HB and is defined when the location of its successful catheter ablation
coincided with either the largest recordable His potential or a His poten-
tial greater than 0.1 mV.67
Electrocardiographic Considerations
The surface ECG can be valuable in anticipating septal or paraseptal
locations of the BT and planning the catheter ablation procedure. Right
superoparaseptal (anteroseptal) and midseptal BTs typically exhibit
positive delta waves in leads I, aVL, and V3 through V6. Delta wave
polarity in leads V1 and V2 can vary. Because of their superior location,
right superoparaseptal BTs are associated with positive delta waves in
all inferior leads (II, III, and aVF). In contrast, the delta wave in mid-
septal BTs is positive in lead II, predominantly negative in lead III, and
negative or isoelectric in lead aVF. The combination of a negative delta
wave in lead V1 and R/S transition in leads V3 to V4 suggests right-
sided midseptal BT, whereas a biphasic delta wave in lead V1 and earlier
QRS transition (in leads V1 to V2) suggest a left-sided location of the
midseptal BT.
The surface ECG can also help distinguish para-Hisian locations of
the BT (which is associated with the highest risk of AV block during
ablation) from other superoparaseptal or septal locations. The presence
of a negative delta wave in leads V1 and V2 was found to carry high
specificity (92%) but poor sensitivity (25%) to detect the ventricular
insertion of BTs with a strict invasive definition of para-Hisian loca-
tion. In addition, the sum of initial r-wave amplitudes in those pre-
cordial ECG leads of less than 0.5 mV could be a useful, adjunctive
marker in the noninvasive identification of these BTs (sensitivity 85%;
specificity 75.5%).67
Technical Considerations
A superoparaseptal location of the BT is initially suggested when the
BT potential and His potential are simultaneously recorded from the
diagnostic EP catheter placed at the HB region.67 AES or short bursts
of atrial pacing can help distinguish BT potential from the His potential.
Atrial impulses that block in the AVN but conduct over the BT results
in fully preexcited QRS morphology preceded by the BT potential but
with concomitant loss of the His potential. On the other hand, atrial
impulses that block in the BT result in loss of preexcitation and BT
potential recording but preserve His potential recording.
The precise location of the BT is verified by mapping this space in
a 30-degree LAO fluoroscopy view using the ablation catheter advanced
via the IVC. The use of a long vascular sheath can help stabilize the
catheter tip during mapping and ablation in the superoparaseptal region.
Also, mapping via the SVC approach is sometimes necessary to optimize
catheter position and contact. Not infrequently, catheter-induced
mechanical trauma can cause conduction block in the BT, which can
hinder BT mapping and ablation. Therefore careful catheter manipula-
tion is warranted during mapping in the region of the BT.
The optimal site of ablation is one from which the atrial and ven-
tricular electrograms are recorded in conjunction with a BT potential,
but with no or only a tiny His potential (less than 0.1 mV). Preferably,
the ventricular insertion site (with V/A electrogram amplitude ratio
greater than 2) of the BT is targeted with ablation to minimize the risk
of damage to the AVN (the HB is more resistant to ablation on the
ventricular aspect, generally within a fibrous sheath at that location).
Occasionally, ablation is required in the presence of a marked (greater
than 0.1 mV) His potential recorded through the ablation catheter (i.e.,
true “para-Hisian” BTs). Ablation of these BTs from the aortic root has
been described and can be an important option to consider in these
challenging cases.68,69
For midseptal BTs, successful ablation is achieved in an area bounded
superiorly by the electrode recording the His potential, and posteroin-
feriorly by the CS os, as marked by the apex of curvature in the CS
catheter. The optimal site of ablation for a right midseptal BT is one
from which atrial and ventricular electrograms are recorded simultane-
ously with a BT potential in between. Ablation is first attempted from
the right side. If it is ineffective or early recurrence occurs after termi-
nation of RF application, then the left-sided approach is attempted.
For manifest BTs, RF application is performed during NSR or atrial
pacing, which helps monitor both BT and AVN-HB conduction during
RF energy delivery. In the setting of concealed para-Hisian BTs, it is
challenging to assess the success of RF application and monitor AV
conduction simultaneously. When RF delivery is performed during
ventricular pacing, monitoring the success of RF application is not
possible because the retrograde atrial activation sequence during ven-
tricular pacing can be similar with either BT or AVN conduction. Atrial
pacing during RF delivery is preferable because it helps monitor AV
conduction and override junctional rhythms that may occur during
RF delivery; however, it is not helpful for assessing the efficacy of RF
application because the BT conducts retrogradely only. RF delivery
during orthodromic AVRT is another option; however, this will certainly
have the potential for catheter dislodgment on SVT termination, and
such dislodgment can endanger the AVN-HB. Moreover, application
of RF energy during orthodromic AVRT will not allow monitoring of
AV conduction. In this setting, monitoring of the mode of termination
of orthodromic AVRT during RF delivery is essential. Termination of
orthodromic AVRT with an atrial electrogram signifies potential damage
to the anterograde limb of the SVT circuit (i.e., the AVN), and therefore
RF delivery should be immediately stopped. On the other hand, ter-
mination of orthodromic AVRT with a ventricular electrogram suggests
successful block in the retrograde limb of the SVT circuit (i.e., the BT),
and therefore RF delivery should be continued, with careful monitoring
of AV conduction during NSR following termination of the SVT. Another
valuable option is RF delivery during atrial-entrained orthodromic
AVRT with manifest atrial fusion. This technique enables continuous
monitoring of effects of RF application on BT function and also obvi-
ates a sudden change in ventricular rate on termination of the SVT. In
addition, this technique allows monitoring of AV conduction during
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 669

