Clinical Electrocardiography

Clinical E lectrocardiography Third Edition

Clinical E Zectrocardiography Third Edition

B L Chia MBBS, FRACP, FRCP (Edin), FAMS, FACC PROFESSOR OF MEDICINE NATIONAL UNIVERSITY OF SINGAPORE CHIEF; CARDIAC DEPARTMENT NATIONAL UNIVERSITY HOSPITAL SINGAPORE

L

World Scientific Singapore New Jersey. London Hong Kong

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First published 1998 Reprinted 2000

CLINICAL ELECTROCARDIOGRAPHY, 3rd Edition Copyright 0 1998 by World Scientific Publishing Co. Re. Ltd.

A11 rights reserved. This book, or parts thereoJ may not be reproduced in any form or by any means, electronic or mechanical, including photocopying, recording or any information storage and retrieval system now known or to be invented, without written permission from the Publisher.

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ISBN 981-02-3761-8 ISBN 981-02-3762-6 (pbk)

Printed in Singapore.

To John and Lin

ACKNOWLEDGEMENTS

It gives me great pleasure to express my thanks and gratitude to the following: (1) Assoc Professor Lim Yean-Teng (Senior Consultant) and the other members of the Cardiac Department, National University Hospital, Singapore who are listed below for their dedication and unfailing support and also for helping to create a stimulating environment where electrocardiography can enjoy a robust growth together with echocardiography, electrophysiology and interventional cardiology: (a) Drs Lim Tai-Tian, Ling Lieng-Hsi, Ng Kheng-Siang, Ng Wai-Lin, Tan Huay-Cheem and Ye0 Tiong-Cheng (all Consultant Cardiologists) (b) Drs Ho Kheng-Thye (Senior Registrar), Bernard Kwok and James Yip (Registrar) (2) Dr Lau Kean-Wah, Senior Consultant Cardiologist at the National Heart Centre, Singapore for reading through the manuscript and for his friendship, invaluable advice and help through the years. (3) Ms Christina Ng for her excellent typing and secretarial skills, without which this book could not have been completed. (4) Mr Tan Lip-Seng for his excellent photography. I would also like to thank the following: Dr Chan I t - Y e e for Fig. 5.18, Dr Bernard Ee for Figs. 2.6,7.9 and 7.13, Dr A Johan for Fig. 5.6, Dr Koo Chee-Choong for Figs. 6.14,6.15 and 7.12, Dr Quek Swee-Chye for Fig. 3.29 and Dr Arthur Tan for Fig. 2.8. The Managing Editor of Asian Medical News for permission to reproduce several of the ECG and cardiovascular quizes which I have previously published. The Editor of the Singapore Medical Journal for permission to reproduce from my previous publications Figs. 2.2 1, 2.27, 2.28, 2.29, 2.30 and 5.19. The Editor-in-Chief, The Canadian Journal of Cardiology for permission to reproduce from my previous publication, Fig. 7.3.

PREFACE

This is the third edition of “Clinical Electrocardiography” which was first published in 1985. There has been tremendous progress in the last 10 years since the second edition, especially in the electrocardiography of acute myocardial infarction. With the advent of the thrombolytic era, many important new insights into the electrocardiography of acute myocardial infarction have evolved. In this new edition, the sections on posterior myocardial infarction, supraventricular tachycardia, ventricular tachycardia and antiarrhythmic drug therapy have all been updated and revised. One of the strengths of the previous two editions has been the quality of the ECG illustrations. In keeping with this tradition, the ECG illustrations in this third edition have been further improved, with 54 (39%) out of the 139 illustrations being new. Books, monographs and scientific papers on electrocardiography abound and it would appear that there is little justification for yet another book on this subject. However, despite the voluminous publications, it is difficult to find books on electrocardiography which are simple, concise, accurate and relevant to patient care. This book is the culmination of about 30 years of experience in the teaching of electrocardiography to coronary care unit nurses, medical undergraduates, interns, residents and cardiology registrars. As the title of the book implies, the approach to the subject has been entirely from the viewpoint of a clinician. Hence, theoretical considerations have been kept to a minimum and clinical-electrocardiographic correlations have been emphasized throughout the text.

