Wellens - EKG in AMI and Unstable Angina - 2002

THE ECG IN
ACUTE MYOCARDIAL
INFARCTION AND UNSTABLE
ANGINA
Developments in Cardiovascular Medicine
232. A. Bayés de Luna, F. Furlanello, B.J. Maron and D.P. Zipes (eds.):
Arrhythmias and Sudden Death in Athletes. 2000 ISBN: 0-7923-6337-X
233. J-C. Tardif and M.G. Bourassa (eds): Antioxidants and Cardiovascular Disease.
2000. ISBN: 0-7923-7829-6
234. J. Candell-Riera, J. Castell-Conesa, S. Aguadé Bruiz (eds): Myocardium at
Risk and Viable Myocardium Evaluation by SPET. 2000.ISBN: 0-7923-6724-3
235. M.H. Ellestad and E. Amsterdam (eds): Exercise Testing: New Concepts for the
New Century. 2001. ISBN: 0-7923-7378-2
236. Douglas L. Mann (ed.): The Role of Inflammatory Mediators in the Failing
Heart. 2001 ISBN: 0-7923-7381-2
237. Donald M. Bers (ed.): Excitation-Contraction Coupling and Cardiac
Contractile Force, Second Edition. 2001 ISBN: 0-7923-7157-7
238. Brian D. Hoit, Richard A. Walsh (eds.): Cardiovascular Physiology in the
Genetically Engineered Mouse, Second Edition. 2001 ISBN 0-7923-7536-X
239. Pieter A. Doevendans, A.A.M. Wilde (eds.): Cardiovascular Genetics for Clinicians
2001 ISBN 1-4020-0097-9
240. Stephen M. Factor, Maria A.Lamberti-Abadi, Jacobo Abadi (eds.): Handbook of
Pathology and Pathophysiology of Cardiovascular Disease. 2001
ISBN 0-7923-7542-4
241. Liong Bing Liem, Eugene Downar (eds): Progress in Catheter Ablation. 2001
ISBN 1-4020-0147-9
242. Pieter A. Doevendans, Stefan Kääb (eds): Cardiovascular Genomics: New
Pathophysiological Concepts. 2002 ISBN 1-4020-7022-5
243. Antonio Pacifico (ed.), Philip D. Henry, Gust H. Bardy, Martin Borggrefe,
Francis E. Marchlinski, Andrea Natale, Bruce L. Wilkoff (assoc. eds):
Implantable Defibrillator Therapy: A Clinical Guide. 2002
ISBN 1-4020-7143-4
244. Hein J.J. Wellens, Anton P.M. Gorgels, Pieter A. Doevendans (eds.):
The ECG in Acute Myocardial Infarction and Unstable Angina: Diagnosis and Risk
Stratification. 2002 ISBN 1-4020-7214-7
Previous volumes are still available

THE ECG IN
ACUTE MYOCARDIAL
INFARCTION AND UNSTABLE
ANGINA
Diagnosis and Risk Stratification
by
Hein J.J. Wellens

Anton P.M. Gorgels
Academic Hospital, Maastricht
The Netherlands
and
Pieter A. Doevendans, MD
Interuniversity Cardiology Institute of The Netherlands
Utrecht, The Netherlands
KLUWER ACADEMIC PUBLISHERS

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eBook ISBN: 0-306-48202-9
Print ISBN: 1-4020-7214-7
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CONTENTS
Chapter 1 Introduction 1
Chapter 2 Determining the size of the area at risk, the severity

of ischemia, and identifying the site of occlusion in
the culprit coronary artery 5
A. The ST segment deviation score 9
B. The terminal QRS-ST segment pattern 11
C. Specific ECG patterns indicating the site of
coronary artery occlusion: 13
I Infero-posterior myocardial infarction with
or without right ventricular infarction 13
II Anterior wall myocardial infarction 24
Chapter 3 Conduction disturbances in acute myocardial

infarction 43
A. The sino-atrial region 45
B. The AV nodal conduction system 49
C. The sub-AV nodal conduction system 53
Chapter 4 Myocardial infarction in the presence of abnormal

ventricular activation 65
A. Left bundle branch block 68
B. Paced ventricular rhythm 76
C. Pre-excitation 79
Chapter 5 Arrhythmias in acute myocardial infarction:
Incidence and prognostic significance 85
A. Supraventricular arrhythmias 87
B. Ventricular arrhythmias 91
Chapter 6 The electrocardiographic signs of reperfusion 99
Chapter 7 The electrocardiogram in unstable angina 117

Recognition of multivessel and left main disease
Recognition of critical narrowing of the left anterior
descending coronary artery
Index 127
ERRATA
The ECG in Acute Myocardial Infarction and Unstable Angina: Diagnosis and
Risk Stratification
by: Hein J.J. Wellens, Anton P.M. Gorgels and Pieter A. Doevendans
ISBN: 1-4020-7214-7
The publisher regrets that due to a publishing error, the incorrect series number
appears on the series page and the back cover. The correct series number is
DICM245. The corrected series page appears below.
Kluwer Academic Publishers
Developments in Cardiovascular Medicine

232. A. Bayés de Luna, F. Furlanello, B.J. Maron and D.P. Zipes (eds.):
Arrhythmias and Sudden Death in Athletes. 2000 ISBN: 0-7923-6337-X
233. J-C. Tardif and M.G. Bourassa (eds): Antioxidants and Cardiovascular Disease.
2000. ISBN: 0-7923-7829-6
234. J. Candell-Riera, J. Castell-Conesa, S. Aguadé Bruiz (eds): Myocardium at
Risk and Viable Myocardium Evaluation by SPET. 2000.ISBN: 0-7923-6724-3
235. M.H. Ellestad and E. Amsterdam (eds): Exercise Testing: New Concepts for the
New Century. 2001. ISBN: 0-7923-7378-2
236. Douglas L. Mann (ed.): The Role of Inflammatory Mediators in the Failing
Heart. 2001 ISBN: 0-7923-7381-2
237. Donald M. Bers (ed.): Excitation-Contraction Coupling and Cardiac
Contractile Force, Second Edition. 2001 ISBN: 0-7923-7157-7
238. Brian D. Hoit, Richard A. Walsh (eds.): Cardiovascular Physiology in the
Genetically Engineered Mouse, Second Edition. 2001 ISBN 0-7923-7536-X
239. Pieter A. Doevendans, A.A.M. Wilde (eds.): Cardiovascular Genetics for Clinicians
2001 ISBN 1-4020-0097-9
240. Stephen M. Factor, Maria A.Lamberti-Abadi, Jacobo Abadi (eds.): Handbook of
Pathology and Pathophysiology of Cardiovascular Disease. 2001
ISBN 0-7923-7542-4
241. Liong Bing Liem, Eugene Downar (eds): Progress in Catheter Ablation. 2001
ISBN 1-4020-0147-9
242. Pieter A. Doevendans, Stefan Kääb (eds): Cardiovascular Genomics: New
Pathophysiological Concepts. 2002 ISBN 1-4020-7022-5
243. Daan Kromhout, Alessandro Menotti, Henry Blackburn (eds.): Prevention
of Coronary Heart Disease: Diet, Lifestyle and Risk Factors in the Seven
Countries Study. 2002 ISBN 1-4020-7123-X
244. Antonio Pacifico (ed.), Philip D. Henry, Gust H. Bardy, Martin Borggrefe,
Francis E. Marchlinski, Andrea Natale, Bruce L. Wilkoff (assoc. eds):
Implantable Defibrillator Therapy: A Clinical Guide. 2002
ISBN 1-4020-7143-4
245. Hein J.J. Wellens, Anton P.M. Gorgels, Pieter A. Doevendans (eds.):
The ECG in Acute Myocardial Infarction and Unstable Angina: Diagnosis and Risk
Stratification. 2002 ISBN 1-4020-7214-7
Previous volumes are still available

Authors
Pieter A. Doevendans, M.D.

Associate Professor of Cardiology,
Department of Cardiology
Academic Hospital Maastricht
University of Maastricht, the Netherlands
Anton P. Gorgels, M.D.

Associate Professor of Cardiology
Department of Cardiology
Academic Hospital Maastricht
University of Maastricht, the Netherlands
Hein J.J.Wellens, M.D.

Professor of Cardiology
Medical Director of the Interuniversity Cardiology Institute of the Netherlands
(ICIN)
Utrecht, the Netherlands
Acknowledgements
Over the years the cardiologists, residents, fellows and nursing staff, working at
the Department of Cardiology of the Academic Hospital of Maastricht, have
carefully collected the electrocardiograms published in this book. We are very
much indebted to them for their enthusiasm and willingness to donate those
pearls to us!
To have the electrocardiograms perfectly reproduced we had the good fortune
to have Adrie van den Dool working for us. She and the medical photography
group of the hospital did a perfect job, demonstrating again their ability to
make beautiful illustrations.
Excellent secretarial assistance was provided by Birgit van den Burg, Miriam
Habex, Vivianne Schellings and Willemijn Gagliardi. We greatly appreciated
their pleasant, never complaining way of helping us again and again!
Manja Helmers played an important role in the final phase by expertly
producing the layout of the manuscript.
Hein J.J. Wellens

Anton P.M. Gorgels
Pieter A. Doevendans
Chapter 1
Introduction
INTRODUCTION 3
The electrocardiogram (ECG) remains the most accessible and inexpensive

diagnostic tool to evaluate the patient presenting with symptoms suggestive of
acute myocardial ischemia. It plays a crucial role in decision making about the
aggressiveness of therapy especially in relation to reperfusion therapy, because
such therapy has resulted in a considerable reduction in mortality from acute
myocardial infarction.
Several factors play a role in the amount of myocardial tissue that can be
salvaged by reperfusion therapy, such as the time interval between onset of
coronary occlusion and reperfusion, site and size of the jeopardized area, type
of reperfusion attempt (thrombolytic agent or an intracoronary catheter
intervention), presence or absence of risk factors for thrombolytic agents, etc.
Most important in decision making on reperfusion therapy and the type of
intervention is to look for markers indicating a higher mortality rate from
The ECG is a reliable, inexpensive, non-invasive instrument to obtain that
information. Recently it has become clear that both in anterior and inferior
myocardial infarction, the ECG frequently allows not only to identify the
infarct related coronary artery, but also the site of occlusion in that artery and
therefore the size of the jeopardized area. Obviously, the more proximal the
occlusion, the larger the area at risk and the more aggressive the reperfusion
attempt. The ECG will also give an indication of the size of the jeopardized
area by making an ST segment deviation score and tell us about the severity
and reversibility of cardiac ischemia by analyzing the pattern of the QRS and
the beginning of ST segment elevation.
It will inform us about other factors of importance for the management and
prognosis of the patient such as heart rate, width of the QRS complex, presence
of abnormalities in impulse formation and conduction, and presence or absence
of a prior infarction.
Following reperfusion therapy the ECG can inform us about the result and
help us to select which patient should receive a rescue angioplasty in case of
failure of thrombolytic therapy.
At present, decision making on management of acute myocardial
infarction should be individualized and the purpose of this book is to show that
the ECG is an indispensable tool to reach that goal.
Often the patient with an acute coronary syndrome presents with different
ST-T segment patterns such as ST elevation, ST depression and T wave
inversion. In recent years it has become clear that the ECG at presentation
allows immediate risk stratification across the whole spectrum of acute
coronary syndromes. For example, we learned that the patient with extensive
ST segment depression may have a worse long term prognosis that the patient
with an acute myocardial infarction.
Risk of the patient with acute myocardial ischemia will depend on site and
severity of coronary artery disease. Therefore the identification of the patient
with left main stenosis, severe three vessel disease or proximal narrowing of
the left anterior descending branch is of obvious importance. Again, also under
4 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA
these circumstances the ECG allows us to select those patients who need
invasive diagnostic studies.
Chapter 2
Determining the size of the area at risk, the severity of

ischemia, and identifying the site of occlusion in the culprit
coronary artery
SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION 7
A. ST SEGMENT DEVIATION SCORE
More than 15 mm indicates an area sufficiently large to attempt

reperfusion
B. THE TERMINAL QRS-ST SEGMENT PATTERN
Grade III ischemia indicates poorer short and long term prognosis
C. SPECIFIC ECG PATTERNS: IDENTIFYING THE SITE OF

OCCLUSION IN THE CULPRIT CORONARY ARTERY
I Infero posterior infarction
RCA or CX?
RCA 1. ST elevation in lead III higher than in lead II

2. ST depression in lead I
CX 1. ST elevation in lead II higher than in lead III

2. ST iso-electric or elevated in lead I
3. ST iso-electric or depressed with negative T wave in lead
Proximal (with right ventricular infarction) or distal RCA?
Proximal RCA
ST elevation with positive T wave in lead
Distal RCA
Iso electric ST with positive T wave in lead
Posterior wall involvement?
ST depression in precordial leads

Lateral wall involvement?
ST elevation in leads I, AVL, and
Atrial infarction?
Pta segment elevation in lead II
II Anterior wall infarction
LAD occlusion proximal to first septal and first diagonal branch
Acquired right bundle branch block

ST elevation lead AVR
ST elevation > 2mm in lead
ST depression in leads II, III and AVF
LAD occlusion distal to first septal and proximal to first diagonal

branch
ST depression lead III> Lead II

Q in lead AVL
LAD occlusion distal to first diagonal and proximal to first septal

branch
Signs of occlusion proximal to first septal branch

ST depression in lead AVL
Distal LAD occlusion
Q waves in leads
Absence of ST depression in leads II, III and AVF
In acute myocardial infarction (MI) the surface electrocardiogram (ECG)

allows risk assessment in the individual patient by estimating the size of the
area involved. This will be of help in selecting those patients most likely to
profit from reperfusion of that area. Risk on admission can be assessed from
several variables 1) The total score of ST segment deviation reflecting the
severity of ischemia and global size of the ischemic area (1-3), 2) the heart rate
(3-5), 3) QRS width (3), 4) the terminal QRS-ST segment pattern (6,7), and 5),
by identifying the leads showing ST segment deviation, because they reflect the
site and size of the ischemic process. As will be shown in this chapter the latter
usually allows to identify not only the culprit coronary artery, but also the site
of occlusion in that artery and thereby the area at risk. This is important
because coronary arteries differ as far as the size of the ventricular area that
they perfuse. In general the left anterior descending coronary artery (LAD)
supplies 50% of left ventricular mass and the right coronary artery (RCA) and
circumflex coronary artery (CX) each 25%.
The size of a MI may differ between patients because of individual
variations of the coronary artery system and the site of occlusion in the culprit
vessel (proximal or distal). Also collateral circulation or multivessel ischemia
will influence the extent of the ischemic area. This may sometimes lead to
paradoxical situations: ST segment elevation in the precordial leads can be
caused by RCA occlusion and ST segment elevation in the inferior leads by
LAD occlusion.
To understand the findings on the ECG, it is helpful to look at the pattern
of ST segment elevation and depression in the different leads by applying the
vectorial concept of electrical forces (8).
A. THE ST SEGMENT DEVIATION SCORE
The number of ECG leads showing ST segment deviation (elevation or

depression) and the ST segment deviation score (using the sum of ST segment
deviation in all 12 leads) are markers for the extent of the ischemic area in
acute coronary syndromes (9).
Soon after the introduction of thrombolytic therapy for treatment of acute
MI, it was shown that the greatest reduction in infarct size could be obtained in
patients showing a large ST segment deviation score (1,10,11). The absolute
ST segment deviation score was especially of great value in estimating the
extent of posterior ischemia in patients with infero-posterior infarction (12,13).
Hathaway et al (3) using the information from the GUSTO-I study showed
that the sum of absolute ST segment deviation added major information about
the area at risk and 30 days mortality of acute MI when included in a
nomogram for risk stratification on admission. As shown in table 2-1 also
included in their nomogram were data on systolic blood pressure, heart rate,
QRS duration, age, height, diabetes, Killip class, prior MI and prior coronary
artery bypass grafting.
It is important to know that in the very acute phase of ischemia locally

marked ST segment elevation may occur. With ongoing ischemia the amount
of ST segment deviation stabilizes after 1 to 4 hours which is the time when
usually the first ECG is made (9).
For practical purposes it is useful to accept a 15mm value of ST segment
deviation as a figure indicating a large area at risk. As will be discussed later,
especially in the precordial leads in anterior wall MI there may be a
discrepancy between the area at risk as determined from the ST segment
deviation score and ECG findings indicating the site of occlusion in the culprit
coronary artery.
B) THE TERMINAL QRS-ST SEGMENT PATTERN AND THE