RF application once the orthodromic AVRT is terminated, and therefore
reduces the risk of damage to the AVN-HB. During successful RF appli-
cation, termination of orthodromic AVRT will be indicated by trans-
formation from the tachycardia P wave morphology and atrial activation
sequence into a fully paced atrial activation sequence at the same rate.
Ablation in the region of the triangle of Koch is associated with 2%
to 10% incidence of AV block and, to reduce this risk, such BTs should
be ablated with the catheter placed on the tricuspid annulus or on the
ventricular side of the tricuspid annulus, preferably with the use of lower
RF power. Titrated RF energy output can be used for true para-Hisian
BTs, starting with 5 W, and increasing by 5 W every 10 seconds of energy
application, up to a maximum of 40 W. For other superoparaseptal BTs,
ablation can be started at 30 W, targeting a temperature of 50°C to 60°C.
During RF ablation within the triangle of Koch, the occurrence of
junctional tachycardia is not uncommon and is associated with loss
of preexcitation; this should not be misinterpreted as successful abla-
tion leading to continuing RF energy delivery. Instead, overdrive atrial
pacing should be performed to monitor AV conduction or RF applica-
tion should be stopped and other sites sought (Fig. 18.58). RF applica-
tion should be stopped after 10 to 15 seconds if no block in the BT is
achieved to minimize potential damage to the AVN-HB.
To reduce the risk of AV block, RF delivery should be immediately
discontinued when the following occur: (1) the impedance rises sud-
denly (greater than 10 Ω); (2) the PR interval (during NSR or atrial
pacing) prolongs; (3) AV block develops; (4) retrograde conduction
block is observed during junctional ectopy; or (5) fast junctional tachy-
cardia (TCL less than 350 milliseconds) occurs, which may herald
imminent heart block.
Cryoablation of Superoparaseptal and
Midseptal Bypass Tracts
Cryothermal ablation of BTs in the superoparaseptal and midseptal
areas, both at high risk of permanent AV block with RF ablation, is
successful and extremely safe. Cryoablation may also be used to ablate
selected cases of epicardial left-sided BTs within the CS, well beyond
the middle cardiac vein, once attempts using the transseptal and
transaortic approaches have failed. The experience with cryoablation
in unselected BTs, however, is more limited and less satisfactory; this
is likely related to multiple factors, including the learning curve and
the smaller size of the lesion produced by cryoablation. In addition,
many of the features of cryothermal energy that distinguish it from RF
energy, and which are optimal for septal ablation, are less important
or even useless for ablation of BTs located elsewhere.70
A 6-mm-tip or 8-mm-tip cryocatheter is usually used. Not infre-
quently, because of the limited maneuverability and the wide distal
electrode spacing of the cryocatheter (which can displace the geometric
center point of the measuring bipole and greatly decreases precision),
mapping of the target BT ablation site may need to be performed using
a steerable quadripolar EP catheter with 2–5–2-mm distal electrode
spacing prior to cryoablation.71
Cryomapping.  Cryomapping, or ice mapping, is designed to verify
that ablation at the chosen site will have the desired effect (i.e., block
in the BT) and to ensure the absence of complications (i.e., AV block).
Cryomapping is performed at −30°C in the selected site. At this tem-
perature, the lesion is reversible (for up to 60 seconds) and the catheter
is “stuck” to the endocardium in an ice ball that includes the tip of the
catheter (cryoadherence). This permits programmed electrical stimula-
tion to test the disappearance of BT conduction during ongoing ablation
and also allows ablation to be performed during AVRT without the
risk of catheter dislodgment on tachycardia termination. In the cry-
omapping mode, the temperature is not allowed to drop below −30°C,
and the time of application is limited to 60 seconds. Formation of an
ice ball at the catheter tip and adherence to the underlying myocardium
are signaled by the appearance of electrical noise recorded from the
ablation catheter’s distal bipole.
In patients with manifest preexcitation, cryomapping may be per-
formed during NSR or atrial pacing (to monitor for loss of delta waves),
during ventricular pacing (to monitor retrograde BT block), or during
AVRT (to monitor tachycardia termination). For concealed BTs, cry-
omapping is preferably performed either during orthodromic AVRT
or during ventricular pacing. Once an ice ball is formed, programmed
electrical stimulation is repeated to verify that the BT has been blocked.