B L CHIA 1998

vii

CONTENTS

Dedications Acknowledgements Preface 1. The Normal Electrocardiogram

V

vi vii

2

2. Ischaemic Heart Disease

11

3. Miscellaneous Conditions

38

4. Cardiac Arrhythmias

62

5 . Supraventricular Arrhythmias

68

6. Ventricular Arrhythmias

90

7. Bundle Branch Block, Hemiblock and Atrioventricular (AV) Block Index

108

120

ix

Clinical Electrocardiography

1

CHAPTER 1

THE NORMAL ELECTROCARDIOGRAM

THE 12-LEAD ELECTROCARDIOGRAM The 12-lead electrocardiogram (ECG) consists of the following leads:

(I)

Bipolar Leads (i) Lead I (between right arm and left arm) (ii) Lead I1 (between right arm and left leg) (iii) Lead I11 (between left arm and left leg)

(11) Augmented Unipolar Leads (i) Lead aVR (right arm) (ii) Lead aVL (left arm) (iii) Lead aVF (left leg) (111) Unipolar Chest Leads These are designated as V leads. There are six V leads (from V1 to V,) depending on where the electrode is placed on the chest (Fig. 1.1). Lead V1 is recorded with the electrode in the fourth intercostal space just to the right of the sternum, and lead V2 in the fourth intercostal space just to the left of the sternum. Lead V3 is recorded at a position exactly mid-way between leads Vz and V4. Lead V4 is recorded in the fifth intercostal space in the mid-clavicular line. Leads V5 and V6 are recorded at the same horizontal level as lead V4, with lead V5 in the anterior axillary line and lead V6 in the mid-axillary line. Apart from the above conventional 12 leads, other leads are also frequently recorded. Right-sided chest leads such as leads V3R, V4R, VSRand V6R are recorded in positions which correspond to leads V3, V4, V5 and V6 respectively, except that the electrode is

2

-I

Fig. 1.1 Diagram showing the positions of the electrode when recording the different left and right-sided chest leads. 1 to 6 = leads V1 to V6 respectively. MCL = mid-clavicularline, AAL = anterior axillary line, MAL = mid-axillary line, V3R and V4R = right-sided chest leads.

now placed on the right side of the chest instead of on the left.' These leads (especially lead V4R) are particularly useful for the diagnosis of right ventricular infarction. Very recently, leads V7,Vg and Vg have been reported to be valuable in the diagnosis of posterior myocardial infarction. These 3 leads are recorded at the same horizontal level as lead Vg, with the electrode being placed in the left posterior axilliary line (V,), left mid-scapular line (V,) and at the left border of the spine (V9).2

CALCULATION OF HEART RATE The ECG is normally recorded at a speed of 25 m d s e c . The horizontal distance between 1 large square on the ECG paper recorded at this speed represents 0.20 sec. Since this distance spans the length of 5 small squares, each small square therefore represents 0.04 sec (Fig. 1.5). There are many different ways of calculating the heart rate. A simple way is to divide 300 by the number of large squares between 2 consecutive beats if the rhythm is regular. For example, the following are the heart rates corresponding to the number of large squares in between 2 consecutive beats.

3

Heart rate

Number of large squares between 2 consecutive beats

300 150 100 75 60 50 43 38

1 (300/1) 2 (300/2) 3 (30013) 4 (300/4) 5 (300/5) 6 (300/6) 7 (300/7) 8 (300/8)

The rationale for the above calculation is as follows. There are 300 fifths of a second in 1 minute (5 x 60). One fifth of a second (i.e. 0.20 sec) is represented by 1 large square. Therefore the heart rate is conveniently calculated by dividing 300 by the number of large squares between 2 consecutive beats.

CALCULATING ELECTRICAL AXIS The term "electrical axis" is used to describe the average direction of the electrical impulse of the heart as it is projected in the frontal, horizontal or sagittal plane. Although the P, QRS and T complexes each has an axis in these 3 planes, this term, when unqualified, usually refers to the axis of the QRS complex in the frontal plane. Like the calculation of the heart rate, there are numerous ways of calculating the electrical axis. To understand the logic behind the method of calculating the axis, one must be familiar with the concept of the Einthoven triangle and the hexaxial reference sy~tern.~ The latter is derived from a combination of the triaxial reference systems of both the standard bipolar leads and the augmented unipolar limb leads (Fig. 1.2). In the hexaxial reference system, which is diagrammed in Fig. 1.3, the frontal plane is divided into 30" intervals.