SEVERITY OF CARDIAC ISCHEMIA
As pointed out by Sclarovsky and Birnbaum (6,7) typical patterns of the end of
the QRS complex and ST segment morphology may be of prognostic signifi-
cance in acute myocardial infarction. They divided the ischemic changes after
occlusion of the coronary artery into three grades (figs 2.1 and 2.2). Grade I is
characterized by tall, peaked, symmetrical T waves without ST segment
elevation. Grade II shows ST segment elevation without changes in the
terminal portion of the preceding QRS complex; while in grade III ischemia,
apart from ST segment elevation, changes are present in the last part of the
QRS complex such as an increase in the amplitude of the R wave and
disappearance of the S wave.
These serial ECG changes following acute coronary occlusion are related
to severity and size of the ischemic area. However, decision making on
necessity and type of reperfusion therapy is usually based on the admission
ECG. Sclarovsky and Birnbaum therefore called attention to two important
signs indicating distortion of the terminal portion of the QRS in grade III
ischemia: presence of the junction point more than 50% of the height of the R
wave in leads with a qR configuration, and disappearance of the S wave in
leads expected to have an RS configuration (6,7).
Several studies looked at the prognostic significance of the three grades of
ischemia on presentation (14-17). They indicated that ischemia grading on the
admission ECG correlated with in-hospital mortality, final infarct size, severity
of left ventricular dysfunction and late mortality. Grade III ischemia had the
most ominous prognosis doubling early and late mortality as compared to grade
II ischemia. It was also shown that early reperfusion therapy (within 2 hours
after onset of symptoms) resulted in similar beneficial results in grade II and
grade III ischemia. This was no longer the case when such therapy was applied
later, grade III ischemia patients having a significantly higher in-hospital
mortality (18). This suggests that ischemia grading in relation to time interval
after onset of complaints can also give an indication of the reversibility of
cardiac ischemia. The same authors also showed a higher incidence of
complications in grade III patients during hospital admission such as high
degree AV block and reinfarction (19). These date suggest that an early
primary percutaneous coronary intervention should be considered in patients
presenting with grade III ischemia.
Birnbaum and Sclarovsky discussed why patients with grade III ischemia
on the admission ECG have worse short and long term prognosis and less
benefit from reperfusion therapy (7). They came to the conclusion that the
difference in infarct size between grade II and Grade III ischemia patients is
probably due to faster progression of necrosis in grade III ischemia possibly
related to thickness of the ventricular wall, lack of collaterals and lack of
protection by ischemic preconditioning (7).
C. SPECIFIC ECG PATTERNS: IDENTIFYING THE SITE OF

OCCLUSION IN THE CULPRIT CORONARY ARTERY
In cardiac ischemia the direction and displacement of the ST segment is

determined by the sum of direction and magnitude of all ST vectors at that
point in time. The resulting main vector will point in the direction of the most
pronounced ischemia. This results in ST elevation in that area. The opposite
area will record (reciprocal) ST segment depression. Although no ischemia
may be present in that area, this is not excluded by the reciprocal changes. The
lead perpendicular to the dominant vector will record an iso-electrical ST
segment (6). This vectorial concept is particularly useful when analyzing the
frontal plane leads. In the horizontal plane the electrodes may be so close to the
myocardium that the local vector overrules the far field electrical forces.
Infarction patterns are usually classified as inferoposterior and anterior. It
will be shown that additional information from the ECG allows the recognition
of the culprit coronary artery and frequently the location of the occlusion in
that artery.
I Infero-posterior wall infarction

Infero-posterior wall infarction is either caused by the occlusion of the RCA or
the CX and is characterized by ST segment elevation in leads II, III and AVF.
Discriminating ECG features between these two coronary arteries are based
upon the specific anatomic location of these vessels.
Coronary patho-anatomy
The perfusion areas of the RCA (1) and the CX are depicted in figure 2.3. The
RCA originates from the right aortic sinus. It passes down the right
atrioventricular groove towards the crux, where it crosses the interventricular
septum and continues to the postero(lateral) area of the left ventricle. The
following side branches are of importance: 2) The conus branch. This branch
may provide blood flow to the basal part of the interventricular septum in case
of a proximal LAD occlusion(20). 3) The sinoatrial branch. This vessel
originates in 60% from the RCA, and in about 40% from the CX (11 in fig. 2.3)
and rarely from both arteries. Involvement of this vessel may lead to sinus node
ischemia with sinus bradycardia, sino-atrial block and atrial infarction and may
favor the occurrence of atrial fibrillation. 4) The right ventricular branch, which
perfuses the anterolateral part of the right ventricle. The RCA before the right
ventricular branch is called the proximal, thereafter the distal RCA. Occlusion
of the proximal RCA leads to right ventricular (RV) infarction, with diminished
function of the RV, possibly leading to underfilling of the LV with hypotension
and cardiogenic shock. In proximal RCA occlusion there is also a high
incidence of high degree AV nodal conduction disturbances (see chapter 3) 5)
The distal RCA has the acute marginal branch perfusing the posterior area of
the RV. 6) The posterior descending branch which brings blood to the
inferobasal septum and the posteromedial papillary muscle. Obstruction of flow
leads to septal involvement, and possibly papillary muscle dysfunction and
mitral regurgitation. It may also result in block or conduction delay in the
posterior fascicle of the left bundle branch, especially when also the proximal
LAD is narrowed or occluded. 7) The branch to the AV node. 8) The
posterolateral branch(es). In case of a dominant RCA, occlusion may result in
posterior wall infarction, and even left lateral involvement. The CX originates
from the main stem of the left coronary artery (9) and runs through the left
atrioventricular groove. The CX usually gives one to three large obtuse
marginal branches (12) supplying the free wall of the LV from superior to
inferior along the lateral border. In case of a dominant CX one or more medial
posterobasal branches may arise from this vessel (13 in fig. 2.3).
Dominance
The RCA is dominant in about 70% of cases, passing the interventricular
septum, giving rise to posterolateral branches. In 30% of patients no RCA
dominance is present, the CX being dominant in about half of them. In those
cases the CX is large and continues down to the diafragmatic surface of the
LV, where it gives rise to the posterolateral branches, reaching the crux, ending
in the posterior descending branch with a branch to the AV node. It is very
important to recognize which vessel is dominant because this identifies patients
at risk for extensive myocardial damage with complications of heart failure,
ventricular arrhythmias and death.
RCA or CX occlusion in acute inferior wall myocardial infarction?

Because of the different anatomic structures perfused and the resulting clinical
consequences in case of ischemia and necrosis, it is important to identify the
culprit coronary artery in infero posterior wall infarction. As pointed out
before, both vessels perfuse the inferior part of the left ventricle, but the RCA
more specifically the medial part including the inferior septum, whereas the CX
perfuses the left postero basal and lateral area. This results in a ST segment
vector directed inferior and rightward in case of a RCA occlusion versus an
inferior and leftward vector in CX occlusion (figure 2.4). In RCA occlusion the
ST vector will therefore result in more ST elevation in III than in II leading to
ST depression in lead I. In case of CX occlusion the vector will point towards
lead II, leading to ST elevation or an isoelectric ST segment in lead I. When the
vector points towards AW, the ST vector is perpendicular to lead I, resulting
in an iso-electric ST segment in lead I. In our experience ST segment

depression in lead I is predictive for RCA occlusion in 86%, and an iso-electric
or positive ST segment for CX occlusion in 77%. Differences in dominance
lead to absence of a 100% positive predictive accuracy.
Figure 2.5, left, shows an example of an acute inferior wall infarction due
to RCA occlusion. Marked ST elevation is present in the inferior leads. Lead
III shows the most pronounced elevation, being higher than in II, resulting in a
depressed ST segment in lead I. Note that also the ST segment in lead AVL is
negative. A greater ST segment depression in lead AVL than in lead I has also
been found to be highly predictive for RCA occlusion (21). The least negative
ST segment is found in lead AVR, indicating an almost perpendicular
orientation of the ST vector in that lead. ST segment elevation in lead AVR in
the setting of inferior wall infarction is rare and suggests in our experience
additional proximal left coronary artery disease, or a dominant posterior
descending branch perfusing large parts of the septum. Figure 2.5, right, shows
inferior wall infarction due to a CX occlusion. Most ST elevation is seen in
lead II, resulting in a positive ST segment in lead I. The ST segment in AVR is
iso-electric indicating that the ST vector is perpendicular to that lead. This
results in a markedly negative ST segment in lead AVL.
Posterior wall involvement

Posterior wall involvement is diagnosed by finding reciprocal ST segment
depression in the precordial leads. When present in RCA occlusion, it indicates
dominance of this vessel.
In case of CX occlusion posterior wall involvement is almost obligatory.
Absence of precordial ST depression in inferior wall infarction is therefore
strongly suggestive of RCA involvement (22). In figure 2.5, left, an example is
given of posterior wall involvement in RCA occlusion. ST depression is
present in leads to with deepest negativity in lead In figure 2.5, right,
a CX occlusion is shown with ST depression in leads to
Recent data indicate that larger infarctions, more postinfarction
complications and a higher mortality rate occur in patients with precordial ST-
depression (20-22). As pointed out by Birnbaum et al (23) when the greatest
amount of ST depression is seen in leads 3-vessel disease and a low left
ventricular ejection fraction should be suspected.
Isolated ST depression in the precordial leads may present the difficulty to
differentiate acute CX occlusion, resulting in true posterior wall infarction,
from nonocclusive anterior myocardial ischemia. It has been suggested that in
that situation maximal ST depression in or is predictive for acute CX
occlusion (24-26). Also the recording of qR complexes with ST segment
elevation in leads has been recommended to diagnose a CX occlusion
(27,28).
Lateral wall involvement

Lateral wall involvement is reflected by ST segment elevation in leads and
It can be seen in both RCA or CX occlusion, but occurs more frequently in
the latter. Independent of the vessel involved, ST segment elevation in these
leads implies a larger ischemic area and the need for aggressive reperfusion
therapy (29).
Figure 2.6 shows an inferior wall infarction due to RCA occlusion as
assessed by the typical changes in the extremity leads and the absence of ST
depression in the precordials. ST elevation in and indicates lateral
involvement and therefore the presence of a dominant RCA.
Figure 2.7 shows an example of a CX occlusion: there is only minor ST
elevation in the inferior leads, with most ST elevation in lead I, suggesting a
non dominant CX. The vector in the frontal plane suggests a more high lateral
localization of the ischemia, consistent with a not very large obtuse marginal
branch. Most ischemia is found in the left posterior wall, due to a prominent
posterolateral branch.
RV infarction
In RCA occlusion the presence of RV involvement is important because it
identifies a subgroup of patients at high risk (30-42). Clinically the patient may
present with hypotension, frequently combined with bradycardia, due to sinus
bradycardia or high degree AV nodal block. AV-nodal conduction disturbances
and late VT are more frequently encountered in inferior wall MI with RV
involvement. As also discussed in chapter 3, patients with AV nodal
conduction disturbances have a higher mortality than patients without AV
nodal conduction disturbances, also in the thrombolytic era (30-33).
Diagnosing RV-involvement in inferior wall infarction is difficult from the
standard 12 lead ECG. The reason being that precordial leads overlying the RV
frequently record ST depression due to reciprocal ST segment changes
of ischemia of the posterior wall.
Therefore it is necessary to record the right precordial leads. Figure 2.6

(right panel) shows ST elevation in the right precordial leads to
has been found to be especially useful for diagnosing right ventricular
involvement. ST-elevation of predicts an occlusion proximal to the
RV-branch with an accuracy of 90% and ST-segment depression an
occlusion of the CX (fig. 2.8) with an accuracy of 100% (43). An isoelectric
ST-segment predicts distal RCA occlusion (fig. 2.9). It is important to stress
that sufficient ST-segment elevation in the inferior leads of the standard ECG
(at least 2mm) is needed to use the right precordial leads for determining the
site of coronary artery occlusion.
In a minority of cases of RV involvement the precordial lead shows ST-

elevation. The sensitivity of ST elevation in lead is 24% but the specificity
100%. Figure 2.10 shows an acute inferior wall infarction due to RCA
occlusion. In lead the ST segment is elevated, indicating RV involvement.
Even less frequent than ST elevation in only, as the result of RV
involvement, is the finding of more leftward precordial leads with ST
elevation. An example is shown in figure 2.11. The extremity leads indicate
inferior wall infarction due to RCA occlusion. The precordial leads to
display ST elevation, most prominent in consistent with RV involvement.
Lack of posterior wall ischemia leads to these findings because of ischemia of
the relatively thin RV anterior wall. This is confirmed by the positive right
precordial leads (right panel).
Isolated RV infarction
Rarely the ECG shows only minor or no changes in the inferior leads and ST
elevation is only seen in leads and in the right precordial area. An
example is given in figure 2.12. This picture reflects a predominant RV
infarction and is related to a non dominant RCA, a collaterally filled RCA or an
isolated occlusion of a RV branch (44). It may also be seen after occlusion of
the RV branch following PTCA or stenting of the right coronary artery (45).
Atrial infarction
Atrial infarction may occur when a RCA or CX occlusion is proximal to the
sinoatrial branch. An example is given in figure 2.6. It shows slight elevation of
the baseline following the P wave, best seen in lead II. This Pta segment
elevation reflects the repolarization phase of the P wave. The presence of atrial
infarction not only identifies a proximal RCA or CX occlusion, but is
frequently accompanied by sinus node dysfunction, sino-atrial conduction
disturbances and episodes of atrial fibrillation.
AV nodal block
AV nodal block is common in inferior wall infarction, especially in case of a
proximal RCA occlusion. ECG features, prognostic significance and
management are discussed in chapter 3.
Difficulties in diagnosing CX occlusion

One of the pitfalls in diagnosing acute MI is the underestimation of the area
involved in CX infarction. This is due to several causes: 1) The left ventricular
area supplied by the CX is activated in the second half of the QRS complex and
therefore both abnormalities in activation and repolarization may be obscured
by preceding and ongoing activation and repolarization of other areas of the
heart. 2) Posterior wall ischemia may only become manifest by ST segment
depression and therefore unstable angina rather than MI is diagnosed. In that
setting it has been suggested that presence of maximal ST depression in leads
or is predictive for acute CX occlusion (24-26). Also the use of
additional leads has been recommended (27,28). A finding in CX
occlusion can be delayed activation of the posterolateral wall. This can be
recognized as a late positive deflection in lead I, and a late negative deflection
in leads III and AVF indicating that the terminal activation vector points to the
left baso lateral area (fig. 2.5, right).
A clue pointing to an extensive CX infarction is shown in figure 2.13. It
shows an inferior wall infarction with an iso-electric ST segment in lead I,
consistent with a CX occlusion. The left and right precordial leads are in
accordance with that diagnosis.
Suggestive of CX dominance is the clearly prolonged PR interval,
indicating AV nodal involvement.
II Anterior wall infarction