II

HRA

His

CSprox

CSdist
RVA

ABLdist
600 msec

Start RF application Junctional tachycardia Stop RF application

Fig. 18.58  Junctional Tachycardia During Radiofrequency (RF) Ablation of a Superoparaseptal Bypass
Tract. The first few complexes demonstrate normal sinus rhythm with preexcitation. A few seconds after
starting RF energy delivery, junctional tachycardia develops, with loss of preexcitation. This prompted
immediate termination of RF application, after which preexcitation resumed. ABLdist, Ablation distal bipolar
electrodes; CSdist, distal coronary sinus; CSprox, proximal coronary sinus; HRA, high right atrium; RVA, right
ventricular apex.
670 CHAPTER 18  Typical Atrioventricular Bypass Tracts
If cryomapping does not produce BT conduction block after 10 to 30
seconds of freezing or results in detrimental effects on AV conduction,
cryomapping is interrupted and, after a few seconds, allowing the cath-
eter to thaw and become dislodged from the tissue, the catheter can be
moved to a different site and cryomapping repeated. Alternatively, if
the test application is unsuccessful but mapping findings are very favor-
able, after rewarming, further 30-second applications are tested, decreas-
ing the temperature by 10°C for every step of the application, up to
the last application at −70°C. This is because the amount of cryothermal
energy required for permanent ablation is individualized, ranging from
an application of −40°C for 40 seconds to one of −75°C for 480 seconds;
limiting test applications to only −30°C can limit the applicability of
cryoablation for these patients. In addition, the use of cryothermal
energy at temperatures lower than −30°C should be considered safer
than RF energy at these critical sites.
Cryoablation.  When sites of successful cryomapping are identified
by demonstrating BT conduction block with no modification of the
normal AVN-HB conduction, the cryoablation mode is activated, in
which a target temperature below about −75°C is sought (a temperature
of −75°C to −80°C is generally achieved). The application is then con-
tinued for up to 480 seconds, creating an irreversible lesion. If the
catheter tip is in close contact with the endocardium, a prompt drop
in catheter tip temperature should be seen as soon as the cryoablation
mode is activated. A slow decline in temperature or very high flow rates
of refrigerant during ablation suggests poor catheter tip–tissue contact
and, in such a case, cryoablation is interrupted and the catheter is
repositioned. Additional cryoablation “bonus” applications (usually two
to three freeze–thaw–freeze cycles) may be applied to consolidate the
lesion formation and improve long-term success rates.
Advantages of cryoablation.  Cryoablation has several distinct
advantages. First, “cryomapping” allows creation of “test lesions,” in
which ablation target sites are cooled to a temperature that reversibly
and temporarily halts local electrical activity. This enables valuation of
the success and safety of the cryotherapy, and untoward effects caused
by cryotherapy can be detected and reversed by interruption of cryo-
therapy before inducing permanent tissue damage. This is of particular
value when ablation is performed in the close vicinity of the compact
AVN or HB. Second, cryoadherence enhances catheter stability during
ablation. This facilitates creating small, discrete cryolesions, which helps
avoid damage to adjacent structures. Also, cryoablation may be per-
formed during SVT without the concern of catheter dislodgement upon
tachycardia termination.
On the other hand, the cryocatheter is not yet as steerable as the
conventional RF catheter. Catheter stiffness and limited maneuverability
can limit proper positioning of the catheter tip and potentially result
in tissue trauma and transient mechanical AV or BT block. Furthermore,
the large electrode spacing decreases the specificity of mapping of the
BT. These limitations can potentially be overcome by the use of an
electroanatomic mapping system and a conventional EP catheter with
2-mm spacing for mapping of the precise BT location before targeting
that site with cryoablation.71
Outcome of cryoablation.  In recent series, the acute success rate
of cryoablation of BTs in the superoparaseptal and midseptal regions
exceeded 90% (range, 60% to 100%). However, recurrence rates after
initially successful cryoablation remain high (occurring in up to 20%
of patients), and overall success rates have been lower than those with
RF ablation of BTs. Nevertheless, whereas RF ablation of some supero-
paraseptal and midseptal BTs may otherwise be abandoned (in up to
17% of patients) because of a prohibitive risk of AV block, cryoablation
is a viable, and often successful, option to eliminate those BTs. Many
patients often prefer a strategy to minimize the risk of procedural AV
block even when associated with a lower rate of procedural success.
Although transient modifications of the normal AV conduction can be
observed during cooling, no permanent modifications have been
observed. RBBB has occurred on occasion, but inadvertent permanent
AV block has yet to be reported. In fact, immediate discontinuation of
cryothermal energy application at any temperature on observation of
modification of AVN conduction results in return to baseline conditions
shortly afterward.71–73
Ablation of Posteroseptal (Inferoparaseptal)
Bypass Tracts
Anatomical Considerations
The posteroseptal region corresponds to a complex anatomic region
where the four cardiac chambers reach their maximal proximity pos-
teriorly (i.e., the crux), and incorporates the converging segments of
the AV rings as well as the CS with its proximal branches. The postero-
septal region spans the area between the central fibrous body (superiorly),
the interventricular septum (anteriorly), the right posterior paraseptal
region (right lateral border), and the left posterior paraseptal region
(left lateral border). Posteroseptal BTs can be located in a relatively
wide area either at an epicardial site around the proximal CS or the
middle cardiac vein or at an endocardial site along the tricuspid annulus
in the immediate vicinity of the CS os, or along the posteromedial
ventricular aspect of the mitral annulus. Because the posteroseptal region
is actually posterior to the septum and not a septal structure, postero-
septal BTs are more appropriately referred to as right- or left-sided
“inferoparaseptal” or “posterior paraseptal” BTs.
Because the interatrial sulcus is displaced to the far left of the inter-
ventricular sulcus, and because the AV valves are not isoplanar (the
tricuspid annulus is displaced apically 5 to 10 mm in relation to the
mitral annulus), the true septal part of the AV junction (the RA to LV
sulcus) actually separates the inferomedial RA from the posterior supe-
rior process of the LV. The undersurface of the CS is about 1 cm above
the mitral annulus. The CS os abuts the superior margin of the RA-to-
LV sulcus and the paraseptal mitral annulus in the pyramidal space,
providing an access for BT ablation. The right margin of the posteroseptal
space includes the area surrounding the CS os and the inferior portion
of the triangle of Koch. The left margin (the junction of the posterior
septum and left free wall) lies as far as 2 to 3 cm from the CS os. The
epicardial dimension of the posteroseptal space at the level of the valve
annuli extends a mean of 3.4 ± 0.5 cm. BTs can be located anywhere
within this relatively large space or in the adjacent right or left free
walls. BTs located close to the edges of the septum can be ablated from
the adjacent atrial or ventricular cavity, but BTs located deep within
the posteroseptal space or near the epicardial aspect require ablation
from within the CS or cardiac veins. BTs located in the proximal 1.5 cm
of the CS are almost always in the posterior septal region. Those located
between 1.5 and 3 cm from the CS os can be in the left free-wall or
posterior septal region, and those located more than 3 cm from the CS
os are almost invariably in the left free wall.
Most posteroseptal BTs are believed to be RA-to-LV BTs, with the
ventricular insertion attaching onto the posterior superior process of
the LV, but some posteroseptal BTs are considered to be left paraseptal
(connecting the LA to the LV) or right paraseptal (connecting the RA
to the RV). Up to 20% of posteroseptal BTs connect the myocardial
coat of the CS (which is connected anatomically and electrically to both
the RA and LA) to the LV.74–76
Electrocardiographic Considerations
Prediction of the site of successful ablation of posteroseptal BTs into
either the right or the left heart has been attempted by analysis of the
preexcitation pattern on the surface ECG. In addition to the obvious
limitation of the surface ECG in the case of concealed BTs (47.5% in
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 671