.' -150."

..

aVF Fig. 1.2 Diagram showing the triaxial reference system.

4

Fig. 1.3 Diagram showing the hexaxial reference system.

When calculating the axis of the heart, it is useful to assess all the limb leads (i.e. leads I, 11,111, aVR, aVL and aVF) and look for the lead where the QRS complex has the smallest or most equiphasic deflection. The axis is perpendicular to this lead. Using Fig. 1.4 as an example, the limb lead where the ventricular complex shows the least deflection is lead aVL. The axis which is perpendicular to lead aVL is therefore lead 11. Examination of lead I1 shows that the ventricular complex is upright and therefore the axis must be directed towards the positive pole of this lead (i.e. the axis is +60"). The following method is an alternative way of calculating the axis: (1) Calculate the algebraic sum of the QRS deflections in leads I and aVF and mark Off each value in arbitrary units in these 2 leads; (2) Draw lines perpendicular to leads I and aVF passing through these 2 points; and (3) Draw a line joining the point of intersection of the constructed lines to the point of intersection of leads I and aVE This line represents the axis. The normal axis is between -30" to +90". Left axis deviation is defined as an axis between -30" to -90" and right axis deviation as an axis between +90" to +180". When the axis is between -90" to -1 80" (i.e. upper right quadrant), the axis is termed "indeterminate".

wwww m

aV F

aVR

kki% v3

v2

V4

V5

Fig. 1.4 Normal 12-lead ECG.

COMPLEXES AND SEGMENTS P Wave The P wave represents atrial depolarization which normally proceeds downwards, anterogradely from the sinoatrial node. It is normally upright in leads I, 11, aVF and the left

5

Fig. 1.5 Diagram showing the various ECG complexes, segments and intervals.

praecordial leads V4 toV6, and inverted in lead aVR. The polarity of the P wave in all the other leads is variable. It should not be more than 0.12 sec in duration and 2.5 mm in height in the limb leads, and it should be less than 1.5 mm in height in the praecordial leads (Figs. 1.4 and 1.5).

PR Segment The PR segment is the portion between the end of the P wave and the beginning of the QRS complex.

QRS Complex The QRS complex reflects depolarization of the 2 ventricles. The nomenclature of the various segments of the ventricular complex is standardized. If the first deflection is downwards, it is called a Q wave. An upright deflection is called an R wave, whether it is preceded by a Q wave or not. Anegative deflection following an R wave is called an S wave, whether the R wave has been preceded by a Q wave or not. Depolarization of the ventricular myocardium begins in the septum, where it takes place in a left to right direction (sequence 1 in Fig. 1.6). Following this, both the left and right ventricles are depolarized simultaneously. However, since the left ventricle has a much larger physical and electrical mass, ventricular depolarization can be conveniently regarded electrically as depolarization of the left ventricle alone. This depolarization proceeds from right to left (sequence 2 in Fig. 1.6). An electrode which is orientated to the left ventricle (e.g. lead V,) will show an initial small q wave (due to septa1 depolarization moving away from the electrode), followed by a large R wave (due to the ventricular depolarization moving towards the electrode). A typical left praecordial lead complex is therefore a qR complex.

h

Fig. 1.6 Diagram showing normal sequence of ventricular depolarization and the ventricular complexes in V1 and V5. S = septum, RV = right ventricle, LV = left ventricle.