The left anterior descending branch (LAD) is usually the largest coronary
artery and supplies the anterior, lateral, septal and in 70% of humans the infero-
apical segment of the left ventricle (figure 2.14). It also perfuses the bundle of
His and the proximal part of the bundle branches. The size of the ischemic area
and the prognosis is dependent on the site of occlusion in the LAD. Depending
upon the site of LAD occlusion, apart from ST segment elevation in the
precordial leads, specific changes will occur in the extremity and lateral leads.
Involvement of the distal AV conduction system leads to impaired conduction,

varying from intra hissal block to right bundle branch block (RBBB) with or
without left fascicular block, to complete sub AV nodal block (46). The clinical
picture may include heart failure and in the subacute phase ventricular
tachycardia and fibrillation may occur, leading to increased in-hospital and one
year mortality (47,48).
Anterior wall infarction is diagnosed by the presence of ST elevation in the
precordial leads to The challenge in anterior wall infarction is to
recognize the size of the area at risk and the site of the occlusion in the LAD.
This information can be obtained by observing additional changes in the other
precordial and extremity leads.
The ST segment vector to localize the site of ischemia

The anteroseptal area of the left ventricle which is perfused by the LAD can be
divided into 3 main parts: 1) The basoseptal part, supplied by the first septal
branch(es), 2) The lateral basal part, perfused by the first diagonal branch(es),
or intermediate branch, 3) The inferoapical part, receiving blood from the distal
LAD, frequently wrapped around the apex (figure 2.14, left panel).
As shown in a recent study by Engelen et al (49) occlusions at different sites

(figure 2.14, right panel) lead to 4 electrocardiographically different pictures:
1. Proximal of the septal and diagonal branches. This results in ischemia of all
3 named areas. 2. Distal of the first septal and diagonal branches. This leads to
ischemia of the inferoapical area only. 3. Occlusion before the first diagonal
but distal of the first septal branch. This leads to ischemia of the baso lateral
wall and the infero apical wall but not the basal septum. 4. Proximal before the
first septal but distal of the first diagonal branch. This leads to ischemia of the
septum and the inferoapical area, whereas the basolateral area remains free. In
the study by Engelen et al (49) the incidence of these sites of occlusion in the
LAD territory were as follows: 40%, 40%, 10% and 10% respectively.
Obviously, risk varies with these different sites of occlusion.
LAD occlusion proximal to the first septal and the first diagonal branch.
High risk!
Typically the ECG shows one or more of the following findings. Acquired
right bundle branch block, ST elevation in AVR, ST elevation of more than
2mm in lead and ST depression in the inferior leads and in lead (42-44).
An example is given in fig. 2.15. Figure 2.16 depicts the likely mechanism of
these findings: Global involvement of the left ventricle with contribution to the
ECG from all ischemic areas. Because of the larger mass of the basal part the
vector of the ST segment will point in the superior direction (figure 2.16, left
panel). In the frontal plane this results in ST elevation in leads AVR and AVL
as the consequence of basal septal and lateral ischemia (figure 2.16, right
panel). The more cranially positioned lead will also record ST elevation.
This upward orientation of the ST vector causes reciprocal ST depression in the
inferior leads (50) and also sometimes in the lateral leads Frequently
the ST vector points not only upward but somewhat more to the left than to the
right. This results in more ST elevation in AVL than in AVR, and more ST
depression in lead III than in lead II. Local conduction delay in the lateral leads
may lead to widening of the Q wave in lead AVL.
Statistical values of criteria to identify a proximal occlusion are listed in table
2.2.
Distal LAD occlusion. Low risk.

Figure 2.17 shows an example of an acute anterior wall infarction due to a
distal LAD occlusion (behind the major proximal septal and diagonal
branches). Typical findings are the presence of Q waves in leads and
and the absence of ST depression in the inferior leads (53,54).
In this situation there is ischemia in the infero-apical part therefore the ST
vector will point inferiorly (figure 2.18 left panel).
The ST segment in the inferior leads will become isoelectric or even
positive (figure 2.18, right panel). The Q waves in the left precordial leads are
likely due to the combination of local conduction delay in that area combined
with persistence of the regular septal q wave in these leads.
LAD occlusion distal to the first septal branch, but proximal to the first
diagonal branch. Intermediate risk.
Figure 2.19 shows the ECG of an acute anterior wall infarction with an
occlusion site distal to the first septal, but proximal to the first diagonal branch.
Typical features are: ST elevation in lead AVL and the left lateral leads and ST
depression in lead III which is more pronounced than in lead II. Figure 2.20
shows a diagram with the distribution of ischemia in that situation, leading to
the ST segment vector pointing in a left lateral direction (left panel). Because
of that direction of the ST segment vector the difference in ST depression
between leads III and II is now much more pronounced than in the LAD
occlusion proximal to both the first septal and the first diagonal (fig. 2.15).
LAD occlusion distal to the first diagonal branch but proximal to the first
septal branch. Intermediate risk
In this situation, the baso-lateral area is not involved, because the occlusion site
is distal to the first diagonal or intermediate branch (fig. 2.21). Signs of an
occlusion proximal to the first septal branch are present such as ST elevation in
AVR and >2mm in with ST depression in In this situation the right
precordial lead has also been described to show ST elevation (55).
However, lead AVL now shows ST depression and the inferior leads positive
ST segments.
Figure 2.22 shows a diagrammatic presentation to explain the findings.
The left panel shows the rightward orientation of the ST segment vector,
leading (right panel) to most negativity of the ST segment in AVL and most
positivity in lead III, whereas leads AVR and II are less positive, or isoelectric.
Negativity in lead AVL is highly specific for an occlusion site below the first
diagonal branch (table 2.2).
Criteria to identify the site of occlusion in anterior wall infarction

Table 2.2 lists the criteria to identify the site of occlusion in anterior wall
infarction. They are especially useful in patients presenting with a first acute
anterior infarction. In contrast to sensitivity, the specificity of these criteria is
high, indicating that their presence accurately predicts the occlusion site, but
that a specific site is not excluded by their absence.
Right bundle branch block remains, as described in chapter 3, a very
specific marker of an occlusion before the first septal branch. ST elevation in
has to be more than 2mm to be sufficiently specific for that location. ST
elevation in AVR is apart from being specific the most sensitive marker for
proximal LAD occlusion. ST depression in is not a very frequent, but
specific marker.
Lead AVL is the most useful lead to identify an occlusion site proximal
(starting with a Q wave) or distal (showing a negative ST segment) to the first
diagonal branch.
Left main occlusion

Figures 2.23 and 2.24 show the tracings of patients with a left main occlusion.
Apart from acquired right bundle branch block and other features of an
occlusion proximal to the first septal branch the ECG also shows signs of
severe posterobasal ischemia. This combination is very suggestive for severe
ischemia caused by an occlusion proximal to the take off of the LAD and the
CX. Recently Yamaji et al (56) reported that left main occlusion should be
suspected when ST segment elevation in AVR is higher than ST segment
elevation in lead
ST deviation score and location of the coronary artery occlusion

In our experience there is an acceptable correlation between the ST segment
deviation score and the location of the occlusion in the culprit coronary artery
(fig. 2.25). There are exceptions however (fig. 2.26), especially in anterior wall
infarction where the precordial leads reflect a more local than global area of
ischemia of the left ventricle.
A new infarction in the presence of an old one

Obviously, the occurrence of a new infarction in a coronary vessel territory
different from the previous one places the patient in a high risk category
because of pre-existent myocardial tissue loss from the old infarction. Such a
situation should be recognized on the ECG and an indication for aggressive
reperfusion therapy. An example is given in figure 2.27.
Limitations
Although the ECG has proven to be very useful to determine the extent and
severity of ischemia and the site of the occlusion in the culprit artery, it may be
limited in the individual patient by factors such as: A location in the CX area,
the presence of old infarction(s), left ventricular hypertrophy, altered activation
as in left bundle branch block, preexcitation or a ventricular paced rhythm (see
chapter 5), preexisting ST-T abnormalities, ischemia at a distance because of
occlusion of a coronary artery which was also supplying the territory of another
coronary artery by collateral circulation, dominance or underdevelopment of
coronary arteries and a congenital abnormal site of origin of coronary arteries.
Conclusion
Anyone involved in decision making in the patient with acute cardiac ischemia
should be familiar with the electrocardiographic signs that indicate the severity
and size of the area at risk. This includes knowledge and understanding of the
importance of the ST segment deviation score; ischemia grading based upon
the behaviour of the terminal portion of the QRS and the beginning of ST
elevation; and the ECG signs that indicate which coronary artery is occluded
and where the occlusion is located.
Such knowledge is essential for optimal decision making in relation to the
use and the type of reperfusion therapy.
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Chapter 3
Conduction disturbances in acute myocardial infarction

Sinus arrest and sino-atrial block
Low incidence
Infero-posterior infarction with proximal occlusion of RCA or CX
Therapy other than reperfusion dictated by hemodynamic and/or
arrhythmic consequences
AV nodal conduction disturbances
Common in proximal RCA occlusion

Worsens prognosis, stressing necessity of aggressive reperfusion
therapy
Temporary pacing in case of pump failure, cardiogenic shock or
frequent ventricular ectopic activity. Permanent pacing rarely needed
Sub-AV nodal conduction disturbances
Differentiate between pre-existent and acquired bundle branch block

Acquired bundle branch block indicates proximal LAD occlusion
Acquired bundle branch block worsens prognosis indicating aggressive
reperfusion therapy
Temporary pacing in case of advanced intra Hissal or sub Hissal block
Permanent pacing rarely needed
CONDUCTION DISTURBANCES IN ACUTE MYOCARDIAL INFARCTION 45
A. THE SINO-ATRIAL REGION
Blood supply of the sinus node and the atrio-ventricular conduction system
In discussing abnormalities in sinus node behavior, sino-atrial conduction and

atrio-ventricular conduction during acute cardiac ischemia, it is essential to
know by which coronary artery these structures receive their blood supply.
Sinus node and sino-atrial region

The sinus node and the sino-atrial region are in 55% of cases perfused by an
atrial branch from the proximal part of the right coronary artery (RCA) and in
45% of cases by a proximal branch of the circumflex (CX) coronary artery (1).
Therefore, a proximal occlusion of the RCA or CX may lead to ischemia of the
sinus node and the surrounding atrium.
The atrio-ventricular (AV) conduction system

As shown in figure 3.1 the RCA perfuses the AV node and the proximal part of
the bundle of His. The distal part of the His bundle, the right bundle branch and
the anterior fascicle of the left bundle branch are supplied by the septal
branches of the left anterior descending (LAD) coronary artery. The posterior
fascicle of the left bundle branch is perfused both by the septal branches of the
LAD and by the RCA (1).
This means that AV nodal conduction disturbances in acute myocardial

infarction point to a RCA occlusion and sub AV nodal conduction
abnormalities are found in case of impaired perfusion of the upper part of the
interventricular septum caused by an LAD occlusion proximal to the first septal
branch.
Slow rhythms and conduction abnormalities at the sinus nodal and sino-
atrial level
ECG findings
Sinus bradycardia
This is defined as the presence of sinus P waves at a rate of less than 60 beats
per minute (figure 3.2).
Sino atrial block and sinus arrest

Sino-atrial (SA) conduction abnormalities can become manifest as second
degree (SA Wenckebach, SA Mobitz-2 block, 2 to 1 block) or complete sino-
atrial block. In the absence of electrogram recordings from the sinus node
itself, it is impossible to know in case of a sinus bradycardia or absence of
sinus P waves whether abnormalities in impulse formation, impulse conduction
or both are responsible.
Figure 3.3 is an example of second degree sino-atrial block of the Mobitz-
2 type. Figure 3.4 shows complete absence of P waves either because of
complete sino-atrial block or absence of impulse formation in the sinus node.
Incidence, mechanisms and prognostic significance

In 1976 Liem et al. (2) published an incidence of sinus bradycardia of 12,5% in
800 consecutive patients with an acute myocardial infarction. It was three times
more common in infero-posterior than in anterior wall myocardial infarction.
They showed that patients with sinus bradycardia had a better prognosis as to
mortality and infarct size than patients without sinus bradycardia.
As indicated in table 1 different mechanisms have been suggested as cause

for sinus bradycardia (1,3,4). Especially, in the early stage of myocardial
infarction slow or absent sinus rhythm seems to be caused by activation of the
parasympathetic nervous system because of pain, anxiety and the Bezold-
Jarisch reflex. In our experience a slow or absent sinus rhythm is much more
common in proximal than in distal RCA occlusion. Emergence at a later stage
of sinus bradycardia and SA block suggests perfusion abnormalities of the
sino-atrial area. The ECG finding of atrial infarction supports ischemia as the
cause. The effect of atropine can be of help to distinguish between a vagal and
an ischemic cause. In the first situation sinus bradycardia or sinus arrest will
disappear. This is not the case when ischemia is responsible for the slow or
absent sinus rhythm. Unfortunately, no information is available on the
incidence of sino-atrial conduction abnormalities in acute infero-posterior
infarction, nor do we have knowledge about their prognostic significance, for
example in relation to the development of the sick sinus syndrome later.
Management
Abnormalities in impulse formation and conduction in the sinus node region
result in slow heart rates and may thereby lead to a lower cardiac output,
increased occurrence of atrial fibrillation and (because of a slow heart rate) to

increased ventricular ectopy.
Differentiation between a vagal and non-vagal origin should be attempted.
Reperfusion of the culprit coronary artery is certainly indicated when ECG
signs are present of atrial infarction or advanced sino-atrial block because they
indicate proximal RCA occlusion with right ventricular involvement or a
proximal CX occlusion.
In general, sinus bradycardia, because it is vagally induced, indicates a
smaller infarction with a good short and long-term prognosis. Atropine
administration or cardiac pacing is seldom indicated.
B. THE AV-NODAL CONDUCTION SYSTEM
Conduction abnormalities at the atrio-ventricular nodal level
ECG findings
In infero-posterior infarction conduction abnormalities in the AV node are most
commonly seen in case of an occlusion of the RCA proximal to the right
ventricular branch leading to a right ventricular infarction as well (see chapter
2). Conduction disturbances in the AV node may become manifest on the ECG
as: 1) a prolonged PR interval of more than 200 msec, 2) second degree AV
block (of the Wenckebach type, or 2 to 1 block) and 3) complete AV nodal
block. Examples of a Wenckebach, a 2 to 1 and a complete AV nodal block are
given in figures 3.5, 3.6 and 3.7. In all 3 examples a proximal RCA occlusion
was responsible and right ventricular involvement was present (lead not
shown in figures 3.5 and 3.6). All three cases show atrial infarction (as
manifested by a PTa shift after the P wave).
Typically for AV nodal Wenckebach and 2 to 1 AV nodal block is the

markedly prolonged PR interval of the conducted P wave. This is in contrast to
Wenckebach conduction or 2 to 1 conduction in the sub AV nodal conduction
system where smaller PR increments are seen during the Wenckebach sequence
and less PR prolongation of the conducted P wave. In fact, in 2 to 1 block sub
AV nodally the PR interval of the conducted beat is often not prolonged.
Left bundle branch block in inferior wall myocardial infarction

In 1974, Lie et al. (5) noted that in patients with inferior wall infarction and
high degree AV nodal block a bundle branch block pattern was present in beats
terminating a long RR interval. However, in contrast to the right bundle branch
block (RBBB) shaped beats terminating a long RR interval, the LBBB shaped
ones had a His potential in front of the QRS and represented conducted beats or
AV junctional escape beats with phase 4 (bradycardia dependent) block in the
left bundle branch. A typical example is shown in figure 3.8. Therefore, LBBB
shaped beats occurring after a critical RR interval in patients with high degree
AV nodal block in acute inferior infarction do not indicate infra AV nodal
block, meaning absence of an indication for implantation of a permanent
pacemaker!
Incidence, mechanism and prognostic significance