a recent report), reports on the accuracy of surface ECG features to
differentiate BTs associated with the three compartments of the inferior
paraseptal space have been conflicting. Furthermore, although ECG
characteristics of ventricular preexcitation can potentially predict the
ventricular insertion site of the BT, the ability to predict the successful
approach to BT ablation remains limited.
Previous reports found that, in patients with preexcitation, a nega-
tive delta wave polarity in lead V1 and positive polarity in lead V2
favors right-sided localization of a posteroseptal BT, whereas left pos-
teroseptal BTs were associated with biphasic or positive delta wave
polarity in leads V1 and V2. Recent reports, however, have questioned
the predictive value of such a criterion. The vast majority of postero-
septal BTs can be successfully ablated at the tricuspid annulus or within
the proximal CS, although the delta wave polarity on the ECG suggests
a left ventricular origin. This phenomenon can be explained by the fact
that many posteroseptal BTs are “RA-to-LV” fibers and an RA approach
for ablation would suffice even though the delta wave polarity in lead
V1 is suggestive of left posteroseptal BTs.74–76
On the other hand, the R/S ratio in lead V1 was found to be an
accurate ECG parameter to predict the site of successful ablation of
posteroseptal BTs. This finding might be related to the observation that
the ventricular insertion of “RA-to-LV” posteroseptal BTs attaches onto
the posterosuperior process of the LV, resulting in earlier activation
of the posterobasal LV with positive delta wave and predominantly
negative QRS morphology (R/S ratio less than 1) in lead V1. In contrast,
the ventricular insertion of “LA-to-LV” BTs attaches to the posteromedial
aspect of the mitral annulus, resulting in a positive delta wave and a
predominantly positive QRS morphology (R/S ratio greater than 1) in
lead V1.75
Posteroseptal BTs typically display deeply negative delta waves in
lead III. Lead aVF is also negative in right posteroseptal BTs, but less
commonly negative in left posteroseptal BTs. A steeply negative delta
wave in lead II is a specific indicator for epicardial posteroseptal BTs
(typically requiring ablation from within the coronary venous system).
Technical Considerations
Ablation of posteroseptal BTs is usually more difficult than other BT
locations because of the complexity of the anatomical structures involved.
Mapping and ablation can be required at either the mitral or the tri-
cuspid annulus, or inside the CS or its proximal branches. Therefore
the ability to discriminate BTs amenable to ablation from the right side
(on the tricuspid ring or inside the coronary venous system) from those
requiring ablation on the mitral annulus can potentially have great
impact on procedure outcome and safety by reducing procedural and
fluoroscopy times, reducing the number of unsuccessful RF applications,
and avoiding unnecessary LA access and its potential complications.74,75
In addition to the ECG criteria discussed above, invasive EP findings
have been used to predict the successful ablation site of manifest or
concealed posteroseptal BTs (Table 18.2; Fig. 18.59). The response of
the VA interval during orthodromic AVRT to the development of BBB
has been suggested to help distinguish between right and left postero-
septal BTs. Prolongation of the surface VA interval in response to BBB
by 10 to 30 milliseconds compared to that with normal QRS predicts
the ventricular insertion of the posteroseptal BT in the ventricle ipsi-
lateral to the side of BBB. However, the utility of this observation in
predicting the successful approach to ablation is limited.74
Measurement of the ΔVA interval during orthodromic AVRT (the
difference in VA intervals measured at the HB catheter and at the site
of earliest atrial activation in the CS) was found to be useful for pre-
dicting the successful approach. A ΔVA interval of 25 milliseconds or
more suggests a left endocardial BT, whereas a ΔVA interval less than
25 milliseconds favors a right endocardial BT. This suggests that atrial
activation is relatively early in the HB region during retrograde conduc-
tion through both right endocardial and CS-associated BTs, compared
with left endocardial BTs.74
Furthermore, a previous report found that a VA interval less than
50 milliseconds recorded at the left posteroseptal region during RV
pacing identified 71% of patients with left posteroseptal BTs, with 100%
specificity. In patients with a VA interval greater than 50 milliseconds,
a difference in the VA intervals of less than 20 milliseconds recorded
at the HB region and at the left posteroseptal region during RV pacing
predicted right posteroseptal BT with a sensitivity of 97%, a specificity
of 85%, and a positive predictive value of 91%.
PJRT is usually caused by a slowly conducting BT, commonly located
in the posteroseptal region. Although the mere presence of a long-RP
orthodromic AVRT has been suggested to favor a right endocardial BT,
in 50% of cases, such BTs can be located in the left posterior or free
wall (greater than 4 cm inside the CS). In the remaining 50%, the BT
is located between the base of the pyramidal space formed by the points
of pericardial deflection that contact the posterior RA and LA. None
have been reported in the anteroseptal region.74
An earliest atrial activation during orthodromic AVRT in the middle
CS favors a left endocardial ablation site. However, recent studies found
that a large proportion (more than one-third) of patients with an

