The ECG in Acute Myocardial Infarction and Unstable Angina (Developments in Cardiovascular Medicine)

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

©2002 Kluwer Academic Publishers New York, Boston, Dordrecht, London, Moscow Print ©2003 Kluwer Academic Publishers Dordrecht All rights reserved No part of this eBook may be reproduced or transmitted in any form or by any means, electronic, mechanical, recording, or otherwise, without written consent from the Publisher Created in the United States of America Visit Kluwer Online at: and Kluwer's eBookstore at:

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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.): ISBN: 0-7923-6337-X Arrhythmias and Sudden Death in Athletes. 2000 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

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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

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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

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Chapter Introduction

1

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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

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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

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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

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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.

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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

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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)

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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

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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.

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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.

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

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.

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

In a minority of cases of RV involvement the precordial lead shows STelevation. 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).

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

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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).

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

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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 inferoapical 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.

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

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).

25

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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

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

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.

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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.

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

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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).

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

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).

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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

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

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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.

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

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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.

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

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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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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Birnbaum Y, Maynard C, Wolfe S, et al. Terminal QRS distortion on admission is better than ST segment measurements in predicting final infarct size and assessing the potential effect of thrombolytic therapy in anterior wall acute myocardial infarction. Am J Cardiol 1999;84:530-539.

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Herz I, Assali AR, Adler Y, Solodky A, Sclarovsky S. New electrocardiographic criteria for predicting either the right or left circumflex artery as the culprit coronary artery in inferior wall acute myocardial infarction. Am J Cardiol 1997;80:1343-1345.

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Kontos M, Desai PV, Jesse RL, Ornato JP. Usefulness of the admission electrocardiogram for identifying the infarct related artery in inferior wall acute myocardial infarction. Am J Cardiol 1997;79:182-184.

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Borgia MC, Gori F, Pellicelli A, Curcio D, Lionetti M, Buccarella PA, Lucidi M. Influence of thrombolytic therapy on inferior acute myocardial infarction with concomitant anterior ST segment depression. Angiology 1999;50:619-628.

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Birnbaum Y, Wagner GS, Barbash GI et al. Correlation of angiographic findings and right versus left precordial ST-segment depression in inferior wall acute myocardial infarction. Am J Cardiol 1999;83:143-148.

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Shah A, Wagner GS, Green CL, et al. Electrocardiographic differentation of the STsegment depression of acute myocardial injury due to left circumflex artery occlusion from that of myocardial ischemia of nonocclusive etiologies. Am J Cardiol 1997;80:512-513.

27.

Casas R, Marriott HJL, Glancy L. Value of leads in diagnosing posterior wall acute myocardial infarction and other causes of tall R waves in Am J Cardiol 1997;80:89.

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28.

Matetzky S, Freimark D, Chouraqui P, et al. Significance of ST segment elevations in posterior chest leads (V7 to V9) in patients with acute inferior myocardial infarction: application for thrombolytic therapy. J Am Coll Cardiol 1998;31:506-511.

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Assali A, Sclarovsky S, Herz I, et al. Comparison of patients with inferior wall acute myocardial infarction with versus without ST-segment elevation in leads V5 and V6. Am J Cardiol 1998;81:81-83.

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Braat SH, Brugada P, de Zwaan C, Wellens HJJ. Value of electrocardiogram in diagnosing right ventricular involvement in patients with an acute inferior wall myocardial infarction. Br Heart J 1983;49:368-372.

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Berger PB, Ruocco N, Ryan T, Frederick M, Jacobs A, Faxon D. Incidence and prognostic implications of heart block complicating acute inferiotr myocardial infarction treated with thrombolytic therapy: results from TIMI II. J Am Coll Cardiol 1992;20:533-540.

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Kimura K, Kosuge M, Ishikawa T, et al. 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;83:731-733.

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Klein HO, Trjordman T, Ninio R, et al. The early recognition of right ventricular infarction: diagnostic accuracy of the electrocardiographic V4R lead. Circulation 1983;67:558-565.

35.

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.

36.

Berger PB, Ryan TJ. Inferior myocardial infarction: high-risk sub-groups. Circulation 1990;81:401-411.

37.

Berger PB, Ruocco NA, Ryan TJ, et al. Frequency and significance of right ventricular dysfunction during inferior wall left ventricular myocardial infarction treated with thrombolytic therapy (results from the Thrombolysis in Myocardial Infarction (TIMI) II trial. Am J Cardiol 1993;71:1148-52.

38.

Zehender M, Kapere W, Kauder E, et al. Right ventricular infarction as independent predictor of prognosis after acute myocardial infarction. N Engl J Med 1993;328:981-988.

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Zeymer U, Neuhaus KL, Wegscheider K, Tebbe U, Molhoek P, Schroder R, for HIT-4 Trial Group. Effects of thrombolytic therapy in acute inferior myocardial infarction with or without right ventricular involvement. J Am Coll Cardiol 1998;32:876-881.

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Buono H, Lopez-Palop R, Bermejo J, Lopez-Sendon JL, Delcan JL. In-hospital outcome of elderly patients with acute myocardial infarction and right ventricular involvement. Circulation 1997;96:436-441.

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Buono H, Lopez-Palop R, Perez-David E, Garcia-Garcia J, Lopez-Sendon JL, Delcan JL. Combined effect of age and right ventricular involvement on acute inferior myocardial infarction. Circulation 1998;98:1714-1720.

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42.