In the prethrombolytic era, Tans et al. (6) found that 144 out of 843 patients (17
%) with an infero-posterior infarction had advanced AV nodal block defined as
second degree AV nodal block or worse. More recently, in the era of
reperfusion, the incidence is similar, varying between 12 and 20% (7,8). Also
as pointed out by Simons et al. (9) the incidence of third degree AV nodal
block remained similar in the thrombolytic era (around 10%). Increased vagal
stimulation because of pain, anxiety and the Bezold Jarisch reflex, and
ischemia of the AV node have been suggested as mechanisms for AV nodal

block. As with sinus bradycardia and sino-atrial block, the distinction between
these two mechanisms can be made by giving atropine. Vagally induced AV
nodal block will disappear and ischemic AV nodal block will persist. Also the
ECG can give a clue as to the most likely mechanism. For example in figure
3.6 during 2 to 1 AV nodal block the ECG shows a sinus rate of 150 beats per
minute, clearly indicating absence of vagal dominance.
AV nodal block is common in case of a proximal RCA occlusion. As
shown by Braat et al. (10), approximately 45% of these patients have advanced
AV nodal block during the acute phase of myocardial infarction. A proximal
RCA occlusion means a larger inferior infarct, with right ventricular
involvement. It is not surprising therefore that AV nodal block is accompanied
by a 2,5 times higher in hospital mortality rate also in the thrombolytic era.
AV nodal block in inferior wall myocardial infarction is typically transient
disappearing after a few days. It may last up to 16 days, as shown by Barold
(11) in a careful analysis of 20 studies of patients with second and third degree
AV nodal block after inferior wall myocardial infarction.
Management
The occurrence of high degree AV nodal block in inferior wall infarction
usually means a proximal RCA occlusion and a large infero-posterior infarct
with right ventricular involvement. This stresses the necessity of early
reperfusion of the occluded RCA. This is frequently followed by a return of
normal AV nodal conduction when reperfusion is accomplished (12), which is
in fact an electrocardiographic marker of reperfusion. Temporary ventricular or
dual chamber pacing is indicated when pump failure, cardiogenic shock or
frequent ventricular ectopic activity accompany high degree AV nodal block in
inferior wall MI. Results of pacing can be disappointing because outcome is
primarily determined by the size of the myocardial infarction and the
associated hemodynamic status. The necessity of permanent pacing in AV
nodal block after inferior MI is very rare (11). In fact only when persistent
symptomatic second or third degree AV nodal block is present more than 2
weeks after inferior MI.
C. CONDUCTION ABNORMALITIES AT THE SUB-AV NODAL

LEVEL
ECG findings
As previously indicated, the bundle of His and the proximal and distal parts of
the bundle branches are perfused by the septal branches from the LAD. The
posterior fascicle of the left bundle branch is frequently also supplied by the
posterior descending coronary artery (which may come from the RCA or CX).
Conduction disturbances in the His bundle and the bundle branch system
occurring in the setting of anterior wall infarction indicate a very proximal
occlusion in the LAD. Figures 3.9 and 3.10 are examples of 2 to 1 and
Mobitz-2 intrahissal block in a proximal LAD occlusion. The presence of

conduction disturbances in or below His means that a large area of the left
ventricle is in jeopardy. Essential in using bundle branch block (BBB) in acute
myocardial infarction as a marker of a large area at risk and the likelihood of a
poor prognosis is to know the duration of BBB. Was BBB present before
myocardial infarction (pre-existent BBB) or is it the consequence (acquired
BBB) of impaired blood supply to the conduction system because of an LAD
occlusion proximal to the first septal branch? Twenty five years ago, Lie et al.
(13) showed that when RBBB was present before infarction and patients were
matched for age and sex, hospital mortality was not different from patients
without RBBB. This was totally different in patients developing bundle branch
block in the setting of their acute myocardial infarction. Acquired BBB is
typically seen in anteroseptal myocardial infarction with right (R) BBB with or
without left fascicular block (figure 3.11). This is much more common than
acquired complete left (L) BBB and has a more ominous prognosis (13).
Occasionally acquired bundle branch block in anterior wall infarction may

occur in the left anterior fascicle only (figure 3.12). Marked left axis deviation
with increased QRS duration in acute anterior wall myocardial infarction
should make one suspicious of a proximal LAD occlusion.
The ECG is helpful in distinguishing between acquired and pre-existent

RBBB. As shown in figure 3.13 and table 3.2 acquired RBBB is characterized
by a QR complex, while pre-existent RBBB shows an RsR1 configuration in
lead Preexistent RBBB is more commonly found in the elderly patient.
When RBBB develops in acute anterior MI it occurs suddenly (figure
3.14) and it may or may not be accompanied by a conduction disturbance in
one of the fascicles of the left bundle branch (figure 3.14)
Time of onset, duration of RBBB and the additional presence of a

conduction problem in one of the fascicles of the left bundle branch all affect
prognosis.
Early onset, long duration and additional disturbances in left fascicular
conduction all increase the chance of the development of complete AV block
and increase early mortality (13). Lie et al. (14) also showed that in these
patients the HV but not the PR interval was helpful in determining which
patient with bifascicular block is at high risk for developing complete infra AV
nodal block. When complete infra AV nodal block develops (figure 3.15) it
usually does so within 3 days after infarction (14).
Complete LBBB secondary to acute anterior wall MI is rare. Already in
1976 (13) Lie et al. showed that in acute anterior wall MI acquired RBBB is
much more common then acquired LBBB. Occasionally, one may observe
acquired complete RBBB followed by acquired complete LBBB (fig 3.16).
Obviously, this finding indicates the necessity to attempt rapid reperfusion.
Figure 3.16 shows the effect of primary PTC A in such a patient.
Incidence, mechanism and prognostic significance

In the pre-thrombolytic era Lie et al. (13) found an incidence of acquired
RBBB of 26% in patients admitted because of an acute anterior wall MI.
Mortality was 3 times higher than in patients with anterior MI without bundle
branch block.
Unfortunately, we have no data on the incidence of acquired BBB in acute
anterior wall MI in the era of reperfusion therapy. Articles have appeared on
the incidence of BBB in patients treated with thrombolytic therapy (15) but
people have not been divided into those with preexistent and acquired BBB.
When all BBB’s (transient and persistent) in all infarct locations were included
Newly et al. (15) found an incidence of 23,6%. Patients with an LAD infarction
had the highest incidence of BBB. The in hospital mortality rates in patients
with BBB were 2½ times higher as compared to those without BBB. Patients
with persistent BBB had a higher mortality rate than those with transient BBB.
When complete AV block develops mortality rate continues to be higher in the
thrombolytic era when compared to patients without complete AV block (16).
Harpaz et al. (16) also found that while the incidence of complete AV block
diminished in the thrombolytic era the higher mortality rate was still present
and similar in thrombolysis-treated and non treated patients with complete AV
block.
In that study no information is available on the timing of complete AV
block in relation to thrombolytic therapy. Was it present before or did it
develop later? The mechanism of RBBB and hemiblock and complete sub AV
nodal block is the interruption of blood supply to the proximal part of the sub-
AV nodal conduction system. This means an LAD occlusion proximal to the
first septal branch resulting in a large anterior wall myocardial infarction with
clear consequences as to mortality and morbidity. Reperfusion should be
attempted as early as possible. Depending upon the rapidity of the intervention
primary PTCA could be more beneficial than thrombolytic therapy in this
situation.
Management
Apart from rapid reperfusion, intravenous beta-blocking therapy and
administration of an ACE-inhibitor, prophylactic insertion of a pacing wire
should be done when in the setting of an acute anterior wall MI RBBB
develops accompanied by a frontal QRS axis to the left of –60° (indicating
additional left anterior hemiblock) or to the right of + 90 (suggesting additional
left posterior hemiblock).
Pacing is indicated in case of: 1) apparent second or third degree
intrahissal block 2) RBBB with prolonged PR (with or without left hemiblock)
or advanced (second or third degree) AV block.
When pacing is indicated it should preferably be done in a dual chamber
fashion.
As pointed out by Hauer et al. (17) chronic pacing is rarely required. Like
in inferior wall MI sub-AV nodal conduction disturbances following anterior
wall myocardial infarction rarely result in persistent high degree conduction
disturbances.
The future of the patient with anterior wall MI and AV conduction
disturbances is determined by the degree of impairment in LV function and the
occurrence of life-threatening ventricular arrhythmias.
Conclusions
As indicated in table 3.3 high degree block in the AV node (infero-posterior

MI) and below the AV node (anterior MI) significantly worsens short and long-
term outcome. Primarily because of the size of the myocardial infarction and its
hemodynamic consequences.
Rapidity of reperfusion of the ischemic area is therefore important. Especially,
in these high risk patients the possible advantages of primary PTCA over
thrombolytic therapy should be evaluated.
References
1. James TN. The coronary circulation and conduction system in acute myocardial infarction.
Progr Cardiovasc Dis 1968; 10:410-428.
2. Liem KL, Lie KI, Louridtz WJ, Durrer D, Wellens HJJ. Sinusbradycardie bij het acute
hartinfarct. Ned T Geneesk 1976;120:604-608.
3. James TN. Cardiac innervation. Anatomic and pharmacological relations. Bull New York
Acad Med 1967;43:1041-1050.
4. Zipes DP. The clinical significance of bradycardiac rhythm in acute myocardial infarction.
Am J Cardiol 1969;24:814-819.
5. Lie KI, Wellens HJ, Schuilenburg RM, Becker AE, Durrer D. Mechanism and significance
of widened QRS complexes during complete AV block in acute inferior myocardial
infarction. Am J Cardiol 1974;33:833-841.
6. Tans A, Lie KI, Durrer D. Clinical setting and prognostic significance of high degree
atrioventricular block in acute inferior myocardial infarction; a study of 144 patients. Am
Heart J 1980;99:4-8.
7. Berger P, Ruocco N, Ryan T, Frederick M, Jacobs A, Faxon D. Incidence and prognostic

implications of heart block complicating acute inferior myocardial infarction treated with
thrombolytic therapy: results from TIMI II. J Am Coll Cardiol 1992;20:533-540.
8. Kimura K, Kosuge M, Ishikawa T, Shimizu M, Hongo Y, Sugiyama M, Tochikubo O,

Umemura S. Comparison of the results of early reperfusion in patients with inferior wall
acute myocardial infarction with and without complete atrioventricular block. Am J
Cardiol 1999;84:731-733.
9. Simons GR, Sgarbossa E, Wagner G, Califf RM, Topol EJ, Natale A. Atrioventricular and
intraventricular conduction disorders in acute myocardial infarction: A reappraisal in the
thrombolytic era. PACE 1992;21:2651-2663.
10. Braat S, de Zwaan C, Brugada P, Coenegracht J, Wellens H. Right ventricular involvement

with acute myocardial infarction identifies high risk of developing atrioventricular nodal
conduction disturbances. Am Heart J 1984;107:1183-7.
11. Barold SS. American College of Cardiology/American Heart Association guidelines for
pacemaker implantation after acute myocardial infarction. What is persistent advanced
block at the atrioventricular node? Am J Cardiol 1997; 80:770-774.
12. Kimura K, Kosuge M, Ishikawa T et al. Comparison of results of early reperfusion in

patients with inferior wall acute myocardial infarction with and without complete
atrioventricular block. Am J Cardiol 1999;84:731-733.
13. Lie KI, Wellens HJ, Schuilenburg RM. Bundle branch block and acute myocardial
infarction. In: The conduction system of the heart, Editors H. Wellens, KI Lie and MJ
Janse. Philadelphia, Lea and Febiger 1976, pp 663-672.
14. Lie KI, Wellens HJ, Schuilenburg RM, Becker AE, Durrer D. Factors influencing
prognosis of bundle branch block complicating acute anteroseptal infarction: the value of
His bundle recordings. Circulation 1974;50:935-941.
15. Newby KH, Pisano E, Krucoff MW, Green C, Natale A. Incidence and clinical relevance
of the occurrence of bundle branch block in patients treated with thrombolytic therapy.
Circulation 1996;94:2424-2428.
16. Harpaz D, Behar S, Gotlieb S, Boyko V, Kishon Y, Eldar M. Complete atrioventricular

block complicating acute myocardial infarction in the thrombolytic era. J Am Coll Card
1999;34:1721-1728.
17. Hauer R, Lie KI, Liem KL, Durrer D. Long-term prognosis in patients with bundle branch
block complicating acute anteroseptal infarction. Am J Cardiol 1982;49:1581-1585.
Chapter 4
Myocardial infarction in the presence of abnormal

ventricular activation
Left bundle branch block, paced ventricular rhythm,

pre-excitation
Presence of pre-existent left bundle branch block (LBBB) worsens

prognosis in acute myocardial infarction.
Abnormal left ventricular activation, as in LBBB, right ventricular pacing

and ventricular pre-excitation, results in low sensitivity and specificity of
the ECG to diagnose site and size of a myocardial infarction.
Serial ECG’s are most helpful to diagnose myocardial infarction in case of

abnormal ventricular activation.
In case of abnormal left ventricular activation the clinical impression

should determine decision making as to reperfusion therapy.
MYOCARDIAL INFARCTION IN THE PRESENCE OF ABNORMAL VENTRICULAR ACTIVATION 67
The use of the electrocardiogram to identify the area at risk and the culprit
coronary artery during acute myocardial ischemia is based upon spread of
ventricular activation during sinus rhythm over an intact bundle branch system.
Locating ischemic or infarcted areas is possible when they are in parts of
the ventricle that under normal circumstances are activated early in the QRS
complex (1) but is more difficult when the infarcted areas are in parts of the
ventricle that are activated late in the QRS complex. Damage to myocardium in
the anterior and inferior areas of the left ventricle, which are activated early by
the left anterior and left posterior fascicle respectively, is thus more easily
identified than is damage in the postero-basal area.
When the sequence of ventricular activation is altered by bundle branch
block, ventricular pacing or ventricular pre-excitation, there will be a change in
the timing of activation in the areas that are normally activated earliest.
In right bundle branch block (RBBB) the diagnosis of ischemia or
infarction is usually not affected. The left ventricle accounts for the largest
mass of myocardium and sites of early activation of the left ventricle are in
general not altered by RBBB. But depending upon the proximity of the exit of
the RBB to the inferior portion of the heart a false diagnosis of inferior wall
infarction can be made in the presence of RBBB (figure 4.1). The closer the
exit of the RBB to the inferior portion of the heart, the larger the delay of
activation of the inferior portion. This is of course aggravated in the presence
of additional left posterior hemiblock.
However, ventricular activation is markedly different when the sequence

of left ventricular activation is completely changed by left bundle branch block,
right ventricular pacing and ventricular pre-excitation.
A. LEFT BUNDLE BRANCH BLOCK (LBBB)
In LBBB the left ventricle is activated by radial spread from the point of
termination of the RBBB. Therefore areas of the left ventricle that are normally
activated early, are activated much later in the QRS complex making it difficult
to recognize ischemia or infarction in those areas.
This problem is not new; it has puzzled experienced electrocardiographers
for more than 50 years (2). It is also known for a long time that the patient with
LBBB and acute MI has a much worse prognosis than a patient with infarction
and normal intraventricular conduction (3). As shown by Lie et al. (4) this is
true both for patients who already have LBBB before infarction (frequently
patients with hypertensive heart disease) and for those in whom LBBB
develops as a result of acute anteroseptal infarction. It is still the case in the
modern era of thrombolytic therapy (5-7). The unfortunate problem is that
because of the difficulties in making the diagnosis of acute myocardial
ischemia in the presence of LBBB these patients are often not receiving therapy
to reperfuse the ischemic area (8).
Twenty years ago Wackers et al. (9) reviewed the various
electrocardiographic criteria that were reported to be of value in making the
diagnosis of acute myocardial infarction in the presence of complete LBBB.
This was done by reviewing ECG findings in patients with LBBB in whom
infarct diagnosis and localization was based upon the outcome of thallium -201
scintigraphy. The conclusion of that study was that the electrocardiographic
criteria suggested to be helpful in diagnosing acute myocardial infarction in
LBBB were relatively insensitive and not specific for a particular location of
infarction. ST segment elevation (the amount not specified!) had a sensitivity
for myocardial infarction of 52 %, and abnormal Q waves a 31 % sensitivity.
Initial positivity in lead and a Q wave in lead and a 20 % sensitivity,
but a 100 % specificity for anteroseptal infarction (figures 4.2 and 4.3).
The most valuable finding was serial electrocardiographic changes having
a 67 % sensitivity for acute myocardial infarction. These serial changes
occurred mainly during the early phase (24-48 hours) of infarction and
frequently disappeared after 4-5 days.
More recently Sgarbossa et al. (10) reported on a retrospective study of
131 patients with LBBB who were among the 26.003 patients enrolled in the
GUSTO-I trial of thrombolytic therapy in patients with acute myocardial
infarction. They were compared with asymptomatic patients with LBBB. Three
ECG findings were found to have independent value in the diagnosis of acute
infarction in the presence of LBBB: 1/ ST segment elevation equal to a greater
than 1 mm in the presence of a positive QRS complex (figure 4.4); 2/ ST
segment depression equal to or greater than 1 mm in lead V1, V2 or V3
(figure 4.5); 3/ ST segment elevation equal to or greater than 5 mm in the

presence of a negative QRS complex (fig 4.6). They also constructed an index
score using these three criteria (see table 4.1)
These findings were recently criticized by Shlipak et al. (11). They

performed a retrospective cohort study in 83 patients with LBBB who
presented 103 times with symptoms suggestive of myocardial infarction. They
could not find an ECG pattern which distinguished the 30 % of patients with
myocardial infarction from those with other diagnoses. They could not confirm
the value of the algorithm proposed by Sgarbossa et al. (10). Similar findings
were reported in abstract form by Kontos et al. (12) and by Eriksson (13).
Obviously a prospective study is needed to evaluate the true value of the
Sgarbossa algorithm.
Information from intermittent LBBB