TABLE 18.2  Electrocardiographic and Electrophysiological Criteria for Discrimination

Between Right and Left Posteroseptal Bypass Tracts
Favors Right Posteroseptal
Bypass Tract
Electrocardiogram • Delta wave negative in lead V1
and positive in lead V2
• R/S ratio in lead V1 <1
Response of orthodromic AVRT to left bundle branch block • Prolongation of VA interval
ΔVA interval during orthodromic AVRT (the difference in VA intervals measured • <25 ms
at the HB catheter and the site of earliest atrial activation in the CS)
ΔVA interval during RV pacing (the difference in VA intervals measured at the • VA >50 ms and ΔVA <20 ms
HB catheter and the left posteroseptal region)
Site of earliest retrograde atrial activation • CS ostium
CS electrogram characteristics at earliest retrograde site • Sharp/blunt CS atrial
electrogram sequence
Favors Left Posteroseptal
Bypass Tract
• Biphasic or positive delta wave
polarity in leads V1 and V2
• R/S ratio in lead V1 >1
• No change in VA interval
• ≥25 ms
• <50 ms
• Mid CS
• Blunt/sharp CS atrial
electrogram sequence

AVRT, Atrioventricular reentrant tachycardia; CS, coronary sinus; HB, His bundle; RV, right ventricular; VA, ventricular-to-atrial.
672 CHAPTER 18  Typical Atrioventricular Bypass Tracts
Concealed
PS BT
Earliest atrial
activation at
middle electrode
YES NO
LPS
Long RP'
tachycardia
YES NO
RPS
∆VA ≥ 25 msec
YES NO
LPS RPS
Fig. 18.59  Algorithm for Identifying the Need for Left Endocardial
Ablation of Concealed Posteroseptal (PS) Bypass Tracts (BTs). ΔVA,
difference in ventricular-to-atrial conduction time between the His bundle
recording and the earliest site in the coronary sinus. LPS, Left postero-
septal; RPS, right posteroseptal; VA, ventriculoatrial. (From Chiang CE,
Chen S, Tai C, et al. Prediction of successful ablation on concealed
posteroseptal accessory pathways by a novel algorithm using baseline
electrophysiological parameters. Circulation. 1996;93:982–991.)
earliest activation site at or distal to the mid-CS required ablation inside
the CS after a failed left endocardial approach, and 35% of all BTs
ablated from the right side produced such an eccentric retrograde atrial
activation. Therefore the ability of the site of earliest atrial activation
during AVRT to predict the successful ablation approach seems very
limited, mainly because CS-associated BTs can produce a very much
eccentric retrograde atrial activation sequence.74
Careful analysis of CS electrograms recorded by a catheter placed
inside the CS can help distinguish between left and right posteroseptal
BTs. “Atrial” electrograms recorded from inside the proximal CS originate
not only from LA myocardium, but also from activation of the CS
myocardial coat. This results in “fragmented” or double potentials, with
a low-amplitude, blunt “far-field” LA component and a larger, sharp
“near-field” signal from the CS musculature. The sequence of LA and
CS myocardial coat activation at the earliest “atrial” electrograms in
the CS recorded during retrograde BT conduction can guide mapping
of these BTs into right- or left-sided compartments of the posteroseptal
space. An activation wavefront traveling from the posteroseptal RA
toward the left (e.g., by pacing posterior to the CS os) will first activate
the muscle coat covering the proximal CS, producing a large, sharp
signal recorded by the electrodes inside the CS. Discrete connections
of the CS musculature with the LA will activate the LA myocardium,
producing a lower-amplitude, blunt, “far-field” signal on the CS elec-
trodes. Thus two-component “fragmented” or double potentials will
be recorded in the proximal CS, with the sharp component preceding
the blunt signal (sharp/blunt sequence). The same sequence (sharp/
blunt) of potentials is expected to happen when a retrogradely conduct-
ing right-sided “endocardial” BT first activates RA myocardium and
when a BT inserts directly into the CS musculature (as is the case with
epicardial CS-associated BTs). In contrast, when pacing is performed
from the lateral LA, the sequence is the opposite (blunt/sharp), with
CS musculature activation following activation of LA myocardium.
This sequence should be produced if a BT connects to LA myocardium
(i.e., left-sided “endocardial” AV BTs), the first signal recorded in the
CS being a “far-field” potential followed by later activation of the CS
musculature resulting in a blunt/sharp sequence of potentials. Different
conduction velocities of LA myocardium and CS musculature can cause
the sequence of potentials to change farther away from the insertion
site of the BT, explaining the importance of analyzing the electrograms
recorded at the earliest site. The recording of double potentials inside
the CS has been found to be especially common during retrograde
conduction through posteroseptal BTs.74
Generally, a right-sided endocardial approach is initially adopted
for mapping and ablation of BTs in the posteroseptal region. The pos-
teroseptal tricuspid annulus, including the CS os and its most proximal
part, and inferomedial RA are carefully mapped. If the ablation site
fails or no appropriate ablation site can be obtained, the left postero-
septal area is mapped (with a transaortic or transseptal approach, as
described for left-sided BTs). A primary left-sided approach may also
be considered if multiple ECG and EP features suggest a left-sided
location of the BT. If endocardial mapping fails, an epicardial approach
via the CS is then considered (see later discussion).
Ablation of Epicardial Bypass Tracts
Anatomical Considerations
Epicardial BTs can be found at any location, but are most common in
the posteroseptal and left posterior regions. Epicardial BTs account for
4% of left-sided BT ablation cases and 10% of those in patients referred
after a failed ablation attempt.77
Embryologically, the CS develops from the sinus venosus, together
with the smooth part of the RA. As a remnant of sinus venosus mus-
culature, a cuff of striated muscle covers the proximal CS, continuous
with RA myocardium at the CS os. The CS muscle coat extends for 25
to 51 mm from the CS os and may extend for several millimeters over
the necks of the middle cardiac vein and posterior coronary vein.
Although this muscle coat is usually separated from the LA by adipose
tissue, broad and extensive muscular strands frequently bridge this
separation, producing electrical continuity between the CS musculature
and the LA. These myocardial sleeves or cords, however, do not usually
extend into the ventricular myocardium. In variations, an AV BT (referred
to as an “epicardial” BT) is formed by a connection between a sleeve-
like extension of the CS myocardial coat (along the middle cardiac vein,
posterior cardiac vein, or another coronary vein) and the epicardial
surface of the LV myocardium (CS-ventricular BT).78 In some cases,
the muscle creating this connection is found in the neck of a CS diver-
ticulum, usually arising within the proximal 1.5 cm of the CS and before
the middle cardiac vein. The prevalence of CS-associated epicardial BTs
is approximately 22% to 36% among patients with posteroseptal or left
posterior BTs, and is up to 47% among patients with a previous failed
ablation attempt. This highlights the difficulty of localizing these BTs.74
Other types of unusual BTs that cannot be ablated with a standard
endocardial approach at the annulus have been described. These include
 CHAPTER 18  Typical Atrioventricular Bypass Tracts
BTs that connect an atrial appendage to its respective ventricle, which
can be successfully ablated using a transcutaneous pericardial approach
or endocardial ablation over a large area; ablation at the valve annulus
is uniformly unsuccessful in these cases. Another example is BTs closely
associated with the ligament of Marshall, which can be ablated by tar-
geting this ligament.79
Electrocardiographic Considerations