Mehta SR, Eikelboom JW, Natarajan MK, et al. Impact of right ventricular involvement on mortality and morbidity in patients with inferior myocardial infarction. J Am Coll Cardiol 2001;37:37-43.

43.

Braat SH, Gorgels APM, Bar FWHM, Wellens HJJ. Value of the ST-T segment in lead V4R in inferior wall acute myocardial infarction to predict the site of coronary artery occlusion. Am J Cardiol 1998;62:140-142.

44.

Mittal SR. Isolated right ventricular infarction. Int J Cardiol. 1994;46:53-60.

45.

Van der Bolt CLB, Vermeersch PHMJ and Plokker HWM. Isolated acute occlusion of a large right ventricular branch of the right coronary artery following coronary balloon angioplasty. Eur Heart J 1996;17:247-250.

46. Li e 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. 47.

Lie KI, Wellens HJ,Schuilenburg RM, David GK, Durrer D. Early identification of patients developing late in-hospital fibrillation after discharge from the CCU. Am J Cardiol 1978;41:674-677.

48.

Melgarejo-Moreno A, Galcera-Tomas J, Garcia-Alberola A, et al. Incidence, clinical characteristics, and prognostic significance of right bundle-branch block in acute myocardial infarction: a study in the thrombolytic era. Circulation 1997;96:1139-1146.

49.

Engelen DJ, Gorgels AP, Cheriex EC, et al. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol. 1999;34:389-395

50.

Birnbaum Y, Solodky A, Herz I et al. Implications of inferior ST-segment depression in acute anterior myocardial infarction: electrocardiographic and angiographic correlation. Am Heart J 1994;127:1467-73.

51.

Tamura A, Kataoka H, Mikuriya Y, Nasu M. Inferior ST-segment depression as a useful marker for identifying proximal left anterior descending artery occlusion during acute anterior wall myocardial infarction. Eur Heart J 1995;16:1795-9.

52.

Porter A, Sclarovsky S, Ben-Gal T, Herz I, Solodky A, Sagie A. Value of T wave inversion with lead III ST-segment depression in acute anterior myocardial infarction: electrocardiographic prediction of a wrapped left anterior descending coronary artery. Clin Cardiol 1998;21:562-6.

53.

Sapin PM, Musselman DR, Dehmer GJ, Cascio WE. Implications of inferior ST-segment elevation accompanying anterior wall acute myocardial infarction for the angiographic morphology of the left anterior descending coronary artery morphology and site of occlusion. Am J Cardiol 1992;69:860-865.

54.

Tamura A, Kataoka H, Nagase K, Mikuriya Y, Nasu M. Clinical significance of inferior ST elevation during acute myocardial infarction. Br Heart J 1995;74:611-614.

55.

Kataoka H, Tamura A,Yano S,Kanzaki K,Mikuriya Y. ST elevation in the right chest leads in anterior wall ventricular acute myocardial infarction. J Am Cardiol 1990;66:1146-1147.

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

56.

Yamaji H, Iwasachi S, Kusachi S, et al. Prediction of acute left main coronary obstruction by 12-lead electrocardiogram:AVR ST-segment elevation with less V, ST-segment elevation. J Am Coll Cardiol 2001;38:1348-1354.

Chapter 3 Conduction disturbances in acute myocardial infarction

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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

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).

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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 sinoatrial 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).

CONDUCTION DISTURBANCES IN ACUTE MYOCARDIAL INFARCTION

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 sinoatrial 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 Mobitz2 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.

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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 BezoldJarisch 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,

CONDUCTION DISTURBANCES IN ACUTE MYOCARDIAL INFARCTION

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).

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

CONDUCTION DISTURBANCES IN ACUTE MYOCARDIAL INFARCTION

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

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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

CONDUCTION DISTURBANCES IN ACUTE MYOCARDIAL INFARCTION

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

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CONDUCTION DISTURBANCES IN ACUTE MYOCARDIAL INFARCTION

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).

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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)

CONDUCTION DISTURBANCES IN ACUTE MYOCARDIAL INFARCTION

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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

CONDUCTION DISTURBANCES IN ACUTE MYOCARDIAL INFARCTION

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.

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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

CONDUCTION DISTURBANCES IN ACUTE MYOCARDIAL INFARCTION

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 subAV 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 longterm 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.

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CONDUCTION DISTURBANCES IN ACUTE MYOCARDIAL INFARCTION

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.

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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

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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

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.

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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

MYOCARDIAL INFARCTION IN THE PRESENCE OF ABNORMAL VENTRICULAR ACTIVATION

(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)

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MYOCARDIAL INFARCTION IN THE PRESENCE OF ABNORMAL VENTRICULAR ACTIVATION

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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.

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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 myocardial infarction.

MYOCARDIAL INFARCTION IN THE PRESENCE OF ABNORMAL VENTRICULAR ACTIVATION

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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).

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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.

MYOCARDIAL INFARCTION IN THE PRESENCE OF ABNORMAL VENTRICULAR ACTIVATION

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.

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MYOCARDIAL INFARCTION IN THE PRESENCE OF ABNORMAL VENTRICULAR ACTIVATION

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.

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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.

MYOCARDIAL INFARCTION IN THE PRESENCE OF ABNORMAL VENTRICULAR ACTIVATION

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;94:23412350. 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.

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Chapter 5 Arrhythmias in acute myocardial infarction Incidence and prognostic significance

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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

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.

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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

ARRHYTHMIAS IN ACUTE MYOCARDIAL INFARCTION

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).