As discussed in chapter 3 in acute infero-posterior infarction intermittent,
frequently bradycardia-related, phase-4 LBBB may occur. This gives the
opportunity to compare the QRS-T complex during normal intraventricular
conduction and LBBB in the same patient. As shown in figures 4.7 to 4.9, in
inferior wall myocardial infarction, ST segment elevation persists during
LBBB in the inferior leads II,III and AVF. This is even more outspoken when
left axis deviation is present during LBBB (figures 4.8 and 4.9). As also shown
in figures 4.7 to 4.9 wide and notched QS-complexes are frequently present in
inferior leads in infero-posterior infarction.
The importance of serial ECG’s

Already 20 years ago Wackers et al. (9) pointed out the importance of
recording serial ECG’s in patients with LBBB admitted with chest pain.
Examples are given in figures 4.10 and 4.11. Note widening of the QRS, axis
shift and ST-T segment changes during chest pain. Serial ECG’s also allow to
document reperfusion of the culprit coronary artery (figure 4.12).
Practical approach
Although as indicated above ECG clues may be present indicating myocardial
ischemia or infarction in the presence of LBBB, the ECG is frequently not a
reliable source of information. Possibly, as suggested by Eriksson et al. (14)
dynamic vector cardiography might be a better tool. In the mean time we (15)
strongly support the guidelines of the American College of Cardiology /
American Heart Association (16) which recommend acute reperfusion therapy
for patients with LBBB and a clinical presentation suggestive of acute
B. PACED VENTRICULAR RHYTHM
At present, when ventricular pacing is indicated, the pacing electrode is usually

placed in the right ventricle. This will lead to sequential activation of first the
right ventricle which is followed by the left ventricle, similar to LBBB. The
consequences in diagnosing myocardial infarction were pointed out by Barold
et al. (17) and Dodinot et al. (18) more than 20 years ago.
Figure 4.13 gives an example in a patient with a circumflex occlusion.
Note the widening and notching of the QRS in the precordial leads
accompanied by marked ST segment depression. Barold (17) and Dodinot (18)
also showed the importance of examining the 12 lead ECG without pacing
which in the older type pacemakers might require chest wall stimulation (figure
4.14 and 4.15). Occasionally, alternation of the paced QRS may be observed
(fig 4.16).
Two important points have to be mentioned when discussing

myocardial infarction in paced ventricular rhythms. First, as pointed out by
Chatterjee et al. (19) in hearts without ischemia abnormal ventricular
depolarization by ventricular pacing may lead to T-wave negativity when
normal intraventricular conduction returns. This can be observed when pacing
is intermittent or suppressed. Characteristically, the T-wave negativity is
present in leads showing a negative or predominantly negative QRS complex
during ventricular pacing (figure 4.17). Second, as pointed out by Dodinot et al.
(18), in myocardial infarction there may be an increase in the interval between
the pacing stimulus and the onset of the QRS complex (so-called latency). This
can be the result of pacing in the infarcted area.
C. VENTRICULAR PRE-EXCITATION
During ventricular pre-excitation part or the whole of the ventricle is activated

by way of an accessory atrio-ventricular pathway. This will result in abnormal
ventricular activation. As in LBBB and ventricular pacing this will hamper the
diagnosis of myocardial infarction. It may also lead to pseudo-infarct patterns
because early activation of for example the inferior portion of the heart by way
of an infero-postero septal accessory pathway may result in initial QRS
negativity (because of the delta wave) in the inferior leads (figure 4.18). The
ability to mask myocardial infarction by ventricular pre-excitation depends
upon the location of the accessory pathway. A pathway inserting in the
posterior wall of the left ventricle may make the diagnosis of anterior wall
myocardial infarction more difficult (figure 4.19). On the other hand inferior
infarction in the presence of a posteroseptal accessory pathway can still be
diagnosed (figure 4.20). In general if the location of the infarction is
contralateral to the accessory pathway it will mask infarction, while an
ipsilateral location will allow recognition of ischemia or infarction.
Conclusion
Abnormal left ventricular activation may hamper or impair the diagnosis of

myocardial infarction. This means that decision making as to a myocardial
reperfusion attempt should be based upon the clinical impression rather than
the electrocardiogram.
References
1. Durrer D, van Dam RTH, Freud GE et al. Total excitation of the isolated human heart.
Circulation 1970;41:899-912.
2. Wilson FN, Rosenbaum FF, Johnston F, Barker PS. The electrocardiographic diagnosis of
myocardial infarction complicated by bundle branch block. Arch Inst Cardiol Mex
1945; 14:201-212.
3. Col JJ, Weinberg SL. The incidence and mortality of intraventricular conduction defects in
acute myocardial infraction. Am J Cardiol 1972;29:344-350.
4. Lie KJ, Wellens HJJ, Schuilenburg RM. Bundle branch block and acute myocardial
infarction. In: Wellens HJJ, Lie KJ, Janse MJ, eds. The conduction system of the heart.
Philadelphia: Lea and Febiger 1976: 662-672.
5. Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. Indications for fibrinolytic

therapy in suspected acute myocardial infarction: Collaborative overview of early mortality
and major morbidity results from all randomized trials of more than 1000 patients. Lancet
1994;343:311-322.
6. Sgarbossa EB, Pinski SL, Topol EJ et al., for the GUSTO-I investigators. Acute myocardial
infarction and complete bundle branch block at hospital admission. Clinical characteristics
and outcome in the thrombolytic era. J Am Coll Cardiol 1998;31:105-110.
7. Go AS, Barron HV, Rundle AC, Ornato JP, Avins AL, for the National Registry of
myocardial infarction 2 Investigators. Bundle branch block and in-hospital mortality in
acute myocardial infarction. Ann Int Med 1998; 129: 690-697.
8. Barron HV, Bowlby BJ, Breen T et al. Use of reperfusion therapy for acute Myocardial
Infarction in the United States. Data from the National Registry of Myocardial Infarction.
Circulation 1998;97:1150-1156.
9. Wackers FJT, Lie KJ, David G, Koster RM, Wellens HJJ, Assessment of the value of
electrocardiographic signs for myocardial infarction in left bundle branch block. In: Wellens
HJJ, Kulbertus HE, eds. What’s new in electrocardiography? The Hague, The Netherlands:
Martinus Nijhoff, 1981:37-57.
10. Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of evolving
acute myocardial infarction in the presence of left bundle branch block. N Engl J Med
1996;334: 481-487.
11. Shlipak MS, Lyons WL, Go AS et al. Should the electrocardiogam be used to guide therapy
for patients with left bundle branch block and suspected myocardial infarction. JAMA
1999;281:714-719.
12. Kontos MC, Mc Green RJ, Jesse R, Tatum J, Omato J. Can the ECG diagnose acute
myocardial infarction in emergency department patients with chest pain and left bundle
branch block (abstract). J Am Coll Cardiol 1999;33:347A.
13. Eriksson P, 1998, personal communication.
14. Eriksson P, Gunnarson G, Dellborg M. Diagnosis of acute myocardial infarction in patients

with chronic left bundle branch block. Standard 12-lead ECG compared to dynamic
vectorcardiography. Scand Cardiovasc J 1999;33:17-22.
15. Wellens HJJ. Acute myocardial infarction and left bundle branch block. Can we lift the
veil? N Engl J Med 1996;334:528-529.
16. Ryan TJ, Anderson JL, Antman EM et al. ACC / AHA guidelines for the management of
patients with acute myocardial infarction: executive summary: a report of the American
College of Cardiology / American Heart Association task force on Practice Guidelines
(Committee on Management of Acute Myocardial Infarction). Circulation 1996;94:2341-
2350.
17. Barold SS, Ong LS, Heinle RA. Electrocardiographic diagnosis of myocardial infarction in
patients with transvenous pacemakers. J Electrocardiol 1976;9:99-111.
18. Dodinot B, Kubler L, Godemir JP. Electrocardiographic diagnosis of myocardial infarction

in pacemaker patients. In Wellens HJJ, Kulbertus HE, eds. What’s new in
electrocardiographs? The Hague, The Netherlands, Martinus Nijhoff, 1981:79-90.
19. Chatterjee K, Harris A, Davies S, Leatham A. Electrocardiographic changes subsequent to

artificial ventricular depolarization. Br Heart J 1969;31:770-779.
Chapter 5
Arrhythmias in acute myocardial infarction
Incidence and prognostic significance

Sinus tachycardia in acute MI indicates poor prognosis and urges a careful

search for the cause.
Atrial fibrillation developing after onset of MI worsens prognosis.
Sustained ventricular tachycardia in acute MI is rare. When present it

usually indicates a closed coronary artery or a scar from a previous MI.
Prognostic significance of successfully resuscitated VF in acute MI is

unclear, probably because its occurrence is not related to the size of the
area at risk and extent of coronary artery disease.
ARRHYTHMIAS IN ACUTE MYOCARDIAL INFARCTION 87
Cardiac arrhythmias, ranging from a premature beat to sustained tachycardias,

are common in acute myocardial infarction. They may be transient, occurring
only during the acute ischemic phase like primary ventricular fibrillation, or
longer lasting because of structural changes or hemodynamic consequences of
myocardial infarction. Their significance may vary from innocent to life
threatening. As will be pointed out in this chapter, correct identification of
arrhythmias is not only of importance for decision making as to treatment, but
also for the short and long term prognosis of the patient.
A. SUPRAVENTRICULAR ARRHYTHMIAS
Sinus tachycardia
Shortly after the introduction of the coronary care unit, it was realized that the
finding of sinustachycardia after a myocardial infarction was of important
prognostic significance (1). This was confirmed by several subsequent studies
both in the pre- and post thrombolytic era (2-8). Both Hathaway et al. (7) and
Zuanetti and coworkers (8) found in the thrombolytic era that in a large series
of patients from respectively the GUSTO-I and the GISSI-2 study early
mortality increased when sinus heart rate on admission was above 80 beats per
minute with mortality increasing threefold at sinus rates above 100 beats per
minute. Zuanetti et al. (8) also noted that sinus tachycardia at the time of
discharge from hospital indicated a marked increase in mortality at 6 months.
When sinus tachycardia is present in the patient with an acute myocardial
infarction, the patient should be carefully examined for additional and possibly
correctable abnormalities. Those may or may not be related to myocardial
infarction.
As shown in table 5.1, related complications include (impending)
myocardial rupture; heart failure because of infarct size, presence of a previous
infarction, mechanical damage from papillary muscle dysfunction or rupture
(figure 5.1); ventricular septal rupture; and ischemia at a distance because the
culprit coronary artery supplies other vessel territories by collateral circulation.
Complications not related to the myocardial infarction itself include anemia,

fever, pulmonary embolism, infection, etc. The important message is that sinus
tachycardia should always be a stimulus for a careful search for the cause!
Atrial fibrillation
Atrial fibrillation is a common complication of acute myocardial infarction.
Depending upon the age of the patient, the incidence may be as high as 20% (9,
10). Approximately half of the patients with atrial fibrillation have the
arrhythmia on admission while in the other half it develops during admission
(10). Interestingly, the prognostic significance of atrial fibrillation varies
between different studies. Some found no effect of atrial fibrillation (9, 11-14)
while others reported increased in-hospital and long term mortality (10, 15-18).
Small sample size, enrollment in different centers, short follow-up and patient
selection may have played a role in these differences.
Twenty five years ago, Liem et al. (19) showed in a consecutive series of
1000 patients admitted to hospital because of a myocardial infarction that 8%
developed atrial fibrillation after admission. If atrial fibrillation occurred in
patients without heart failure, the arrhythmia did not affect in-hospital cardiac
mortality. Also when severe heart failure was present, occurrence of atrial
fibrillation did not change the high in-hospital mortality. Interestingly, in case
of mild heart failure, the development of atrial fibrillation was accompanied by
a 2,5 times higher in-hospital mortality rate. Atrial fibrillation may occur
during the initial phase of acute inferior infarction as an expression of (pain and
anxiety induced) increased vagal tone and is than accompanied by high degree
AV nodal block (fig. 5.2). When atrial fibrillation develops in acute anterior
wall myocardial infarction, it is frequently a marker of manifest or impending
pump failure (fig. 5.3).
Recently, Rathore et al. (10) reported on 106.780 Medicare patients

years who were included in the Cooperative Cardiovascular Project and treated
for acute myocardial infarction. They found that 10,5% of those patients
presented with atrial fibrillation on admission, while 11,6% developed the
arrhythmia later. Particularly when atrial fibrillation develops during
hospitalization, the prognosis becomes worse as reflected by higher in-hospital,
30 days and 1-4 year mortality.
These data indicate that loss of atrial contribution to ventricular filling and
an inappropriate ventricular rate during atrial fibrillation often result in a worse
outcome. Unfortunately, no studies are available showing that in acute
myocardial infarction pharmacological or non-pharmacological attempts to
convert atrial fibrillation to sinus rhythm is rewarded by a better prognosis.
That question has to be answered by prospective studies.
B. VENTRICULAR ARRHYTHMIAS
Ventricular premature beats