ECG predictors of epicardial posteroseptal BTs include the following:
(1) steep negative delta wave in lead II; (2) steep positive delta wave in
lead aVR; and (3) deep S wave in lead V6. A negative delta wave in lead
II has the highest sensitivity and a positive delta in lead aVR has the
highest specificity for prediction of the presence of epicardial (i.e.,
requiring ablation within the CS and its branches) versus endocardial
posteroseptal BTs.75
Technical Considerations
An epicardial location of the BT is suggested when the earliest site of
endocardial ventricular activation does not precede the onset of the
delta wave, and when a very large BT potential can be easily recorded
on the CS electrodes. During anterograde conduction over a CS-
ventricular BT, endocardial mapping of the RV and LV identifies far-field
activation (unipolar potential has a wide initial R wave), with the earliest
far-field ventricular potential recorded 1 to 3 cm apical to the tricuspid
and mitral annuli. At those sites, the local endocardial ventricular acti-
vation (as indicated by a rapid downstroke on the unfiltered unipolar
electrogram) is recorded late (greater than 15 milliseconds after the
onset of the far-field ventricular potential), reflecting ventricular activa-
tion from epicardium to endocardium.
On the other hand, mapping within the CS during anterograde
conduction over a CS-ventricular BT reveals the earliest ventricular
activation, usually recorded from the branch of the CS containing the
myocardial extension. At this location, the local ventricular activation
is preceded by a high-frequency potential (similar to an anterograde
BT potential) generated by activation of the CS myocardium extending
along the venous branch (CS myocardial extension potential).
During retrograde conduction over a CS-ventricular BT, the CS
muscular coat is activated prior to the LA myocardium, and the high-
frequency component generated by the CS myocardial extension (similar
to a retrograde BT potential) precedes the low-frequency component gen-
erated by activation of the LA. In contrast, with left-sided “endocardial”
BTs, the impulse activates the LA before the CS and the low-frequency,
far-field signal from the LA will precede the sharp CS component.74
Elimination of CS-ventricular BT requires ablation within the coro-
nary venous system. Ablation of these BTs from the endocardial aspect
at the mitral annulus often fails because of the extensive connections
between the CS myocardial coat and the LA and the absence of a clear
endocardial location for the ventricular insertion of the CS-ventricular
BT. Generally, ablation is ineffective when attempted endocardially
targeting the site of earliest anterograde ventricular activation or target-
ing the site of earliest retrograde atrial activation. Of note, endocardial
ablation at the site of earliest retrograde atrial activation often produces
only a shift in the site of earliest atrial activation (mimicking multiple
BTs) because ablation usually results in interruption of one of the mul-
tiple connections of the CS myocardial coat to the atria.74
The CS provides a useful route for mapping and ablation of epicardial
BTs. CS-ventricular BTs are generally ablatable on the floor of the CS at
the orifice of a venous branch or within a CS diverticulum. The middle
(or “posterior interventricular”) cardiac vein is a well-established site for
posterior epicardial BTs, and is useful for approaching AV BTs located
in the inferior pyramidal space. This vein courses with the posterior
descending coronary artery in the posterior interventricular groove
673
and enters the CS close to the RA orifice or, rarely, enters directly into
the RA. At its junction with the CS, the venous entrance is occasion-
ally much dilated, forming a venous diverticulum. CS venography is
typically required to help delineate its anatomy and guide ablation.77,78
The ideal ablation site is located within the branch of the CS con-
taining the CS myocardial extension (coronary vein or neck of a CS
diverticulum), at the site recording the largest, sharpest CS myocardial
extension potential (similar to a BT activation potential) on the unipolar
electrogram recorded from the ablation electrode. Typically, an irrigated-
tip ablation catheter is used to allow more consistent delivery of RF
energy, with less heating at the electrode-tissue interface. Standard RF
energy delivery is often limited because of impedance or temperature
rise (due to limited cooling from surrounding blood flow). Irrigated
RF energy output of 10 to 20 W is initially delivered at sites within the
CS, with the ablation catheter tip directed toward the ventricle within
the CS (by maintaining a gentle counterclockwise torque on the abla-
tion catheter).
Importantly, in some patients, branches of the distal right coronary
artery (posterolateral branch) or left circumflex artery (posterior descend-
ing artery) course between the vein and the ventricle, just below the
CS, adjacent to the ideal ablation site. RF ablation in close proximity
to a coronary artery is associated with a high risk of arterial injury and
should be avoided. Therefore once the ablation catheter is positioned
at the target site, and before RF energy delivery, coronary arteriography
is performed to outline the spatial relationship between the target vein
and the adjacent coronary artery. Although the minimal safe distance
between ablation sites and coronary arteries is not clear, the risk is
highest for distances less than 2 mm and is negligible for distances
more than 5 mm. Coronary arteriography is also performed after abla-
tion to rule out damage to coronary arteries.80
When close proximity of a coronary artery (within 2 to 4 mm)
prohibits RF ablation, cryoablation offers a safe and reasonably effective
alternative (albeit less effective than RF ablation).81 Freezing seems less
likely to damage adjacent coronary arteries. Cryoablation may also be
considered because it is not limited by high impedance and is likely
facilitated by low blood flow. However, the cryocatheter can be difficult
to maneuver in the coronary venous system.80
The coronary venous approach can also be useful for mapping and
ablation of left-sided AV BTs around the mitral valve and those travers-
ing the inferior pyramidal space, the inferior BTs. Nevertheless, BTs
located very close to the hinge of the mitral valve can be difficult to
ablate because the CS is some distance away. Rarely, a transcutaneous
pericardial approach is required to ablate epicardial BTs that are pos-
teroseptal or right-sided. The success of this approach, however, remains
limited, likely due to the anatomy of the AV groove, the thick epicardial
fat layer covering the region where BTs are located, as well as the close
proximity to the epicardial coronary arteries.77,78
Causes of Failed Bypass Tract Ablation
Technical difficulties are the most common cause of failed BT ablation.
These difficulties are typically related to catheter manipulation and
stability (eFig. 18.9) or inability to access the target site. Catheter insta-
bility can lead to poor tissue contact and insufficient tissue heating at
the optimal target site. These challenges are more common with right-
sided BTs because of the smooth atrial aspect of the tricuspid annulus.
Such difficulties can be overcome by using preformed guiding sheaths
to help stabilize the catheter, using different catheter curvatures and
shaft stiffness, changing the approach for ablation (e.g., from transseptal
to transaortic, or from IVC to SVC), or changing the ablation modality.
Also, cryoablation can help achieve better catheter stability and target
sites that might otherwise be avoided because of the risk of damage to
neighboring structures. Large (8-mm) ablation electrodes and cooled
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 673.e1