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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.

ARRHYTHMIAS IN ACUTE MYOCARDIAL INFARCTION

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.

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Chiladakis et al. (24) recently showed that also in the thrombolytic era Ron-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

ARRHYTHMIAS IN ACUTE MYOCARDIAL INFARCTION

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).

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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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References 1.

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Crimm A, Severance HW Jr, Coffey K. Prognostic signifiance of isolated sinus tachycardia during the first three days of acute myocardial infarction. Am J Med 1984;76:983-988.

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Lee KL, Woodlief LH, Topol EJ, et al., for the GUSTO-1 Investigators. Predictors of 30day mortality in the era of reperfusion for acute myocardial infarction. Results from an international trial of 41021 patients. Circulation 1995;91:1659-1668.

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Goldberg RJ, Seeley D, Becker RC. Impact of atrial fibrillation on the in-hospital and long term survival of patients with acute myocardial infarction: a community wide perspective. Am Heart J 1990;114:996-1003.

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Rathore SS, Berger AK, Weinfurt KP et al. Acute myocardial infarction complicated by atrial fibrillation in the elderly. Prevalence and outcomes. Circulation 2000; 101:969-974.

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Madias JE, Patel DC, Singh D. Atrial fibrillation in acute myocardial infarction: a prospective study based on data from a consecutive series of patients admitted to the coronary care unit. Clin Cardiol 1996;19:180-186.

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Vaage-Nilsen M, Hansen JF, Mellemgaard K, Hagerup L, Sigurd B, Steinmetz E, for the DAVIT II Study Group. Short- and long-term prognostic implications of in-hospital postinfarction arrhythmias. Cardiology 1995:86:49-55.

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Sugiura T, Iwasaka T, Ogawa A, Shiroyama Y, Tsuji H, Onoyama H, Inada M. Atrial fibrillation in acute myocardial infarction. Am J Cardiol 1985;56:27-29.

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Serrano CV, Ramiers JAF, Mansur AP, Pileggi F. Importance of the time of onset of supraventricular tachyarrhythmias on prognosis of patients with acute myocardial infarction. Clin Cardiol 1995;18:84-90.

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15.

Behar S, Zahavi Z, Goldbourt U, Reicher-Reiss H, for the SPRINT-study group. Long-term prognosis of patients with paroxysmal atrial fibrillation complicating acute myocardial infarction. Eur Heart J 1992;13:45-50.

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Eldar M, Canetti M, Rotstein Z, Boyko V, Gottlieb S, Kaplinsky E, Behar S, for the SPRINT and Thrombolytic Survey groups. Significance of paroxysmal atrial fibrillation complicating acute myocardial infarction in the thrombolytic era. Circulation 1998;97:965970.

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Crenshaw BS, Ward SR, Granger CB, Stebbins AL, Topol EJ, Califf RM, for the GUSTOI Trial Investigators. Atrial fibrillation in the setting of acute myocardial infarction; the GUSTO-I experience. J Am Coll Cardiol 1997;30:406-413.

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Sakata K, Kurihara H, Iwamori K, et al. Clinical and prognostic significance of atrial fibrillation in acute myocardial infarction. Am J Cardiol 1997;80:1522-1527.

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Liem KL, Lie KI, Durrer D, Wellens HJJ. Clinical setting and prognostic significance of atrial fibrillation complicating acute myocardial infarction. Eur J Cardiol 1976;4:59-62.

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Lown B, Fakhro AM, Hood WB, et al. The coronary care unit: new perspectives and directions. JAMA 1967;119:188-198.

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Lawrie DM, Higgins MR, Godman MJ, et al. Ventricular fibrillation complicating acute myocardial infarction. Lancet 1968;2:523-528.

22.

Dhurandar RW, MacMillan RL, Brown KWG. Primary ventricular fibrillation complicating acute myocardial infarction. Am J Cardiol 1971;27:347-351.

23.

Lie KI, Wellens HJJ, Durrer D. Characteristics and predictability of primary ventricular fibrillation. Eur J Cardiol 1974;1:379-384.

24.

Chiladakis JA, Karapanos G, Davlouros P, Aggelopoulos G, Alexopoulos D, Manolis AS. Significance of R-on-T phenomenon in early ventricular tachyarrhythmia susceptibility after acute myocardial infarction in the thrombolytic era. Am J Cardiol 2000;85:289-293.

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Lie KI, Wellens HJJ, Van Capelle FJ, Durrer D. Lidocaine in the prevention of primary ventricular fibrillation. New Engl J Med 1974;291:1324-1326.

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Antman EM, Berlin JA. Declining incidence of ventricular fibrillation in myocardial infarction. Implications for the prophylactic use of lidocaime. Circulation 1992; 86: 764773.

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Wellens HJJ, Lie KI, Durrer D. Further observations on ventricular tachycardia as studied by electrical stimulation of the heart. Chronic recurrent ventricular tachycardia and ventricular tachycardia during acute myocardial infarction. Circulation 1974;49:647-653.

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Newby KH, Thompson T, Stebbins A, Topol EJ, Califf RM, Natale A; for the GUSTO investigators. Sustained ventricular arrhythmias in patients receiving thrombolytic therapy. Incidence and outcomes. Circulation 1998;98:2567-2573.

29.

Wellens HJJ, Bär FW, Vanagt EJ, Brugada P. Medical treatment of ventricular tachycardia. Considerations in the selection of patients for surgical treatment. Am J Cardiol 1982;49:186-193.