Shortly after the introduction of the coronary care unit for the management of
acute myocardial infarction, attention was focussed on certain characteristics of
ectopic ventricular beats that qualified them as malignant (so-called warning
arrhythmias) because of their ability to initiate life-threatening ventricular
arrhythmias. Early occurrence, close to the summit of the T wave of the
previously conducted sinus beat, frequent occurrence, multiform configuration
and runs of ventricular premature beats were all suggested as pointing to a
malignant character and an indication to treat the patient with lidocaine (20).
However, a few years later, several investigators (21-24) indicated that early
premature ventricular beats showing the R (of the premature ventricular beat)
on T (of the preceding conducted sinus beat) phenomenon were just as
common in patients developing ventricular fibrillation as in patients not
developing that arrhythmia.
Examples are shown in figure 5.4. Panel A in figure 5.4 shows very
frequent, early occurring ventricular premature beats in the setting of an acute
inferior myocardial infarction. As shown in panel B and C from the same
patient, ventricular fibrillation could be initiated both by an early or a late
ventricular premature beat.
Chiladakis et al. (24) recently showed that also in the thrombolytic era R-
on-T ventricular premature beats and R-on-T ventricular tachycardias are rare
features in acute myocardial infarction, and that R-on-T ventricular premature
beats do not serve as triggers for severe ventricular tachyarrhythmias.
Because of the inability to predict which ventricular premature beat (early or
late) would initiate ventricular fibrillation, Lie et al. (25) made a plea to treat
the patient with an acute myocardial infarction with prophylactic lidocaine.
Over the years, the enthusiasm to give lidocaine prophylactically has
decreased, primarily because of the side effects of lidocaine and the fact that
both in the out-of-hospital advanced life support situation and in the coronary
care unit, personnel is available which is well trained in the recognition and
treatment of ventricular fibrillation. Antman and Berlin (26), in reviewing all
the randomized studies on prophylactic lidocaine use in acute myocardial
infarction, came to the conclusion that lidocaine should not be used
prophylactically because of the declining incidence of VF after a myocardial
infarction and the reported trend towards excess mortality in lidocaine treated
patients. Another factor decreasing the use of lidocaine is the routine
administration of a beta-blocking agent to patients with acute myocardial
infarction.
Ventricular tachycardia
Sustained monomorphic ventricular tachycardia (VT) defined as a tachycardia
with identical wide, QRS complexes at a rate of at least 130 beats per minute,
is rare in acute myocardial infarction (27) because a stable re-entry circuit is
required. This is usually not the case in acute myocardial infarction. VT either
stops spontaneously after a limited number of beats (non-sustained VT) or
degenerates into VF. In our experience, sustained VT in acute MI either occurs
during reinfarction in the same coronary artery territory as the previous
infarction (fig. 5.5), or in a scar from a previous infarction in another location.
Typically, therefore the patient with sustained monomorphic VT in the
acute phase of MI is older, and has a diminished left ventricular ejection
fraction because of a previous MI. In the GUSTO-I study (28) 2423/40895
(5,7%) patients were reported as having sustained VT during the acute phase of
MI. Unfortunately, no information is given about time of occurrence (before,
during or after thrombolytic therapy) and on the rate and configurational
characteristics of the arrhythmia. It is therefore likely that long episodes of
accelerated idioventricular rhythm (AIVR) were classified as monomorphic
sustained VT. Outcome of patients with VT was worse as compared to no VT
in the GUSTO-I study (28). This was the case in early and late (more than 2
days after infarction) VT patients. The poor prognosis of patients developing
sustained monomorphic VT during the late phase of hospital admission for
acute MI has been reported before (29), because these patients have larger
(usually anterior) infarcts. Heidbüchel et al. (30) found that in acute MI patients
with VT after thrombolytic therapy, the culprit coronary artery was usually
occluded in contrast to VF patients. They suggested that presence of a
sustained VT should be a reason to perform coronary angiography to assess the

patency status of the coronary artery and to perform a reperfusion procedure
when needed. As discussed more extensively in chapter 6, accelerated
idioventricular rhythm (AIVR) is also a ventricular arrhythmia (monomorphic,
rate 60-120/min) occurring in acute myocardial infarction during reperfusion. It
was initially thought to be a benign arrhythmia, but as indicated by Gorgels et
al (31) always accompanied by myocardial muscle loss. Recently, work by
Engelen et al. (32) indicated that incidence and duration of AIVR is related to
left ventricular wall motion abnormalities late after MI. This may explain the
outcome of the GUSTO-I study that indicated a poorer short and long term
prognosis of patients with ventricular tachycardias after MI (28).
Ventricular fibrillation
Several studies have addressed the question whether occurrence of ventricular
fibrillation (VF) in the acute phase of myocardial infarction has prognostic
significance after the arrhythmia has been treated successfully (33-38).
Volpi et al. (33) reported that primary VF worsened in-hospital mortality

but not long term prognosis. Similar findings were described by Behar et al.
(34) In contrast, Tofler et al.(35) found no difference in hospital mortality in
patients with primary VF.
Chiriboga et al. (36) found in a community-wide observational study that
neither the incidence (around 5 % of patients developed VF) nor the prognosis
associated with primary VF in acute myocardial infarction changed over a
period of 15 years (1975-1990).
Berger and coworkers (37) looked at the significance of primary VF in the
thrombolysis era. They found that VT and VF are not markers for reperfusion.
These arrhythmias were associated with occlusion, not patency of the infarct
related coronary artery. Early mortality, but not long term mortality was
increased in VT/VF patients even in the absence of heart failure and
hypotension.
Brezins et al. (38) found that in hospital primary VF was rare in non Q
wave myocardial infarction. Most cases of primary VF occurred out-of-hospital
or in the emergency room. Smoking, atrial fibrillation, left bundle branch block
and hypokalemia were found more often in the primary VF patients.
Thrombolytic therapy reduced the incidence of primary VF.
Recently, Gheeraert et al. (39) looked at coronary angiographic findings in
patients with out-of-hospital VF in patients with acute myocardial infarction.
They found that patients with an occlusion of the left anterior descending or
circumflex coronary artery had a greater risk for out-of-hospital VF than
patients with an occlusion of the right coronary artery. Interestingly, the
location (proximal or distal in the vessel) of the occlusion, the amount of
myocardium at risk for necrosis and the extent of coronary artery disease were
not related to out-of-hospital VF. These findings are important because they
indicate that many patients suffering from cardiac arrest outside hospital have
hearts too good to die.
Early ischemia related, so-called primary VF has to be distinguished from
secondary VF occurring in the presence of hypotension or heart failure. This
happens in patients with large (usually anteriorly located with acquired right
bundle branch block) infarcts having pump failure. Such episodes occur late
after the acute phase of a myocardial infarction usually in the second or third
week (40). The poor prognosis of these patients is not so much related to VF, if
treated appropriately, but to the degree of left ventricular muscle loss.
Conclusion
Cardiac arrhythmias are common in acute myocardial infarction, varying from

benign to life threatening. Proper identification should be followed by
understanding their significance and be the basis for decisions about treatment.
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Chapter 6
The electrocardiographs signs of reperfusion

Resolution of ST segment deviation of more than 70% within one hour

after thrombolytic therapy strongly suggests patency of the infarct related
coronary artery.
Patients with anterior infarction may show less ST segment resolution on

reperfusion than patients with inferior infarction.
An accelerated idioventricular rhythm is more common after reperfusion

by thrombolytic therapy than by coronary angioplasty.
Severity and duration of an accelerated idioventricular rhythm correlates

with left ventricular wall motion abnormalities late after myocardial
infarction
Non-invasive ECG parameters are helpful to determine the presence of

reperfusion, but do not distinguish between TIMI II or TIMI III flow.
THE ELECTROCARDIOGRAPHIC SIGNS OF REPERFUSION 101
As pointed out in chapter 2, the surface ECG is of great value in acute

myocardial infarction, to decide whether an aggressive approach to regain
coronary artery patency is required or conservative treatment is the preferred
treatment modality. Once the decision is made that the area at risk is such that
reperfusion should be attempted different strategies are possible, such as
thrombolytic therapy, primary percutaneous transluminal coronary angioplasty
(PTCA) with or without stenting, or when thrombolytic therapy fails,
secondary (rescue) PTCA. The choice of treatment depends on local facilities
and experience, the recognition of site and size of an acute myocardial
infarction and the time elapsed from the onset of symptoms.
Assessment of reperfusion of the myocardial tissue at risk is important to
guide treatment in the acute phase of the infarction, with in addition prognostic
consequences for the future (1). Furthermore, new treatments are being
developed to limit myocardial damage during the process of reopening of the
infarct-related vessel. To analyze efficacy of these new treatments to limit
reperfusion damage, the ECG may provide useful information. To recognize
reperfusion non-invasively most attention has been given towards ST-T
segment behavior (1) and the occurrence of brady-and tachyarrhythmias.
ST-T segment behavior
ST segment changes
Monitoring the 12 lead electrocardiogram during the treatment of patients
suffering from an acute myocardial infarction is an inexpensive and reliable
tool to determine vessel patency. It is crucial to realize that in the absence of
reperfusion during the first hours after occlusion of the coronary artery only
minor (<25%) changes in the amount of ST segment deviation occur. During
recovery of blood flow different patterns of ST segment behavior can be
recognized. The most important change being normalization of the ST segment
(2) (fig. 6.1). For practical purposes Zeymer et al. (3) recently indicated that a
more than 70% ST resolution is an excellent marker for reperfusion following
thrombolysis. However, the absence of ST resolution does not accurately
predict an occluded culprit coronary artery. Approximately 50% of patients
with no (<30%) ST resolution have a patent culprit coronary artery.
In about half of the patients receiving thrombolytic therapy, the initial
change is an increase in ST segment elevation at the time of reperfusion (fig.
6.2) (4,5) followed by a significant decrease of ST segment deviation. It is of
interest that the initial ST segment elevation on reperfusion less frequently
occurs in patients undergoing primary PTCA compared with thrombolytic
therapy (10 % versus 50% respectively)(6).
One should realize that important differences may exist between anterior
and inferior MI with regard to ST segment resolution. On restoration of
epicardial blood flow patients with anterior infarction frequently develop
significantly less ST resolution than those with inferior infarction (7). This led
de Lemos et al. (8) to the suggestion that resolution of ST deviation by > 70%
is the optimal threshold for patients with inferior MI but > 50% may be optimal
for anterior MI.
Normalization of the ST segment can be explained by recovery of
myocardial blood flow. The mechanism of the initial increase in ST segment
deviation, which is often accompanied by a marked increase in chest pain, is
less clear. Possible explanations include peripheral embolization of thrombotic
material, increased microvascular resistance and reperfusion damage.
Preliminary data suggest that reperfusion damage may occur in the human
heart (9). From experimental models we know that damage to the myocardium
is inflicted by reperfusion. Reperfusion injury occurs in two stages, acute due
to the formation of oxygen derived free radicals and calcium overload in
damaged myocytes and later by activation of neutrophils (10,11). These
changes may lead to apoptotic cell death (9). Whether pharmacological
interventions during reperfusion can reduce infarct size has yet to be proven in
man.
The normalization of the ST segment has important prognostic
significance. Van ‘t Hof et al., analyzed mortality in patients after primary
PTCA and reported an increased relative risk of 8.7 in the absence of ST
segment normalization and of 3.6 when ST segment recovery was incomplete
after one hour of reperfusion (12). Also, increased mortality rates have been
reported in patients with persisting ST segment elevation in the setting of
anterior MI (15% versus 2%). (13).
The absence of ST segment resolution following PTCA worsens prognosis
as indicated by increased in-hospital and long term mortality. In addition,
impaired left ventricular function and congestive heart failure were more often
found in patients with persistent ST segment elevation after return to the
coronary care unit following reopening of the vessel (14).
In patients with large infarcts treated with thrombolytics absence of ST
resolution should be an indication for a percutaneous coronary intervention.
Although, as indicated above, the vessel may be open one has to be certain in
view of the prognostic consequences of an occluded coronary artery.
Several groups have shown that continuous ST segment monitoring is the
best way to document flow in the infarct related coronary artery (15-21).
Recently Johanson et al (22) indicated that even small variations in ST segment
shift during the first 4 hours of acute myocardial infarction predict worse
outcome. Continuous ST segment monitoring allows early recognition of
reocclusion making optimal management possible.
T wave changes
T wave inversion occurring within the first two hours after the start of
thrombolytic therapy indicates reperfusion (fig. 6.3). In anterior wall MI a
decrease in the ST segment elevation is found together with the development of
terminal T-wave negativity in the precordial leads. A similar phenomenon can
be observed in leads II, III and AVF in inferior MI. In posterior MI, indicated
by ST segment depression in the precordial leads, the reverse pattern can be

found as the terminal part of the T-wave becomes positive.
The recognition of terminal T-wave inversion development during
thrombolytic therapy is important as it indicates successful reperfusion. When
terminal T-wave inversion is already present on the admission ECG in the
setting of an acute MI, it gives no information with respect to artery patency.
Late T wave inversion > 4 hours is not an indicator of reperfusion as it is a
feature of the ST segment behavior after acute myocardial infarction. Changes
in T-wave polarity can be a sign of unstable angina (see chapter 7).
Incidence, mechanism and prognostic implications

The development of early T-wave inversion during thrombolytic therapy is
highly specific for reperfusion (>90%). However, T-wave inversion occurs in
only approximately 60% of the recordings (5,6). Therefore, the absence of
terminal T-wave inversion can not be considered indicative of failed
thrombolysis. When the blood supply to the ischemic and partially necrotic
myocardium is restored, many changes occur at the cellular level. Areas where
electrical activation and conduction were absent are gradually recovering. This
process of recovery is responsible for segments with delayed repolarization
(23). Recovery occurs more rapidly in the epicardial than in the midmyocardial
and endocardial layers. This dispersion in the duration of repolarization in the
infarcted area relative to the normal myocardium increases during reperfusion.
When in anterior MI the restored repolarization current lasts longer in the endo-
than the epicardium, the terminal portion of the T-wave becomes negative in
the precordial leads.
Ectopic activity
ECG findings
The moment patency of an occluded infarct artery is restored, arrhythmias can
occur. Most often premature ventricular beats are seen and sometimes
ventricular tachycardias or ventricular fibrillation.
The value of these arrhythmic events for decision making as to the
reopening of the coronary vessel, depends upon their specificity or positive
predictive value. Rarely, supraventricular arrhythmias mark reopening of the
vessel and in the setting of an inferior wall myocardial infarction, bradycardia
can be observed. To compare the relevance of these findings in different
studies the definitions used are essential (table 6.1). Special attention must be
directed to Accelerated Idiopathic Ventricular Rhythms (AIVR) as they are
very specific and are observed from the moment of the start of reperfusion (24).
AIVR is defined by the rate (60-120 beats/min.), and the mechanism of
initiation and termination. In general, the arrhythmia starts with a long coupling
interval to the preceding sinus beat and stops when sinus rhythm recaptures the
ventricles (24) (see fig. 6.4).
VPB and AIVR

AIVR is a very specific reperfusion arrhythmia, and only occurring in the
setting of myocardial damage (figure 6.5). The specificity of AIVR for
reperfusion has been reported to be >80% with a positive predictive value of
>90%. (25,26). The characteristics of the QRS complex during AIVR depend
upon the site of occlusion, and can be helpful to determine which vessel caused
the myocardial infarction (table 6.2).
The width of the QRS complex is smaller in anterior wall MI because the
AIVR arises close to the midline (fig. 6.6) resulting in more symmetrical
activation of the ventricles. In reperfusion of an RCA occlusion the electrical
axis is always superior, and in CX lesions RBBB patterns have been reported
exclusively (25). Interestingly, the site of AIVR origin may shift down the
coronary artery, when reperfusion occurs (fig. 6.7). An increase in the number
of VPBs often marks the reperfusion event. In many patients this will be
followed by AIVRs. The value of the number of VPBs per time interval (for
example 5 min.) is less specific and has lower positive predictive value for
reperfusion (approximately 70 and 80% respectively). The mechanism of VPBs
and AIVR is possibly related to calcium overload in the surviving
cardiomyocytes in the border of the myocardial infarction. The calcium
overload is secondary to an increased influx of sodium into the vulnerable
myocytes. The increased calcium load and calcium cycling through the
sarcoplasmatic reticulum upon restoration of energy supplies (ATP) provokes
delayed after depolarizations and induces triggered arrhythmias (27). AIVRs
can be prevented or blocked by treatment with dipyridamole and reduced
cellular adenosine uptake (28).
AIVR is probably caused by reperfusion damage. The arrhythmia in itself
has no major acute hemodynamic consequences, and is no precursor of more
malignant tachycardias. A reduction in frequency and duration of AIVR could
therefore be indicative for a reduction in reperfusion damage and be beneficial
(23). Following primary PTCA less AIVR was found compared with
reperfusion after thrombolytic treatment (6,29). AIVR is a transient, self-
terminating arrhythmia that does not need treatment. In general, it should be
considered a positive sign of reperfusion in an acute myocardial infarction.
Future studies should be performed to confirm that AIVR indicates reperfusion
damage and that interventions resulting in less AIVR indicate improved
salvage of myocardial tissue.
The analysis of reperfusion arrhythmias in general, may therefore be of
help in comparing different reperfusion strategies and pharmacological
interventions aimed at reducing reperfusion damage and cell death after
NSVT and VF

Sustained monomorphic ventricular tachycardia is not a reperfusion
arrhythmia. When it occurs in the setting of an acute myocardial infarction, a
scar from a previous myocardial infarction is usually present (30). During
reperfusion non-sustained ventricular tachycardias (NSVT) have been reported
(fig. 6.8). However, NSVTs are also frequently seen in the absence of
reperfusion. Therefore the clinical importance of this arrhythmia as an indicator
of reperfusion is limited. Polymorphic ventricular tachycardia and ventricular
fibrillation are common reperfusion arrhythmias in experimental models of
ischemia and reperfusion and do occur but rarely during reopening of the
infarct-related vessel in man. However, in a large randomized trial, assessing
the safety of thrombolytic therapy at home the incidence of VF was higher in
patients receiving thrombolytics compared with placebo (2.5 vs. 1.6%)
indicating that VF can be a reperfusion arrhythmia (31). No information is
available on the short-term prognostic importance of NSVT and VF occurring
during reperfusion. As discussed in chapter 5 the effect of primary VF on long
term prognosis of patients with MI is not clear (32).
Supraventricular arrhythmias
ECG findings
Atrial tachycardia and atrial fibrillation (fig. 6.9) have been observed in the
setting of reperfusion. Ectopic atrial activity is seen predominantly in the
setting of an inferior wall myocardial infarction based on a proximal occlusion
of the RCA. In most cases a short lasting (<1 min.) episode of ectopic atrial
activity is observed.