I
II
III
V1
V6
HRA
Hisprox
Hismid
Hisdist
CSprox

CSdist
RV
Abluni
A
A V V A V V
Abldist

Ablprox
200 msec

eFig. 18.9  Poor Choice of Ablation Sites Because of Unstable Recordings. In the distal ablation bipolar
(Abldist) recording, the atrial and ventricular electrograms have constantly changing amplitudes, signifying
unstable electrode contact with tissue. Ablation should not be performed until the recordings are stable.
Ablprox, Ablation proximal bipolar electrodes; Abluni, ablation distal unipolar electrode; CSdist, distal coronary
sinus; CSprox, proximal coronary sinus; Hisdist, distal His bundle; Hismid, middle His bundle; Hisprox, proximal His
bundle; HRA, high right atrium; RVA, right ventricular apex.
674 CHAPTER 18  Typical Atrioventricular Bypass Tracts
RF ablation can also help generate large RF lesions; however, other
causes of ablation failure should be considered first before shifting to
those approaches, which are only rarely required for BT ablation because
the target tissue (BT) is generally a thin strand, ablation of which should
not require a large amount of tissue damage.
Mapping errors are the second most common cause of ablation
failure. Mapping pitfalls are largely related to inaccurate localization
of a BT that has an oblique course. This is more likely to occur when
retrograde atrial activation mapping is performed with the ablation
catheter positioned at the ventricular side of the annulus; because of
the oblique course of the BT, the site of earliest atrial activation recorded
from the ventricular aspect of the annulus does not correspond to the
ventricular insertion site. Similar situations can occur when the ablation
catheter is positioned on the atrial aspect of the annulus and RF appli-
cations are delivered where the earliest ventricular activation is recorded.
In these situations, mapping for the earliest atrial activation site with
the catheter on the atrial side of the annulus, or mapping for the earliest
ventricular activation site with the catheter on the ventricular side of
the annulus, should be undertaken.
Failure to recognize that a posteroseptal BT is left-sided rather than
right-sided, and epicardial location of a left-sided or a posteroseptal
BT, are other potential causes of failed ablation of those BTs. Detailed
mapping in the CS should be considered in such situations. Furthermore,
some BTs insert in the ventricle at a distance from the annulus, in which
case a search for a presumed BT potential within the ventricle adjacent
to the region of the earliest ventricular activation recorded at the annulus
can be helpful. Unusual BTs (e.g., atriofascicular BTs) and anatomical
abnormality (e.g., congenital heart disease) also account for some failures
in BT ablation.
Failure to recognize the existence of multiple pathways can result
in apparent failure of ablation of the target BT or recurrent tachycar-
dia. Subtle changes in delta wave morphology during ablation of the
target BT can help recognize the presence of more than one manifest
BT. Furthermore, the use of a multielectrode EP catheter around the
mitral annulus (via the CS) or tricuspid annulus (Halo catheter) can
help recognize changes in retrograde atrial activation sequence or local
VA timing during ablation of the target BT, which can be indicative
of the presence of a second BT. In addition, concealed septal or para-
septal BTs can be missed after ablation of a free-wall BT. Programmed
ventricular and HB stimulation is important to avoid tachycardia
recurrence.
Catheter-induced trauma to the BT also can lead to ablation failure
(eFig. 18.10). Mechanical injury to the BT often persists for some time,
leading to discontinuation of the mapping and ablation procedure in
many cases, and the long-term risk for recovery of BT function is high.
Superoparaseptal and atriofascicular BTs exhibit the highest susceptibil-
ity to mechanical trauma, followed by left free-wall BTs. The outcome
can still be improved in these situations by close observation of the
ECG recordings to recognize catheter-induced trauma of a BT promptly
and, whenever conduction block in the BT does not resolve within 1
minute, by immediate application of RF energy, provided that the cath-
eter has not moved from the site of presumed trauma. The location of
the catheter tip when mechanical trauma occurred can be logged on
electroanatomic mapping systems; some of these allow the user to “play
back” where the catheter was seconds before the trauma occurred (if
there is a question as to whether it has moved from that location). In
addition, adenosine (likely due to its hyperpolarizing effects on atrial
and BT tissues) can potentially transiently revive conduction through
the injured BT secondary to mechanical trauma or partially successful