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30.

Heidbuchel H, Tack J, Vanneste L, Ballet A, Ector H, Van de Werf F. Significance of arrhythmias during the first 24 hours of acute myocardial infarction treated with alteplase and effect of early administration of beta-blocker or a bradycardiac agent on their incidence. Circulation 1994;89:1051-1059.

31.

Gorgels AP, Vos MA, Letsch JS, et al. Usefulness of the accelerated idioventricular rhythm as a marker for myocardial necrosis and reperfusion during thrombolytic therapy in acute myocardial infarction. Am J Cardiol 1988;61:231-235.

32.

Engelen DJ, Gressin V, Theuns DA, et al. Incidence and duration of reperfusion arrhythmias predict left ventricular wall motion abnormalities in reperfused anterior wall myocardial infarction. Submitted.

33.

Volpi A, Maggioni A, Franzosi MJ, Pampallona S, Mauri F, Tognoni G. In hospital prognosis of patients with acute ventricular infarction complicated by primary ventricular fibrillation. N Engl J Med 1987; 317:257-261.

34.

Behar S, Goldbourt U, Reicher-Reiss H, Kaplinsky E, and the principal investigators of the SPRINT-study. Prognosis of acute myocardial infarction complicated by primary ventricular fibrillation. Am J Cardiol 1990;66:1208-1211.

35.

Tofler GH, Stone PH, Muller JE, et al. Prognosis after cardiac arrest due to ventricular tachycardia or ventricular fibrillation associated with acute myocardial infarction (the Milis study). Am J Cardiol 1987;60:755-761.

36.

Chiriboga D, Yarzebski J, Goldberg RJ, Gore JM, Alpert JS. Temporal trends (1975 through 1990) in the incidence and case fatality rates of primary ventricular fibrillation complicating acute myocardial infarction. Circulation 1994; 89: 998-1003.

37.

Berger PB, Ruocco NA, Ryan TJ, Frederick MM, Podrid PJ, and the TIMI investigators. Incidence and significance of ventricular tachycardia and fibrillation in the absence of hypotension or heart failure in acute myocardial infarction treated with recombinant tissuetype plaminogen activator: results from the thrombolysis in myocardial infarction (TIMI) phase II trial. J Am Coll Cardiol 1993; 22: 1773-1779.

38.

Brezins M, Elyassov S, Elimelech I, Roguin N. Comparison of patients with acute myocardial infarction with and without ventricular fibrillation. Am J Cardiol 1996;78:948950.

39.

Gheeraert PJ, Henriques JPS, de Buyzere ML, et al. Out-of-hospital ventricular fibrillation in patients with acute myocardial infarction. J Am Coll Cardiol 2000; 35: 144-150.

40.

Lie KI, Liem KL, Schuilenburg RM, David GK, Durrer D. Early identification of patients developing late in-hospital ventricular fibrillation after discharge from the CCU. Am J Cardiol 1978;41:674-677.

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Chapter

6

The electrocardiographs signs of reperfusion

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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

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%

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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

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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

THE ELECTROCARDIOGRAPHIC SIGNS OF REPERFUSION

(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 endothan 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).

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VPB and AIVR Incidence, mechanism and prognostic implications 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

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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, selfterminating 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 myocardial infarction. NSVT and VF Incidence, mechanism and prognostic implications 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).

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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. Incidence, mechanism and prognostic implications 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.

THE ELECTROCARDIOGRAPHIC SIGNS OF REPERFUSION

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. Incidence, mechanism and prognostic implications 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.

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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 noninvasively 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).

THE ELECTROCARDIOGRAPHIC SIGNS OF REPERFUSION

References 1.

de Lemos JA, Braunwald E, ST segment resolution as a tool for assessing the efficacy of reperfusion therapy. J Am Coll Cardiol 2001 ;38:1283-1294.

2.

Ganz W, Buchbinder N, Marcus A, et al. Intracoronary thrombolysis in acute myocardial infarction. Am Heart J 1981; 101 -4-13.

3.

Zeymer U, Schroder R, Tebbe U, Molhoek GP, Wegscheider K, Neuhaus KL. Non invasive detection of early infarct vessel patency by resolution of ST-segment elevation in patients with thrombolysis for acute myocardial infarction. Eur Heart J 2001;22:769-775.

4.

Arstall MA, Stewart S, Haste MA, Horowitz JD. Streptokinase-induced transient aggravation of myocardial injury. Int J Cardiol 1995; 50:107-116.

5.

Doevendans PA, Gorgels AP, van der Zee R, Partouns J, Bar FW, Wellens HJ. Electrocardiographic diagnosis of reperfusion during thrombolytic therapy in acute myocardial infarction. Am J Cardiol 1995;75:1206-1210.

6.

Wehrens XH, Doevendans PA, Oude Ophuis TJ, Wellens HJ. A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or PTCA. Am Heart J 2000; 139:430-436.

7.

Buszman P, Szafranek A, Kalarus Z, Gasior M. Use of changes in ST segment elevation for prediction of infarct artery recanalization in acute myocardial infarction. Eur Heart J 1995;16:1207-1214.

8.

de Lemos JA, Antman EM, McCabe CH, et al. ST segment resolution and infarct related artery patency and flow after thrombolytic therapy. Am J Cardiol 2000;85:299-304.

9.

Hofstra L, Liem IH, Dumont EA, et al. Visualization of cell death in vivo in patients with acute myocardial infarction. Lancet 2000;356:209-212.

10.