The same electrical events are recorded in an opposite fashion in an electrode orientated to the right ventricle (e.g. lead Vl). The initial deflection is a small r wave due to septa1 depolarization moving towards the electrode, followed by an S wave due to ventricular depolarization moving away from the electrode. A typical right praecordial lead complex is therefore an rS complex (Fig. 1.6). In the praecordial leads, rS complexes are seen in leads V1 and V2, and qR complexes in leads V4 to V6 There is a gradual increase in the height of the r wave and a corresponding decrease in the depth of the S wave from leads V1 to V3. In lead V3, which represents the transitional zone, the height of the R wave and the depth of the S wave are approximately equal. In the limb leads, the ventricular complexes may show either a left or a right praecordial lead pattern. The only exception is lead aVR, where the ventricular complex normally shows a negative deflection in the form of either a deep Q wave or a rS complex (Fig. 1.4). Normally, the 2 ventricles are depolarized simultaneously, resulting in a narrow QRS complex which is between 0.05 to 0.10 sec in duration. In ventricular ectopic beats, bundle branch block or supraventricular ectopic beats with aberrant ventricular conduction, the QRS complex is widened. There is a wide variation in the amplitude of the QRS complex. The generally accepted upper limit for the R wave in lead V5 is between 25 to 30 mm. However, voltages greater than this are commonly present in asthenic, normal, young individuals and in those whose ECG show the early repolarization pattern (see Chapter 3).

ST Segment The ST segment is that portion of the ECG between the end of the S wave and the beginning of the T wave. Normally, the ST segment blends smoothly and imperceptibly with the T wave. It is also normally isoelectric, i.e. at the same horizontal level as the T-P segment which is taken as the isoelectric line (Figs. 1.4 and 1.5). The ST segment may be either elevated or depressed with reference to the isoelectric line. T Wave The T wave comes after the ST segment and represents ventricular repolarization (Fig. 1.5). It is normally upright in leads I, 11, V4 to v6 and inverted in lead aVR. In all the other leads, the polarity of the T wave is variable. T wave inversion is commonly present in leads V1 to V4 in children up to the age of 14 years. After this age, it is considered abnormal except in lead V1 in males, and leads V1 and V2 in females. Rarely, T wave inversion may be present up to lead V3 in normal individuals. The 2 limbs of the T wave are usually asymmetrical and the apex is slightly rounded (Fig. 1.4). It is frequently stated that the height of the T wave should not exceed 5 mm in any standard limb lead and 10 mm in any praecordial lead. However, in subjects with the early repolarization pattern, tall T waves exceeding 10 mm are frequently encountered, even though there is no cardiac or other disease (see Chapter 3).

U Wave The U wave follows the T wave (Figs. 1.4 and 1.5). The genesis of the U wave is unclear but it has been postulated to be due to repolarization of the Purkinje fibres or the papillary muscles. It is normally of low voltage and has the same polarity as the T wave. It is usually most prominent in leads V2 to V, and generally does not exceed 2 mm or one quarter of the height of the preceding T wave (Fig. 1.5).

INTERVALS PR Interval The PR interval is measured from the onset of the P wave to the beginning of the QRS or rS complex (Fig. 1.5). It represents the time taken for the sinus impulse to travel across the atria, down the atrioventricular (AV) node, bundle of His, bundle branches, Purkinje fibres and finally to the ventricular myocardium. It is normally between 0.12 to 0.20 sec in duration. QT Interval The QT interval is measured from the onset of the QRS or rS complex to the end of the T wave (Fig. 1.5). Since the normal QT interval varies with the heart rate, the QTc or the corrected QT interval is used clinically instead of the QT interval. The QTc is calculated from the QT interval and the heart rate using the formula: QTc = QT interval divided by the square root of the R-R i n t e r ~ a l . ~ T hnormal e QTc should not exceed 0.42 sec.

8

REFERENCES 1. Tan CC, Hiew TM, Chia BL. Right chest electrocardiographic patterns in normal subjects. Chest 1990; 97: 572. 2. Matetzky S, Freimak D, Chouraqui P, et al. Significance of ST segment elevations in posterior chest leads (V, to V,) in patients with acute inferior myocardial infarction: application for thrombolytic therapy. J A m Coll Curdiol 1998; 31: 506. 3. Schamroth L. An Introduction to Electrocardiography, Blackwell Scientific Publications, Oxford, 7th ed., 1990; p. 35. 4. Bazett H 0.An analysis of the time relations of electrocardiograms. Heart 1920; 7: 353.

