THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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.):
ISBN: 0-7923-6337-X
Arrhythmias and Sudden Death in Athletes. 2000
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
NEW YORK, BOSTON, DORDRECHT, LONDON, MOSCOW


eBook ISBN:
Print ISBN:

0-306-48202-9
1-4020-7214-7

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CONTENTS

Chapter 1

Introduction

Chapter 2

Determining the size of the area at risk, the severity

1

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:
I

Infero-posterior myocardial infarction with
or without right ventricular infarction

II Anterior wall myocardial infarction

Chapter 3

Chapter 4

13

13
24

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

Myocardial infarction in the presence of abnormal
ventricular activation

65

A. Left bundle branch block

68

B.

76

Paced ventricular rhythm

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.
233.
234.
235.
236.
237.
238.
239.
240.
241.

242.
243.
244.

245.

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
J-C. Tardif and M.G. Bourassa (eds): Antioxidants and Cardiovascular Disease.
2000.
ISBN: 0-7923-7829-6
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
M.H. Ellestad and E. Amsterdam (eds): Exercise Testing: New Concepts for the
New Century. 2001.
ISBN: 0-7923-7378-2
Douglas L. Mann (ed.): The Role of Inflammatory Mediators in the Failing
Heart. 2001
ISBN: 0-7923-7381-2
Donald M. Bers (ed.): Excitation-Contraction Coupling and Cardiac
ISBN: 0-7923-7157-7
Contractile Force, Second Edition. 2001
Brian D. Hoit, Richard A. Walsh (eds.): Cardiovascular Physiology in the
Genetically Engineered Mouse, Second Edition. 2001 ISBN 0-7923-7536-X
Pieter A. Doevendans, A.A.M. Wilde (eds.): Cardiovascular Genetics for Clinicians
2001
ISBN 1-4020-0097-9
Stephen M. Factor, Maria A.Lamberti-Abadi, Jacobo Abadi (eds.): Handbook of
Pathology and Pathophysiology of Cardiovascular Disease. 2001

ISBN 0-7923-7542-4
Liong Bing Liem, Eugene Downar (eds): Progress in Catheter Ablation. 2001
ISBN 1-4020-0147-9
Pieter A. Doevendans, Stefan Kääb (eds): Cardiovascular Genomics: New
ISBN 1-4020-7022-5
Pathophysiological Concepts. 2002
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
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
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
Introduction

1


INTRODUCTION

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
myocardial infarction.
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

3

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

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.
2.

ST elevation in lead III higher than in lead II
ST depression in lead I

CX

1.
2.
3.

ST elevation in lead II higher than in lead III
ST iso-electric or elevated in lead I
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

7


8

THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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


SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION

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.

9


10

THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA


SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION

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 significance 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

11


12

THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA


SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION

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)

13


14

THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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


SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION

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

15


16

THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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


SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION

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 STdepression (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.

17