Both atrial tachycardia and atrial fibrillation are rare during reperfusion
occurring in 10, respectively 5% of all cases (5,6). There is no definite
explanation for the occurrence of these arrhythmias. However, the relation
between atrial damage and reperfusion suggests a similar mechanism as
described above for ventricular reperfusion arrhythmias involving calcium
overload and triggered activity.
The significance of these arrhythmias in patients treated for an acute MI is
not clear. Although the arrhythmias can indicate successful reopening of the
vessel, also complications of the MI could initiate ectopic atrial activity and
atrial fibrillation.
Therefore, the interpretation of these events depends on other concomitant
changes on the ECG and the clinical condition of the patient.
Brady arrhythmias
ECG findings
The occurrence of bradycardia during reperfusion has been reported by several
groups (5, 24, 33). It occurs almost exclusively in inferior wall MI (figure 3.2).
In most patients sinus bradycardia is observed whereas in some patients
complete sino-atrial block leads to a slow AV nodal escape rhythm.

Bradycardia in response to restoration of blood flow to the inferior wall is seen
in approximately 30% of the patients. The mechanisms behind this
phenomenon were discussed in chapter 3, table 3.1.
Damage to the sinus node, atrial tissue or atrio-ventricular node during
reperfusion may contribute. A transient bradycardia occurring during vessel
reopening does not influence the short or long-term prognosis.
Management
Reperfusion brady- and tachyarrhythmias require treatment only when they
affect the hemodynamic condition or, as in reperfusion induced VF, threaten
the life of a patient.
Conclusion
The described ECG changes are of help to document reperfusion non-

invasively and are of value to determine the need of other strategies to obtain
reperfusion. One should keep in mind however that we do not have ECG
criteria to distinguish reliably between TIMI II and TIMI III flow (34).
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Chapter 7
The electrocardiogram in unstable angina

ST segment depression on admission identifies a high risk group of patients

with unstable coronary artery disease
Magnitude and distribution of ST segment depression should determine

invasive versus conservative management strategy
In patients with acute myocardial ischemia continuous 12 lead ECG or

serial ECG’s recordings may be needed to diagnose unstable angina or non
ST-segment elevation myocardial infarction
Determine troponin level to document recent loss of myocardial tissue
In left main or 3 vessel disease ST segment changes in 8 or more ECG

leads develop during chest pain
In critical LAD narrowing precordial T wave negativity develops after

chest pain has subsided
THE ELECTROCARDIOGRAM IN UNSTABLE ANGINA 119
An unstable plaque in a coronary artery may lead to critical narrowing or

complete occlusion resulting in acute ischemia and/or necrosis of the
myocardium. The resulting clinical entities are called acute coronary
syndromes and include unstable angina and acute myocardial infarction.
Initially it may not be clear which of the two is present, and the determination
of biochemical cardiac markers such as troponin requires time and may have a
low sensitivity in the early phase of myocardial ischemia.
The importance of ST segment depression

In unstable angina and non-ST-segment elevation myocardial infarction, the 12
lead surface electrocardiogram (ECG) on admission can give important
information about the site and the extent of ischemia. Antman et al (1) showed
that in those patients the number of leads showing ST depression and the
amount of ST depression indicate size and severity of the ischemic area. This
was recently confirmed by Kaul et al (2). It was also shown that patients with
ST segment depression may have a poorer long-term prognosis than patients
with an acute myocardial infarction (3,4). Magnitude and distribution of ST
depression should determine which patient will profit from an invasive versus a
conservative management strategy (5). Recent data from the FRISC II study
indicate that the presence of ST depression on admission is already sufficient
evidence to propose early invasive treatment to the patient (6).
The ECG also allows identification of high-risk syndromes such as
unstable angina due to a lesion proximal in the left anterior descending (LAD)
branch of the left coronary artery or due to either 3 vessel disease or left main
stem stenosis. Recognizing these entities is important in the decision making to
re-open the culprit artery, either pharmacologically or invasively using a
percutaneous coronary intervention or bypass surgery. These strategies have
led to a marked improved in-hospital and post discharge prognosis of unstable
angina during the last decade (7).
The value of serial ECG’s

Diagnosing unstable angina and also non-ST-segment elevation myocardial
infarction can be particularly difficult both in relation to the presence or
absence of chest pain and the changes on the ECG. At the time of recording the
ECG the chest pain may have already subsided. In that situation it is very
important to look for the development of postischemic T wave changes.
They may occur within a few hours. Ideally they should be picked up by a
continuous recording of the 12-lead ECG (8). The importance of this was
recently shown by Akkerhuis et al. (9) who used continuous multilead ST-T
segment monitoring to identify patients with acute coronary syndromes at high
risk of adverse cardiac events. They especially recommended this approach in
patients not showing on admission either clear ST elevation pointing to acute
MI or definite ST segment depression. In those patients diagnostic ST-T
segment changes may occur during continuous multilead ECG monitoring and
can be helpful to identify patients that will profit from an early invasive
intervention. When continuous ECG monitoring is not possible, it is

recommended to keep the patient in the emergency room, to wait for the
troponin value and to record at least one more ECG before deciding to send the
patient home.
Occasionally the ECG findings are not specific even during chest pain,
especially in case of a circumflex coronary artery narrowing or occlusion. Also
in that situation it is very helpful to record sequential ECG’s during the
observation period, to demonstrate ischemia. Keep in mind that a single normal
ECG in a patient with a typical syndrome of chest pain is insufficient to
exclude myocardial ischemia.
The ECG in 3 vessel or left main stem disease

Unstable angina, such as angina at rest carries an increased risk for myocardial
infarction or sudden death. It is important to record the ECG during chest pain,
not only to document the ischemic nature of the complaints, but also to assess
the site and the extent of ischemia. Typically, high-risk situations are proximal
LAD involvement (10,11) 3-vessel disease and left main stem stenosis (12)
(fig. 7.1). The latter 2 conditions result in a typical ECG pattern during chest
pain (figure 7.2) with generalized, often marked ST-segment depression
combined with ST-segment elevation in lead AVR and frequently in In a
study of 120 patients with rest angina we found that the larger the number of
leads with and the greater the amount of ST segment depression, the higher the
risk of 3-vessel disease or main stem stenosis: A 75% positive predictive
accuracy of 3 vessel disease or a left main stenosis was present when 8 leads or
more showed ST-segment changes during chest pain (11), with leads AVR and
showing ST-elevation!
These ECG findings are also valid for determining the extent of ischemia
when they are observed during exercise (figure 7.3). The unstable nature of the
syndrome is confirmed by the persistence of changes during the recovery phase
(figure 7.3C)
The proximal LAD syndrome
During chest pain: Peaked T-waves in the precordial leads

Changes in the ST segment and the T-wave are important to diagnose both
acute and subacute ischemia. During acute ischemia predominant T-wave
changes can be found, without marked changes in the ST-segment. Typically,
the T-waves become peaked, more symmetric and shorter in duration (figure
7.4). These changes reflect ischemia rather than injury and are probably
explained by shortening of the subendocardial repolarization phase with intact
duration of repolarization in the subepicardial layers (13). The coronary
perfusion is not completely blocked either because there is a subtotal stenosis
or a complete occlusion but with collateral circulation.
After chest pain: T wave negativity in the precordial leads

Recording the development of negative T waves in at least the precordial leads
to following the episode of chest pain has been very useful to identify a
subgroup of patients with unstable angina having an increased risk of
subsequent MI or sudden cardiac death (figure 7.5). Coronary angiographic
correlations invariably showed severe proximal stenosis in the left anterior
descending (LAD) branch or total LAD occlusion in the presence of collateral
circulation (10,14,15). LAD obstruction will lead to MI of the anterior wall as
shown in fig. 7.5, which was recorded before the advent of thrombolytic
therapy. Recognition of the ECG pattern of a critical LAD stenosis is important
because vessel occlusion will lead to a large anterior wall myocardial infarction
and early death may occur due to pump failure or high degree sub-AV nodal
block. Ventricular tachycardia may appear later during the subacute and the
chronic phase and can be prevented by prompt measures to restore flow (16).
After an acute coronary syndrome in the anterior wall occasionally giant T
wave negativity can be observed (figure 7.6). This latter phenomenon has
recently been described to predict good prognosis, as evidenced by recovery of
R-waves and preservation of left ventricular function (17).
Recovery of T wave abnormalities following ischemia

In patients having unstable angina because of a proximal LAD stenosis and
surviving for at least 6 months after the ischemic event, our group found
normalization of the ST-T-segment within 6 weeks in half of the population,
and in 80% within 6 months (16). Similar findings were reported in another
study after balloon angioplasty, revealing normalization of the T wave in 90%
of patients after 28 weeks (14). A more recent study also confirmed the rapid
resolution of postischemic T wave inversion (within 3-21 days of presentation
in 75% of cases). Persistence of T wave inversion was related to a worse
outcome: More new events were found during follow-up of these patients,
when compared with an unstable angina group without postischemic T wave
abnormalities (14).
Conclusion
While Troponin determination will document loss of myocardial tissue in

unstable angina the standard 12 lead ECG gives important information about
the site and extent of ischemia. It is possible to identify high risk situations
such as unstable angina due to a proximal LAD lesion or caused by either 3
vessel disease or left main stem stenosis. Recognizing these entities is
important for decision making to restore adequate patency in the culprit
vessel(s).
References
1. Antman EM, Cohen M, Bernink PJ et al. The TIMI risk score for unstable angina from ST
elevation MI: a method for prognosticitation and therapeutic decision making. JAMA 2000;
284:835-842.
2. Kaul P, Fu Y, Shang WC, et al. Prognostic value of ST segment depression in acute

coronary syndromes : insights from PARAGON-A applied to GUSTO-II b. J Am Coll
Cardiol 2001;38:64-71.
3. Savonitto S, Ardissino D, Granger CB, et al. Prognostic value of the admission

electrocardiogram in acute coronary syndromes. JAMA 1999;281:707-713.
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segment depression. Am J Cardiol 1999;84:379-385.
5. Solomon DH, Stone PH, Glynn RJ, et al. Use of risk stratification to identify patients with
unstable angina likeliest to benefit from an invasive versus conservative management
strategy. J Am Coll Cardiol 2001;38:969-976.
6. Didenholm E, Andren B, Frostfeldt G, et al. ST depression in ECG at entry indicates severe

coronary lesions and large benefits of an early invasive treatment strategy in unstable
coronary artery disease. Eur Heart J 2002;23:41-49.
7. Widdershoven JW, Gorgels AP, Vermeer F, et al. Changing characteristics and in-hospital
outcome of patients admitted with acute myocardial infarction. Observations from 1982-
1994. Eur Heart J 1997;1073-1080.
8. Klootwijk P, Mey S, Van Es GA, et al. Comparison of usefulness of computer-assisted

continuous hour 3-lead with 12-lead ECG-ischemia monitoring for detection and
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9. Akkerhuis KM, Klootwijk PAJ, Lindeboom W, et al. Recurrent ischemia during continuous
multilead ST-segment monitoring identifies patients with acute coronary syndromes at high
risk of adverse cardiac events. Eur Heart J 2001; 22:1997-2006.
10. De Zwaan C, Bar FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a
critical stenosis high in left anterior descending coronary artery in patients admitted because
of impending myocardial infarction. Am Heart J 1982;103:730-735.
11. De Zwaan C, Bar FW, Gorgels AP, Wellens HJ. Unstable angina: are we able to recognize
high-risk patients? Chest 1997;112:224-50.
12. Gorgels APM, Vos MA, Mulleneers R, de Zwaan C, Bar FW, Wellens HJ. Value of the
electrocardiogram in diagnosing the number of severely narrowed coronary arteries in rest
angina pectoris. Am J Cardiol 1993;72:999-1003.
13. Fozzard HA, Makielski JC.The electrophysiology of acute myocardial ischemia. Annual
review of medicine 1985;36:275-280.
14. Simon K, Hackett D, Szelier A, et al. The natural history of postischemic T wave inversion:
a predictor of poor short-term prognosis? Coronary Artery Disease 1994;5:937-942.
15. Shawl FA, Velasco CE, Goldbaum TS, Forman BM. Effect of coronary angioplasty on
electrocardiographic changes in patients with unstable angina secondary to left anterior
descending coronary artery disease. J Am Coll Cardiol 1990;16:325-331.
16. De Zwaan C, Bar FW, Janssen JH, et al. Angiographic and clinical characteristics of
patients with unstable angina showing an ECG pattern indicating critical narrowing of the
proximal LAD coronary artery. Am Heart J. 1989;117:657-666.
17. Agetsuma H, Hirai M, Hirayama H, et al. Transient giant negative T-wave in acute anterior
wall infarction predicts R-wave recovery and preservation of left ventricular dysfunction.
Heart 1996;75:229-234.
Index
A sub-AV nodal conduction disturbances, 44
Abnormal ventricular activation, myocardial supraventricular arrhythmias, 87–90
infarction with, 65–83 atrial fibrillation, 88–90
left bundle branch block, 68–75 sinus tachycardia, 87–88
intermittent, 72–73 ventricular arrhythmias, 91–94
practical approach, 74–75 ventricular fibrillation, 93–94
serial ECG’s, 74 ventricular premature beats, 91–92
paced ventricular rhythm, 76–79 ventricular tachycardia, 92–93
ventricular pre-excitation, 79–81 Angina, unstable, ECG in, 117–126
Accelerated idiopathic ventricular rhythm, chest pain
106–109 peaked T-waves in precordial leads,
Acute myocardial infarction 120–122
arrhythmias in, 85–98 T wave negativity in precordial leads, 123
AV-nodal conduction system, 49–53 ischemia, recovery of T wave abnormalities
atrio-ventricular nodal level following, 124
ECG findings, 49–51 left main stem disease, 120
incidence, 52–53 proximal LAD syndrome, 120–124
left bundle branch block, inferior serial ECG’s, 119–120
wall myocardial infarction, ST segment depression, 119
51–52 Anterior wall infarction, coronary artery
conduction abnormalities, occlusion, 24–37
atrio-ventricular nodal level, 49–53 distal LAD occlusion, 28–29
management, 53 LAD occlusion
conduction abnormalities, sub-AV-nodal distal to first diagonal branch, proximal to
level, 53–63 first septal branch, 31–32
ECG findings, 53–59 distal to first septal branch, proximal to first
incidence, 60–61 diagonal branch, 30
management, 61–62 proximal to first septal, first diagonal
conduction disturbances, 43–64 branch high risk, 26–28
sino-atrial region, 45–49 left main occlusion, 33–34
atrio-ventricular conduction system, new infarction in presence of old one, 36
45–46 site of occlusion in, criteria to identify, 33
blood supply of sinus node, ST deviation score, location, coronary artery
atrio-ventricular conduction occlusion, 34–36
system, 45 ST segment vector, to localize site of
ECG findings, 46 ischemia, 25–26
incidence, 47 Anterior wall myocardial infarction, coronary
management, 48–49 artery occlusion, grades of ischemia, 12
sino atrial block, sinus arrest, 47–48 Arrhythmias in acute myocardial infarction,
sinus bradycardia, 46 85–98
sinus node, sino-atrial region, 45 supraventricular arrhythmias, 87–90
slow rhythms, conduction atrial fibrillation, 88–90
abnormalities, sinus nodal, sinus tachycardia, 87–88
sino-atrial level, 46 ventricular arrhythmias, 91–94
sinus arrest, sino-atrial block, 44 ventricular fibrillation, 93–94
ventricular premature beats, 91–92 Conduction disturbances, acute myocardial