9

CHAPTER 2

ISCHAEMIC HEART DISEASE

The two major clinical applications of electrocardiography are the diagnosis of myocardial ischaemia and cardiac arrhythmias. The birth of electrocardiography more than 9 decades ago opened a new dimension in the study of the heart, by allowing the cardiac electrical currents (voltages, potentials) to be clinically recorded for the first time. This heralded a milestone in the diagnosis and treatment of coronary artery disease and cardiac arrhythmias. Despite the introduction in recent years of many new investigative techniques such as myocardial perfusion scintigraphy, stress echocardiography and coronary angiography, the electrocardiogram today still maintains its pivotal role in the evaluation of myocardial ischaemia, chiefly because it is very useful, very simple to perform, noninvasive and inexpensive. In this chapter, various ECG patterns in ischaemic heart disease will be discussed. The many problems and pitfalls that are frequently encountered in the ECG diagnosis of ischaemic heart disease will be highlighted in the next chapter which deals with ECG abnormalities seen in miscellaneous conditions.

DIAGNOSIS OF ISCHAEMIC HEART DISEASE Coronary artery disease may present in several different ways. A significant number of individuals who suffer from this disease have no symploms at all even though the disease is very severe. They have what is known as “silent myocardial ischaemia”.’Others, however, manifest with stable and unstable angina pectoris, acute myocardial infarction or “sudden death”. Whenever an ECG is recorded in a patient suspected of having ischaemic heart disease, the following questions should be routinely asked:

11

(1) Is the ECG normal or abnormal? (2) If it is abnormal, do the abnormalities indicate myocardial infarction or angina pectoris? (3) If the ECG is indicative of myocardial infarction, do the changes suggest an acute or an old myocardial infarction?

These questions are of obvious importance, because the clinical significance in terms of urgency of management in patients suffering from acute myocardial infarction versus patients suffering from stable angina pectoris or chronic ischaemic heart disease is completely different.

MYOCARDIAL INFARCTION Early diagnosis of acute myocardial infarction is of crucial importance because (1) Mortality is highest in the first few hours; and (2) Thrombolytic therapy, which is today frequently given, is most effective if it is administered within 3 hours after the onset of infarction. In the evaluation of a patient who is suspected of suffering from acute myocardial infarction, the 3 principal parameters are: (1) Clinical history (2) ECG (3) Serum markers of acute myocardial infarction such as creatine phosphokinase (CK), CKMB fraction (CKMB) and troponin T. Since the levels of the serum markers of acute myocardial infarction may not be significantly elevated in the first few hours after the onset of the infarction, early diagnosis frequently must depend on the clinical history and ECG.

TRANSMURAL (Q WAVE) MYOCARDIAL INFARCTION Every year in Singapore, which has a population of about 3 million people, approximately 1300 patients aged 20-64 years suffer from acute myocardial infarction.2 Acute myocardial infarction is very often due to a thrombus which is superimposed on a ruptured atherosclerotic plaque resulting in total obstruction of coronary blood flow. In transmural myocardial infarction, the whole thickness of the myocardium is involved. There is a central core of necrotic myocardium which is surrounded in turn by a shell of injured tissue, and then a zone of ischaemic tissue. An ECG lead which is placed over the site of infarction will record the following changes: (1) Pathological Q waves reflecting tissue necrosis (2) Elevated ST segments reflecting tissue injury (3) T wave inversion reflecting tissue ischaemia. These ECG changes have been described as “the indicative changes” of acute transmural myocardial infar~tion.~

12

Normally, small and narrow q waves are always present in the left praecordial leads. The following are the characteristics of a pathological Q wave which distinguish it as being abnormal: (1) It is broad (0.04 sec or longer in duration); (2) It is deep (greater than 4 mm in depth); ( 3 ) It is usually associated with a substantial loss of the height of the R wave resulting in a Q wave/R wave ratio which is 25% or greater; and (4) It is frequently seen in multiple leads. For example, in inferior infarction, it is present in leads 11, I11 and aVF and in anterolateral infarction, it is seen in leads V4, Vg, Vg, I and aVL. Lastly, to be significant, the pathological Q wave must be present in leads which do not normally show wide and deep Q waves, e.g. lead aVR. In the “hyperacute phase” (i.e. during the first few hours), the ST segments are elevated with a slope which is either straight upwards to the apices of tall and widened T waves or concave upwards. ST segments in leads overlying normal myocardium which are opposite to the infarct site will show “reciprocal” ST segment depression. In this phase of acute myocardial infarction, pathological Q waves and T wave inversion are not seen (B in Fig. 2.1). It is important to note that the initial ECG shows the classical “hyperacute” changes in only about 50% of patients. In another 45% of cases, the ECG shows either ST segment depression or nondiagnostic abnormalities, and in the remaining 5% of cases, no ECG abnormality is d e t e ~ t e d If . ~ the initial ECG is normal or shows nondiagnostic abnormalities, it is crucial to repeat 12-lead ECG recordings every 15-30 minutes, because serial ECGs will very frequently show diagnostic changes in patients who have suffered a myocardial infarction. All the studies so far have shown that thrombolytic therapy is beneficial only in acute myocardial infarction patients presenting with ST segment elevation.