Jordan JE, Zhoa ZQ, Vinten-Johansen J. The role of neutrophils in myocardial ischemia reperfusion injury. Cardiovasc Res 1999;43:860-878.

11.

McCord JM. Oxygen-derived free radicals in postischemic tissue injury. N Engl J Med 1985;312:159-163.

12.

‘t Hof AW van, Liem A, de Boer MJ, Zijlstra F. Clinical value of the 12-lead electrocardiogram after succesful reperfusion therapy for acute myocardial infarction. Zwolle Myocardial Infarction Study Group. Lancet 1997;350:615-619.

13.

Clays MJ, Bosnians J, Veenstra L, et al. Determinants and prognostic implications of persistent ST-segment elevation after primary angioplasty for acute myocardial infacrtion: importance of microvascular reperfusion injury on clinical outcome. Ciculation 1999;99:1972-1977.

14.

Matetzky, Novikov M, Gruberg L, et al. The significance of persistent ST elevation versus early resolution of ST segment elevation after primary PTCA. J Am Coll Cardiol 1999;1932-1938.

15.

Krucoff MW, Green CE, Satler LF, et al. Noninvasive detection of coronary artery patency using continuous ST-segment monitoring. Am J Cardiol 1986;57:916-22.

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16.

Klootwijk P, Langer A, Meij S, et al. Non-invasive prediction of reperfusion and coronary artery patency by continuous ST segment monitoring in the GUSTO-I trial. Eur Heart J 1996;17:689-98.

17.

Schroder R, Wegscheider K, Schroder K, Dissmann R, Meyer-Sabellek W. Extent of early ST segment elevation resolution: a strong predictor of outcome in patients with acute myocardial infarction and a sensitive measure to compare thrombolytic regimens. A substudy of the International Joint Efficacy Comparison of Thrombolytics (INJECT) trial. J Am Coll Cardiol 1995;26:1657-64.

18.

Langer A, Krucoff MW, Klootwijk, et al. Prognostic significance of ST segment shift early after resolution of ST elevation in patients with myocardial infarction treated with thrombolytic therapy: the GUSTO-I ST Segment Monitoring Substudy. J Am Coll Cardiol 1998; 31:783-9.

19.

Carlsson J, Kamp U, Hartel D, et al. Resolution of ST-segment elevation in acute myocardial infarction—early prognostic significance after thrombolytic therapy. Results from the COBALT trial. Herz 1999;24:440-7.

20.

Shah A, Wagner GS, Granger CB, et al. Prognostic implications of TIMI flow grade in the infarct related artery compared with continuous 12-lead ST-segment resolution analysis. Reexamining the “gold standard” for myocardial reperfusion assessment. J Am Coll Cardiol 2000;35:666-72.

21.

Holmvang L, Andersen K, Dellborg M, et al. Relative contributions of a single admission 12-lead electrocardiogram and early 24-hour continuous electrocardiographic monitoring for early risk stratification in patients with unstable coronary artery disease. Am J Cardiol 1999;667-74.

22.

Johanson P, Svensson AM, Dellborg M. Clinical implications of early ST-segment variability. A report from the ASSENT 2 ST-monitoring substudy. Cor Art Dis 2001; 12:277-283.

23.

Gottwald E, Gottwald M, Dhein S. Enhanced dispersion of epicardial activation recovery at sites of histological inhomogenity during regional cardiac ischemia and reperfusion. Heart 1998;474-480.

24.

Goldberg S, Greenspon AJ, Urban PL, et al. Reperfusion arrhythmia: a marker of restoration of antegrade flow during intracoronary thrombolysis for acute myocardial infarction. Am Heart J 1983; 105:26-32.

25.

Gorgels AP, Vos MA, Letsch IS, et al. Usefulness of the accelerated idioventricular rhythm as a marker for myocardial necrosis and reperfusion during thrombolytic therapy in acute myocardial infarction. Am J Cardiol 1988;61:231-235.

26.

Gressin V, Louvard Y, Pezzano M, Lardoux H. Holter recording of ventricular arrhythmias during intravenous thrombolysis for acute myocardial infarction. Am J Cardiol 1992;69:152-159.

27.

Piper HM, Garcia-Dorado D. Prime causes of rapid cardiomyocyte death during reperfusion. Ann Thorac Surg 1999;68:1913-1919.

28.

Yoshida Y, Hirai M, Yamada T, et al. Antiarrhythmic efficacy of dipyridamole in treatment of reperfusion arrhythmias : evidence for cAMP-mediated triggered activity as a mechanism responsible for reperfusion arrhythmias. Circulation 2000; 101:624-630.

THE ELECTROCARDIOGRAPHIC SIGNS OF REPERFUSION

29.

Engelen DJ, Gressin V, Krucoff MW, et al. Reperfusion arrhythmias in acute anterior myocardial infarction are related to the mode of reperfusion and predict worsening of left ventricular function after the acute phase. In press.

30.

Wellens HJ, Lie KI, Durrer D. Further observations on ventricular tachycardia as studied by electrical stimulation of the heart. Chronic recurrent ventricular tachycardia and ventricular tachycardia during acute myocardial infarction. Circulation 1974; 49: 647-653.

31.

Boissel JP, Castaigne A, Mercier C, Lion L, Leizorovicz A. Ventricular fibrillation following administration of thrombolytic treatment. The EMIP experience. European Myocardial Infarction Project. Eur Heart J 1996; 17:213-221.

32.