ventricular tachycardia, 92–93 infarction, 43–64
Atrial fibrillation, 88–90 AV-nodal conduction system, 49–53
Atrial tachycardia, 106 atrio-ventricular nodal level
Atrio-ventricular conduction system ECG findings, 49–51
acute myocardial infarction, 45 incidence, 52–53
conduction disturbances, 45 left bundle branch block, inferior wall
acute myocardial infarction, sino-atrial myocardial infarction, 51–52
region, 45–46 mechanism, 52–53
sino-atrial region, 45 prognostic significance, 52–53
sinus node, blood supply of, 45 conduction abnormalities, atrio-ventricular
Atrio-ventricular nodal level nodal level, 49–53
acute myocardial infarction, ECG management, 53
findings, 49–51 conduction abnormalities, sub-AV-nodal level,
AV-nodal conduction system, conduction 53–63
disturbances, 49–51 ECG findings, 53–59
AV nodal conduction disturbances, incidence, 60–61
conduction disturbances, acute management, 61–62
myocardial infarction, 44 mechanism, 60–61
AV-nodal conduction system, conduction prognostic significance, 60–61
disturbances, acute myocardial sino-atrial region, 45–49
infarction, 49–53 atrio-ventricular conduction system, 45–46
atrio-ventricular nodal level blood supply of sinus node,
ECG findings, 49–51 atrio-ventricular conduction system, 45
incidence, 52–53 ECG findings, 46
left bundle branch block, inferior wall incidence, 47
myocardial infarction, 51–52 management, 48-49
conduction abnormalities, mechanisms, 47
atrio-ventricular nodal level, 49–53 prognostic significance, 47
management, 53 sino atrial block, sinus arrest, 47–48
sinus bradycardia, 46
sinus node, sino-atrial region, 45
B slow rhythms, conduction abnormalities,
Blood supply of sinus node, 45 sinus nodal, sino-atrial level, 46
Brady arrhythmias, 111–112 sinus arrest, sino-atrial block, 44
ECG findings, 111 sub-AV nodal conduction disturbances, 44
incidence, 111 Coronary artery
mechanism, 111 anterior wall infarction, 24–37
prognosis, 111 distal LAD occlusion, 28–29
LAD occlusion
distal to first diagonal branch, proximal
C to first septal branch, 31–32
Chest pain distal to first septal branch, proximal to
peaked T-waves in precordial leads, first diagonal branch, 30
120–122 proximal to first septal, first diagonal
T wave negativity in precordial leads, 123 branch high risk, 26–28
Conduction abnormalities left main occlusion, 33–34
acute myocardial infarction, new infarction in presence of old one, 36
sub-AV-nodal level, 53–63 site of occlusion in, criteria to identify, 33
ECG findings, 53–59 ST deviation score, location of coronary
incidence, 60–61 artery occlusion, 34–36
management, 61–62 ST segment vector, to localize site of
AV-nodal conduction system, acute ischemia, 25–26
myocardial infarction, anterior wall myocardial infarction, grades of
atrio-ventricular nodal level, 49–53 ischemia, 12
INDEX 129
coronary artery, infero-posterior wall atrial, 88–90

infarction, 13–24 ventricular, 93–94
identification of, 5–42
anterior wall infarction, 8–9
distal LAD occlusion, 8–9 I
LAD occlusion Inferior wall myocardial infarction, left bundle
distal to first diagonal, proximal to branch block, atrio-ventricular nodal level,
first septal branch, 8 51–52
distal to first septal, proximal to Infero posterior myocardial infarction, coronary
first diagonal branch, 8 artery occlusion, grades of ischemia, 12
proximal to first septal, first Infero-posterior wall infarction, coronary artery
diagonal branch, 8 occlusion
ECG patterns, 7–9 atrial infarction, 24
infero posterior infarction, 7–8 AV nodal block, 24
atrial infarction, 8 coronary patho-anatomy, 13–15
lateral wall involvement, 8 CX occlusion, diagnosing, difficulties in, 24
posterior wall involvement, 7 dominance, 15
ST depression in precordial leads, inferior wall myocardial infarction, RCA, CX
7 occlusion in, 15–17
proximal, distal RCA, 7 isolated RV infarction, 22–23
RCA, CX, 7 lateral wall involvement, 17
infero posterior myocardial infarction, posterior wall involvement, 17
grades of ischemia, 12 RV infarction, 18–21
infero-posterior wall infarction
atrial infarction, 24
AV nodal block, 24 L
coronary patho-anatomy, 13–15 Left bundle branch block, 68–75
CX occlusion, diagnosing, difficulties acute myocardial infarction, 51–52
in, 24 AV-nodal conduction system, conduction
dominance, 15 disturbances, 51–52
inferior wall myocardial infarction, inferior wall myocardial infarction,
RCA, CX occlusion in, 15–17 atrio-ventricular nodal level, 51–52
isolated RV infarction, 22–23 intermittent, 72–73
lateral wall involvement, 17 practical approach, 74–75
posterior wall involvement, 17 serial ECG’s, 74
RV infarction, 18–21 Left main stem disease, 120
mortality, clinical, ECG variables, 10
severity of ischemia, 5–42
site of occlusion, coronary artery, ECG M
patterns, 13–37 Myocardial infarction, with abnormal ventricular
size of area at risk, 5–42 activation, 65–83
ST segment deviation score, 7, 9–11 left bundle branch block, 68–75
terminal QRS-ST segment pattern, 7 intermittent, 72–73
severity of cardiac ischemia, 11–13 practical approach, 74–75
Coronary artery occlusion, severity of serial ECG’s, 74
ischemia, 5–42 paced ventricular rhythm, 76–79
ventricular pre-excitation, 79–81
E
Ectopic activity, 105 N
ECG findings, 105 Non-sustained ventricular tachycardia, 106, 109
F O
Fibrillation Occlusion, coronary artery
anterior wall infarction, 24–37 atrial infarction, 8

distal LAD occlusion, 28–29 lateral wall involvement, 8
LAD occlusion posterior wall involvement, 7
distal to first diagonal branch, ST depression in precordial leads, 7
proximal to first septal branch, proximal, distal RCA, 7
31–32 RCA, CX, 7
distal to first septal branch, proximal size of area at risk, 5–42
to first diagonal branch, 30 ST segment deviation score, 7, 9–11
proximal to first septal, first diagonal terminal QRS-ST segment pattern, 7
branch high risk, 26–28 severity of cardiac ischemia, 11–13
left main occlusion, 33–34
new infarction in presence of old one,
36 P
site of occlusion in, criteria to identify, Pre-excitation, ventricular, 79–81
33 Premature beats, ventricular, 91–92
ST deviation score, location of
coronary artery occlusion, 34–36
ST segment vector, to localize site of R
ischemia, 25–26 Reperfusion, ECG signs of, 99–116
anterior wall myocardial infarction, accelerated idiopathic ventricular rhythm, 106
grades of ischemia, 12 atrial tachycardia, 106
infero posterior myocardial infarction, brady arrhythmias, 111–112
grades of ischemia, 12 ECG findings, 111
infero-posterior wall infarction incidence, 111
atrial infarction, 24 ectopic activity, 105
AV nodal block, 24 ECG findings, 105
coronary patho-anatomy, 13–15 non-sustained ventricular tachycardia, 106,
CX occlusion, diagnosing, difficulties 109
in, 24 reperfusion arrhythmias, defined, 106
dominance, 15 sinus bradycardia, 106
inferior wall myocardial infarction, ST-T segment behavior, 101–105
RCA, CX occlusion in, 15–17 incidence, 104–105
isolated RV infarction, 22–23 ST segment changes, 101–103
lateral wall involvement, 17 T wave changes, 103–104
posterior wall involvement, 17 supraventricular arrhythmias, 110
RV infarction, 18–21 ECG findings, 110
mortality, clinical, ECG variables, 10 incidence, 110
site of, identification, 5–42 ventricular premature beats, 106–109
site of occlusion increase in, 106
coronary artery Reperfusion arrhythmias, defined, 106
ECG patterns, 13–37
infero-posterior wall infarction,
13–24 S
identification of Sino-atrial block
anterior wall infarction, 8–9 conduction disturbances, acute myocardial
distal LAD occlusion, 8–9 infarction, sinus arrest, 44
LAD occlusion sino-atrial region, conduction disturbances,
distal to first diagonal, proximal acute myocardial infarction, sinus arrest,
to first septal branch, 8 47–48
distal to first septal, proximal to Sino-atrial region
first diagonal branch, 8 conduction disturbances, acute myocardial
proximal to first septal, first infarction, 45–49
diagonal branch, 8 atrio-ventricular conduction system, 45–46
ECG patterns, 7–9 blood supply of sinus node,
infero posterior infarction, 7–8 atrio-ventricular conduction system, 45
INDEX 131
ECG findings, 46 Slow rhythms

incidence, 47 conduction disturbances, acute myocardial
management, 48–49 infarction, sino-atrial region, conduction
sino atrial block, sinus arrest, 47–48 abnormalities, sinus nodal, sino-atrial
sinus bradycardia, 46 level, 46
sinus node, sino-atrial region, 45 sinus nodal, sino-atrial level, conduction
slow rhythms, conduction disturbances, acute myocardial
abnormalities, sinus nodal, infarction, sino-atrial region, 46
sino-atrial level, 46 ST segment deviation score, coronary artery
sinus node, conduction disturbances, occlusion, 7, 9–11
acute myocardial infarction, ST-T segment behavior, 101–105
sino-atrial region, 45 incidence, 104–105
Sinus arrest mechanism, 104–105
sino atrial block, sino-atrial region, prognastic implications, 104–105
conduction disturbances, acute ST segment changes, 101–103
myocardial infarction, 47–48 T wave changes, 103–104
sino-atrial block, conduction disturbances, Sub-AV nodal conduction disturbances,
acute myocardial infarction, 44 conduction disturbances, acute myocardial
Sinus bradycardia, 106 infarction, 44
sino-atrial region, conduction Supraventricular arrhythmias, 87–90, 110
disturbances, acute myocardial atrial fibrillation, 88–90
infarction, 46 ECG findings, 110
Sinus node incidence, 110
blood supply of, atrio-ventricular mechanism, 110
conduction system, conduction prognosis, 110
disturbances, acute myocardial sinus tachycardia, 87–88
infarction, sino-atrial region, 45
sino-atrial region, conduction
disturbances, acute myocardial T
infarction, sino-atrial region, 45 Tachycardia
Sinus tachycardia, 87–88 sinus, 87–88
Site of occlusion ventricular, 92–93
coronary artery Terminal QRS-ST segment pattern
coronary artery occlusion coronary artery occlusion, 7
ECG patterns, 13–37 severity of cardiac ischemia, coronary artery
infero-posterior wall infarction, occlusion, 11–13
13–24
identification of, 5–42
identification of, coronary artery occlusion U
anterior wall infarction, 8–9 Unstable angina, ECG in, 117–26
distal LAD occlusion, 8–9 chest pain
LAD occlusion, 8 peaked T-waves in precordial leads,
proximal to first septal, first 120–122
diagonal branch, 8 T wave negativity in precordial leads, 123
ECG patterns, 7–9 ischemia, recovery of T wave abnormalities
infero posterior infarction, 7–8 following, 124
atrial infarction, 8 left main stem disease, 120
lateral wall involvement, 8 proximal LAD syndrome, 120–124
posterior wall involvement, 7 serial ECG’s, 119–120
ST depression in precordial leads, ST segment depression, 119
7
proximal, distal RCA, 7
RCA, CX, 7 V
Size of area at risk, coronary artery Ventricular activation, abnormal, myocardial
occlusion, 5–42 infarction with, 65–83
left bundle branch block, 68–75 ventricular premature beats, 91–92

intermittent, 72–73 ventricular tachycardia, 92–93
practical approach, 74–75 Ventricular fibrillation, 93–94, 109
serial ECG’s, 74 Ventricular pre-excitation, 79–81
paced ventricular rhythm, 76–79 Ventricular premature beats, 91–92, 106–109
ventricular pre-excitation, 79–81 increase in, 106
Ventricular arrhythmias, 91–94 Ventricular tachycardia, 92–93

Wellens - EKG in AMI and Unstable Angina - 2002

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THE ECG IN

Previous volumes are still available

Diagnosis and Risk Stratification

Hein J.J. Wellens

KLUWER ACADEMIC PUBLISHERS

©2002 Kluwer Academic Publishers

Print ©2003 Kluwer Academic Publishers

All rights reserved

Created in the United States of America

Visit Kluwer Online at: http://kluweronline.com

Chapter 2 Determining the size of the area at risk, the severity

Chapter 3 Conduction disturbances in acute myocardial

Chapter 4 Myocardial infarction in the presence of abnormal

Chapter 7 The electrocardiogram in unstable angina 117

Kluwer Academic Publishers

Developments in Cardiovascular Medicine

Previous volumes are still available

Pieter A. Doevendans, M.D.

Anton P. Gorgels, M.D.

Hein J.J.Wellens, M.D.

Hein J.J. Wellens

The electrocardiogram (ECG) remains the most accessible and inexpensive

Determining the size of the area at risk, the severity of

A. ST SEGMENT DEVIATION SCORE

More than 15 mm indicates an area sufficiently large to attempt

B. THE TERMINAL QRS-ST SEGMENT PATTERN

C. SPECIFIC ECG PATTERNS: IDENTIFYING THE SITE OF

I Infero posterior infarction

RCA 1. ST elevation in lead III higher than in lead II

CX 1. ST elevation in lead II higher than in lead III

Proximal (with right ventricular infarction) or distal RCA?

Posterior wall involvement?

ST depression in precordial leads

Lateral wall involvement?

ST elevation in leads I, AVL, and

Pta segment elevation in lead II

II Anterior wall infarction

LAD occlusion proximal to first septal and first diagonal branch

Acquired right bundle branch block

LAD occlusion distal to first septal and proximal to first diagonal

ST depression lead III> Lead II

LAD occlusion distal to first diagonal and proximal to first septal

Signs of occlusion proximal to first septal branch

Distal LAD occlusion

In acute myocardial infarction (MI) the surface electrocardiogram (ECG)

A. THE ST SEGMENT DEVIATION SCORE

The number of ECG leads showing ST segment deviation (elevation or

It is important to know that in the very acute phase of ischemia locally

B) THE TERMINAL QRS-ST SEGMENT PATTERN AND THE

C. SPECIFIC ECG PATTERNS: IDENTIFYING THE SITE OF

In cardiac ischemia the direction and displacement of the ST segment is

I Infero-posterior wall infarction

RCA or CX occlusion in acute inferior wall myocardial infarction?

in an iso-electric ST segment in lead I. In our experience ST segment

Posterior wall involvement

Lateral wall involvement

Therefore it is necessary to record the right precordial leads. Figure 2.6

In a minority of cases of RV involvement the precordial lead shows ST-

Difficulties in diagnosing CX occlusion

II Anterior wall infarction

Involvement of the distal AV conduction system leads to impaired conduction,

The ST segment vector to localize the site of ischemia

As shown in a recent study by Engelen et al (49) occlusions at different sites