NORMAL

iYPERACUTE

‘ULLY EVOLVED

RESOLUTION

CHRONIC

kf k-

3n +A

C

E

Fig. 2.1 Diagram showing the ECG changes in transmural myocardial infarction. Top panel shows the ECG changes in the leads facing the infarct site (i.e. “indicative changes”). Bottom panel shows the ECG changes in the leads facing the opposite normal myocardium (i.e. “reciprocal changes”).

13

Generally, within 24 hours of the onset of acute myocardial infarction, the ST segment elevation decreases and pathological Q waves start to develop. The elevated ST segments, unlike those seen in the “hyperacute phase”, are now convex upwards. Later in this phase which is called “the fully evolved phase”, deep and symmetrically inverted arrowhead T waves are seen (C in Fig. 2.1 and Fig. 2.4).

Fig. 2.2 “Hyperacute phase” of transmural anterior infarction in a 51-year-old man. Note: (1) Markedly elevated ST segments (concave upwards) in V2 to V,, I and aVL, merging with tall T waves in V2 to V4 (ST segment and T wave in V2 = 10 mm and 20 mm respectively). (2) Reciprocal ST segment depression in 11, I11 and aVE Coronary angiography revealed a 90% stenosis of the proximal left anterior descending artery.

II-

II

v1

m v3

aV R

4 aV F

V6

Fig. 2.3 The ECG was recorded approximately 24 hours after Fig. 2.2. It shows the “fully evolved phase” of transmural anterior infarction as reflected by: (1) Pathological Q waves in V1 and V2. (2) Elevated ST segments in V, to V3. (3) Deep and symmetrically inverted T waves in V2 to V,, I and aVL.

Figures 2.2 and 2.3 are ECGs of a patient with transmural, anterior myocardial infarction recorded about 2 and 24 hours respectively, after the onset of chest pain. Figure 2.2 shows ECG changes reflecting the “hyperacute phase” and Fig. 2.3, the “fully evolved phase” of transmural, anterior myocardial infarction.

14

I

v1

aVR

v3

aVL

V6

Fig. 2.4 “Fully evolved phase” of transmural anterior infarction. Note: (1) Pathological Q waves in V, to V3. (2) Elevation of the ST segment (convex upwards) and T wave inversion in V , to v,.

Following the “fully evolved phase”, the ECG begins to show the “resolution phase”. During this period, the ST segments fall to the isoelectric line, but the T waves remain inverted (D in Fig. 2.1 and Fig. 2.8). Still later, in the “chronic phase”, the T waves become upright and all that remains are the pathological Q waves (E in Fig. 2.1 and Fig. 2.5). The terms “chronic phase” of myocardial infarction and “old myocardial infarction” are frequently used synonymously. In some patients, the pathological Q waves become less prominent or may even disappear completely after several months or years. With the passage of time, small r waves are occasionally resurrected in leads which originally showed pathological Q waves. If this occurs in leads V1 to V3, the height of the r waves may not increase progressively as in the normal ECG. This phenomenon is referred to as “poor r wave progression”, which often indicates an old anteroseptal infarction (Fig. 2.5). This abnormality may also be seen in left ventricular hypertrophy and dilated cardiomyopathy. To illustrate the sequence, an ECG abnormality shown in B in Fig. 2.1 indicates a very recent myocardial infarction perhaps a few hours old, in C slightly later in time, in D a few weeks old and in E a few months old. However, it is important to note that all these evolutionary changes described above may be accelerated with thrombolytic therapy or percutaneous transluminal coronary angioplasty. In some patients, especially those with anterior myocardial infarction, there is persistent elevation of the ST segment. This usually suggests a ventricular a n e ~ r y s m . ~