Doevendans PA, Cheriex E, van der Zee R, et al. Risk stratification in the thrombolytic era: results of a prospective study. Cardiologie 1996; 3:319-323.

33.

Hohnloser SH, Zabel M, Kasper W, Meinertz T, Just H. Assesment of coronary artery patency after thrombolytic therapy: accurate prediction utilizing the combined analysis of three non-invasive markers. J Am Coll Cardiol 1991; 18:44-49.

34.

Chesebro JH, Knatterud G, Roberts R, et al. Thrombolysis in Myocardial Infarction (TIMI) Trial, Phase I: A comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Clinical findings through hospital discharge. Circulation 1987; 76:142-154.

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Chapter

7

The electrocardiogram in unstable angina

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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

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

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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.

THE ELECTROCARDIOGRAM IN UNSTABLE ANGINA

121

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THE ELECTROCARDIOGRAM IN UNSTABLE ANGINA

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).

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

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).

THE ELECTROCARDIOGRAM IN UNSTABLE ANGINA

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.

4.

Hyde TA, French JK, Wong CK, et al. Four-year survival of patients with acute coronary syndromes without ST-segment elevation and prognostic significance of 0,5 mm STsegment 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 19821994. 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 quantification of ischemia in patients with unstable angina. Eur Heart J 1997; 18: 931-940.

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.

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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 Abnormal ventricular activation, myocardial infarction with, 65–83 left bundle branch block, 68–75 intermittent, 72–73 practical approach, 74–75 serial ECG’s, 74 paced ventricular rhythm, 76–79 ventricular pre-excitation, 79–81 Accelerated idiopathic ventricular rhythm, 106–109 Acute myocardial infarction arrhythmias in, 85–98 AV-nodal conduction system, 49–53 atrio-ventricular nodal level ECG findings, 49–51 incidence, 52–53 left bundle branch block, inferior wall myocardial infarction, 51–52 conduction abnormalities, atrio-ventricular nodal level, 49–53 management, 53 conduction abnormalities, sub-AV-nodal level, 53–63 ECG findings, 53–59 incidence, 60–61 management, 61–62 conduction disturbances, 43–64 sino-atrial region, 45–49 atrio-ventricular conduction system, 45–46 blood supply of sinus node, atrio-ventricular conduction system, 45 ECG findings, 46 incidence, 47 management, 48–49 sino atrial block, sinus arrest, 47–48 sinus bradycardia, 46 sinus node, sino-atrial region, 45 slow rhythms, conduction abnormalities, sinus nodal, sino-atrial level, 46 sinus arrest, sino-atrial block, 44

sub-AV nodal conduction disturbances, 44 supraventricular arrhythmias, 87–90 atrial fibrillation, 88–90 sinus tachycardia, 87–88 ventricular arrhythmias, 91–94 ventricular fibrillation, 93–94 ventricular premature beats, 91–92 ventricular tachycardia, 92–93 Angina, unstable, ECG in, 117–126 chest pain peaked T-waves in precordial leads, 120–122 T wave negativity in precordial leads, 123 ischemia, recovery of T wave abnormalities following, 124 left main stem disease, 120 proximal LAD syndrome, 120–124 serial ECG’s, 119–120 ST segment depression, 119 Anterior wall infarction, coronary artery occlusion, 24–37 distal LAD occlusion, 28–29 LAD occlusion distal to first diagonal branch, proximal to first septal branch, 31–32 distal to first septal branch, proximal to first diagonal branch, 30 proximal to first septal, first diagonal branch high risk, 26–28 left main occlusion, 33–34 new infarction in presence of old one, 36 site of occlusion in, criteria to identify, 33 ST deviation score, location, coronary artery occlusion, 34–36 ST segment vector, to localize site of ischemia, 25–26 Anterior wall myocardial infarction, coronary artery occlusion, grades of ischemia, 12 Arrhythmias in acute myocardial infarction, 85–98 supraventricular arrhythmias, 87–90 atrial fibrillation, 88–90 sinus tachycardia, 87–88 ventricular arrhythmias, 91–94 ventricular fibrillation, 93–94

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

ventricular premature beats, 91–92 ventricular tachycardia, 92–93 Atrial fibrillation, 88–90 Atrial tachycardia, 106 Atrio-ventricular conduction system acute myocardial infarction, 45 conduction disturbances, 45 acute myocardial infarction, sino-atrial region, 45–46 sino-atrial region, 45 sinus node, blood supply of, 45 Atrio-ventricular nodal level acute myocardial infarction, ECG findings, 49–51 AV-nodal conduction system, conduction disturbances, 49–51 AV nodal conduction disturbances, conduction disturbances, acute myocardial infarction, 44 AV-nodal conduction system, conduction disturbances, acute myocardial infarction, 49–53 atrio-ventricular nodal level ECG findings, 49–51 incidence, 52–53 left bundle branch block, inferior wall myocardial infarction, 51–52 conduction abnormalities, atrio-ventricular nodal level, 49–53 management, 53

B Blood supply of sinus node, 45 Brady arrhythmias, 111–112 ECG findings, 111 incidence, 111 mechanism, 111 prognosis, 111

C Chest pain peaked T-waves in precordial leads, 120–122 T wave negativity in precordial leads, 123 Conduction abnormalities acute myocardial infarction, sub-AV-nodal level, 53–63 ECG findings, 53–59 incidence, 60–61 management, 61–62 AV-nodal conduction system, acute myocardial infarction, atrio-ventricular nodal level, 49–53