ablation. This can help facilitate intermittent mapping during the tran-
sient adenosine effect.82 Finally, pace mapping the annulus to replicate
the delta wave morphology can help guide ablation.
Outcome
RF ablation is a highly effective and curative treatment for AVRT, with
acute success rates greater than 95%. Acutely successful RF ablation is
usually persistent and late recurrence of BT conduction after ablation
is rare (4%). Short runs of palpitations after ablation are frequent, are
usually caused by isolated or short runs of PACs or PVCs and not by
recurrence of BT conduction, and can be easily managed with symp-
tomatic treatment. When BT-mediated tachycardia does recur, symptoms
are usually observed during the first month after ablation; on the other
hand, later onset of symptoms (more than 3 months after the ablation)
are highly suggestive of SVTs not related to the ablated BT and justify
a thorough evaluation (e.g., event monitoring, long-term ECG moni-
toring, new EP study).
In a survey of 6065 patients, the long-term success rate was 98%
and a repeat procedure was necessary in 2.2% of cases. Serious com-
plications (e.g., cardiac tamponade, AV block, coronary artery injury,
retroperitoneal hemorrhage, stroke) occurred in 0.6% of patients,
with one fatality (0.02%). Thus the one-time risk of catheter abla-
tion appears to be considerably lower than the cumulative annual risk
associated with the WPW syndrome. Hence, catheter ablation remains
the treatment of choice for patients with the WPW syndrome who
may be at risk for life-threatening arrhythmias. In addition, the highly
favorable risk-benefit ratio justifies the use of catheter ablation as first-
line therapy for any patient with BT-dependent tachycardia requiring
treatment.
Success rates and risk of complications vary with different BT loca-
tions. Acute and long-term success rates are highest for left free-wall
BTs. The immediate success rate of transaortic ablation of left free-wall
BTs is 86% to 100% (highest with anterograde BT activation), and the
recurrence rate is 2% to 5%, less frequent than for BTs at other loca-
tions. Complications of this approach include vascular complications
(50% of all complications: groin hematoma, aortic dissection, and
thrombosis), cardiac tamponade, stroke, coronary dissection (from
direct catheter trauma), injury to the left circumflex coronary artery
(from subannular RF application), valvular damage, and systemic embo-
lism (from aortic atherosclerosis, catheter tip coagulum, or ablation
site thrombosis). The transseptal approach, on the other hand, is associ-
ated with a success rate of 85% to 100%, a recurrence rate of 3% to
6.6%, and a complication rate of 0% to 6%. Such complications include
coronary spasm, cardiac tamponade, systemic embolization (0.08%),
and death (0.08%).
As compared with other BT locations, ablation of right free-wall
BT is associated with the lowest acute success rate (88%), and highest
recurrence rate (21%), but a low complication rate. On the other hand,
ablation of posteroseptal BTs is associated with higher success rates (up
to 98%) and a recurrence rate of 12%. For superoparaseptal BT abla-
tion, the reported success rate is up to 97%, with a risk of RBBB in 5%
to 10% of cases. Similarly, ablation of midseptal BTs is associated with
a success rate of 98%, with an incidence of first-degree AV block in 2%
and second-degree AV block in 2%. Although with superoparaseptal
BT ablation RF energy is frequently applied at locations with visible
His potential, the risk of high-grade AV block is higher for ablation of
midseptal BTs because the compact AVN is located in the midseptum.
In contrast to the well-insulated HB, the compact AVN is fragile and
more vulnerable to damage during ablation.62,76
The ablation of epicardial BTs (within the CS) is associated with a
success rate of 62% to 100% and a complication rate of 0% to 6%.
Complications associated with this approach include CS spasm, cardiac
tamponade, pericarditis, and right coronary artery spasm or occlusion.
The overall incidence of coronary artery injury is low (0.1%) and it
can present immediately or several weeks after ablation.83
 CHAPTER 18  Typical Atrioventricular Bypass Tracts 674.e1

eFig. 18.10  Catheter Trauma Leading to Loss of Preexcitation. Red arrow shows sudden absence of
preexcitation with no change in cycle length or premature complexes. The black arrows in the distal ablation
(Abl D) bipolar recording point to a possible bypass tract potential, with conduction interrupted distal to the
bypass tract potential. CS, Coronary sinus; HRA, high right atrium; RVA, right ventricular apex
 CHAPTER 18  Typical Atrioventricular Bypass Tracts
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