Conduction disturbances, acute myocardial infarction, 43–64 AV-nodal conduction system, 49–53 atrio-ventricular nodal level ECG findings, 49–51 incidence, 52–53 left bundle branch block, inferior wall myocardial infarction, 51–52 mechanism, 52–53 prognostic significance, 52–53 conduction abnormalities, atrio-ventricular nodal level, 49–53 management, 53 conduction abnormalities, sub-AV-nodal level, 53–63 ECG findings, 53–59 incidence, 60–61 management, 61–62 mechanism, 60–61 prognostic significance, 60–61 sino-atrial region, 45–49 atrio-ventricular conduction system, 45–46 blood supply of sinus node, atrio-ventricular conduction system, 45 ECG findings, 46 incidence, 47 management, 48-49 mechanisms, 47 prognostic significance, 47 sino atrial block, sinus arrest, 47–48 sinus bradycardia, 46 sinus node, sino-atrial region, 45 slow rhythms, conduction abnormalities, sinus nodal, sino-atrial level, 46 sinus arrest, sino-atrial block, 44 sub-AV nodal conduction disturbances, 44 Coronary artery anterior wall infarction, 24–37 distal LAD occlusion, 28–29 LAD occlusion distal to first diagonal branch, proximal to first septal branch, 31–32 distal to first septal branch, proximal to first diagonal branch, 30 proximal to first septal, first diagonal branch high risk, 26–28 left main occlusion, 33–34 new infarction in presence of old one, 36 site of occlusion in, criteria to identify, 33 ST deviation score, location of coronary artery occlusion, 34–36 ST segment vector, to localize site of ischemia, 25–26 anterior wall myocardial infarction, grades of ischemia, 12

INDEX

coronary artery, infero-posterior wall infarction, 13–24 identification of, 5–42 anterior wall infarction, 8–9 distal LAD occlusion, 8–9 LAD occlusion distal to first diagonal, proximal to first septal branch, 8 distal to first septal, proximal to first diagonal branch, 8 proximal to first septal, first diagonal branch, 8 ECG patterns, 7–9 infero posterior infarction, 7–8 atrial infarction, 8 lateral wall involvement, 8 posterior wall involvement, 7 ST depression in precordial leads, 7 proximal, distal RCA, 7 RCA, CX, 7 infero posterior myocardial infarction, grades of ischemia, 12 infero-posterior wall infarction atrial infarction, 24 AV nodal block, 24 coronary patho-anatomy, 13–15 CX occlusion, diagnosing, difficulties in, 24 dominance, 15 inferior wall myocardial infarction, RCA, CX occlusion in, 15–17 isolated RV infarction, 22–23 lateral wall involvement, 17 posterior wall involvement, 17 RV infarction, 18–21 mortality, clinical, ECG variables, 10 severity of ischemia, 5–42 site of occlusion, coronary artery, ECG patterns, 13–37 size of area at risk, 5–42 ST segment deviation score, 7, 9–11 terminal QRS-ST segment pattern, 7 severity of cardiac ischemia, 11–13 Coronary artery occlusion, severity of ischemia, 5–42

129

atrial, 88–90 ventricular, 93–94

I Inferior wall myocardial infarction, left bundle branch block, atrio-ventricular nodal level, 51–52 Infero posterior myocardial infarction, coronary artery occlusion, grades of ischemia, 12 Infero-posterior wall infarction, coronary artery occlusion atrial infarction, 24 AV nodal block, 24 coronary patho-anatomy, 13–15 CX occlusion, diagnosing, difficulties in, 24 dominance, 15 inferior wall myocardial infarction, RCA, CX occlusion in, 15–17 isolated RV infarction, 22–23 lateral wall involvement, 17 posterior wall involvement, 17 RV infarction, 18–21

L Left bundle branch block, 68–75 acute myocardial infarction, 51–52 AV-nodal conduction system, conduction disturbances, 51–52 inferior wall myocardial infarction, atrio-ventricular nodal level, 51–52 intermittent, 72–73 practical approach, 74–75 serial ECG’s, 74 Left main stem disease, 120

M Myocardial infarction, with abnormal ventricular activation, 65–83 left bundle branch block, 68–75 intermittent, 72–73 practical approach, 74–75 serial ECG’s, 74 paced ventricular rhythm, 76–79 ventricular pre-excitation, 79–81

E Ectopic activity, 105 ECG findings, 105

N Non-sustained ventricular tachycardia, 106, 109

F

O

Fibrillation

Occlusion, coronary artery

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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

anterior wall infarction, 24–37 distal LAD occlusion, 28–29 LAD occlusion distal to first diagonal branch, proximal to first septal branch, 31–32 distal to first septal branch, proximal to first diagonal branch, 30 proximal to first septal, first diagonal branch high risk, 26–28 left main occlusion, 33–34 new infarction in presence of old one, 36 site of occlusion in, criteria to identify, 33 ST deviation score, location of coronary artery occlusion, 34–36 ST segment vector, to localize site of ischemia, 25–26 anterior wall myocardial infarction, grades of ischemia, 12 infero posterior myocardial infarction, grades of ischemia, 12 infero-posterior wall infarction atrial infarction, 24 AV nodal block, 24 coronary patho-anatomy, 13–15 CX occlusion, diagnosing, difficulties in, 24 dominance, 15 inferior wall myocardial infarction, RCA, CX occlusion in, 15–17 isolated RV infarction, 22–23 lateral wall involvement, 17 posterior wall involvement, 17 RV infarction, 18–21 mortality, clinical, ECG variables, 10 site of, identification, 5–42 site of occlusion coronary artery ECG patterns, 13–37 infero-posterior wall infarction, 13–24 identification of anterior wall infarction, 8–9 distal LAD occlusion, 8–9 LAD occlusion distal to first diagonal, proximal to first septal branch, 8 distal to first septal, proximal to first diagonal branch, 8 proximal to first septal, first diagonal branch, 8 ECG patterns, 7–9 infero posterior infarction, 7–8

atrial infarction, 8 lateral wall involvement, 8 posterior wall involvement, 7 ST depression in precordial leads, 7 proximal, distal RCA, 7 RCA, CX, 7 size of area at risk, 5–42 ST segment deviation score, 7, 9–11 terminal QRS-ST segment pattern, 7 severity of cardiac ischemia, 11–13

P Pre-excitation, ventricular, 79–81 Premature beats, ventricular, 91–92

R Reperfusion, ECG signs of, 99–116 accelerated idiopathic ventricular rhythm, 106 atrial tachycardia, 106 brady arrhythmias, 111–112 ECG findings, 111 incidence, 111 ectopic activity, 105 ECG findings, 105 non-sustained ventricular tachycardia, 106, 109 reperfusion arrhythmias, defined, 106 sinus bradycardia, 106 ST-T segment behavior, 101–105 incidence, 104–105 ST segment changes, 101–103 T wave changes, 103–104 supraventricular arrhythmias, 110 ECG findings, 110 incidence, 110 ventricular premature beats, 106–109 increase in, 106 Reperfusion arrhythmias, defined, 106

S Sino-atrial block conduction disturbances, acute myocardial infarction, sinus arrest, 44 sino-atrial region, conduction disturbances, acute myocardial infarction, sinus arrest, 47–48 Sino-atrial region conduction disturbances, acute myocardial infarction, 45–49 atrio-ventricular conduction system, 45–46 blood supply of sinus node, atrio-ventricular conduction system, 45

INDEX

ECG findings, 46 incidence, 47 management, 48–49 sino atrial block, sinus arrest, 47–48 sinus bradycardia, 46 sinus node, sino-atrial region, 45 slow rhythms, conduction abnormalities, sinus nodal, sino-atrial level, 46 sinus node, conduction disturbances, acute myocardial infarction, sino-atrial region, 45 Sinus arrest sino atrial block, sino-atrial region, conduction disturbances, acute myocardial infarction, 47–48 sino-atrial block, conduction disturbances, acute myocardial infarction, 44 Sinus bradycardia, 106 sino-atrial region, conduction disturbances, acute myocardial infarction, 46 Sinus node blood supply of, atrio-ventricular conduction system, conduction disturbances, acute myocardial infarction, sino-atrial region, 45 sino-atrial region, conduction disturbances, acute myocardial infarction, sino-atrial region, 45 Sinus tachycardia, 87–88 Site of occlusion coronary artery coronary artery occlusion ECG patterns, 13–37 infero-posterior wall infarction, 13–24 identification of, 5–42 identification of, coronary artery occlusion anterior wall infarction, 8–9 distal LAD occlusion, 8–9 LAD occlusion, 8 proximal to first septal, first diagonal branch, 8 ECG patterns, 7–9 infero posterior infarction, 7–8 atrial infarction, 8 lateral wall involvement, 8 posterior wall involvement, 7 ST depression in precordial leads, 7 proximal, distal RCA, 7 RCA, CX, 7 Size of area at risk, coronary artery occlusion, 5–42

131

Slow rhythms conduction disturbances, acute myocardial infarction, sino-atrial region, conduction abnormalities, sinus nodal, sino-atrial level, 46 sinus nodal, sino-atrial level, conduction disturbances, acute myocardial infarction, sino-atrial region, 46 ST segment deviation score, coronary artery occlusion, 7, 9–11 ST-T segment behavior, 101–105 incidence, 104–105 mechanism, 104–105 prognastic implications, 104–105 ST segment changes, 101–103 T wave changes, 103–104 Sub-AV nodal conduction disturbances, conduction disturbances, acute myocardial infarction, 44 Supraventricular arrhythmias, 87–90, 110 atrial fibrillation, 88–90 ECG findings, 110 incidence, 110 mechanism, 110 prognosis, 110 sinus tachycardia, 87–88 T Tachycardia sinus, 87–88 ventricular, 92–93 Terminal QRS-ST segment pattern coronary artery occlusion, 7 severity of cardiac ischemia, coronary artery occlusion, 11–13 U Unstable angina, ECG in, 117–26 chest pain peaked T-waves in precordial leads, 120–122 T wave negativity in precordial leads, 123 ischemia, recovery of T wave abnormalities following, 124 left main stem disease, 120 proximal LAD syndrome, 120–124 serial ECG’s, 119–120 ST segment depression, 119 V Ventricular activation, abnormal, myocardial infarction with, 65–83

132

THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

left bundle branch block, 68–75 intermittent, 72–73 practical approach, 74–75 serial ECG’s, 74 paced ventricular rhythm, 76–79 ventricular pre-excitation, 79–81 Ventricular arrhythmias, 91–94

ventricular premature beats, 91–92 ventricular tachycardia, 92–93 Ventricular fibrillation, 93–94, 109 Ventricular pre-excitation, 79–81 Ventricular premature beats, 91–92, 106–109 increase in, 106 Ventricular tachycardia, 92–93