aV R

aVL

aVF

V6

v3 Fig. 2.5 ECG of a 70-year-old man showing the “chronic phase” of transmural anterior and inferior infarction. Note: (1) Very deep and wide pathological Q waves in leads 111 and aVF (arrowheads) reflecting old inferior infarction. (2) Poor r wave progression from V1 to V3 reflecting old anterior infarction. Coronary angiography showed severe triple vessel disease.

LOCALIZATION OF INFARCT SITE The presence of the “indicative” ECG infarct pattern in certain leads suggest that myocardial infarction has occurred in specific sites of the heart, e.g. leads 11, I11 and aVF - inferior infarction, leads V1 to V3 - anteroseptal infarction, leads V4, V5, V6, I and aVL - anterolateral infarction of the left ventricle. The conventional 12-lead ECG does not directly record electrical currents from the posterior wall of the left ventricle. Therefore, infarction at this site does not manifest the usual “indicative” infarct pattern in any of the conventional 12 leads. However, “indicative changes” of posterior infarction can be detected in leads V7, V8 or Vg (Fig. 2.7) or in the oesophageal lead (ie ECG recorded from an electrode placed in the oesophagus facing the posterior wall of the left ventricle) which is seldom performed today because of its inconvenience. Posterior wall infarction can also be diagnosed from the 12-lead ECG using indirect criteria, such as reciprocal ST segment depression in leads V1to V4in the “hyperacute phase” (Figs. 2.6 and 2.7), or tall R and tall T waves in leads V1 and V2 in the “resolution phase” (Figs. 2.8 and 2.9). In the past 20 years, there has been considerable controversy over whether ST segment depression in the praecordial leads V1 to V4 in patients with acute inferior infarction, reflects reciprocal changes or represent additional ischaemia in the anterior myocardial waK6 Very recently however, this ST segment depression has been confirmed to be due to reciprocal changes from acute posterior infarction which frequently accompanies inferior infarction7. A major advance in recent years has been the finding that right ventricular infarction, which is present in approximately 30% of patients with inferior infarction of the left ventricle, can be accurately diagnosed from right-sided chest leads, especially lead V4R.8Figures 2.6 and 2.7 are examples of the “hyperacute phase” of right ventricular infarction, as well as inferior and posterior infarction of the left ventricle.

16

~~

.-

___ - - - -

v1

V6

V4R

V5R

V6R

Fig. 2.6 Acute inferior, posterior and right ventricular infarction in a 60-year-old woman. Note: (1) Elevated ST segments in 11, I11 and aVF, merging with tall T waves and reciprocal ST segment depression in I and aVL reflecting the “hyperacute phase” of transmural inferior infarction. (2) ST segment depression in V2 to V, reflecting the reciprocal changes of acute posterior infarction. (3) Pathological Q waves and elevated ST segments in V,R, VSR and V6R reflecting acute right ventricular infarction.

V1

V6 v2

V8

v3

v4

VS

V9

V4 R

VSR

V6R

Fig. 2.7 Acute inferior, posterior and right ventricular infarction in a 49-year-old man. Note: (1) Elevated ST segments in 11,111 and aVF (associated with pathological Q wave in 111) and reciprocal ST segment depression in I and aVL reflecting acute, transmural inferior infarction. (2) ST segment elevation in V7, Vg, V, and ST segment depression in V1 to V3 reflecting acute posterior infarction. (3) ST segment elevation and pathological Q waves in V4R, V5R and V6R reflecting acute right ventricular infarction. (4) First degree AV block (PR interval = 0.28 sec). Coronary angiography showed subtotal occlusion of the right coronary artery.

17

I

II

Ill

aVR

aVL

aV F

Fig. 2.8 ECG of a 39-year-old man showing inferolateral and posterior transmural myocardial infarction. Note: (1) Pathological Q waves and T wave inversion in 11, 111, aVF, V5 and V6 reflecting the “resolution phase” of transmural inferolateral infarction. (2) Tall R and T waves in V1 to V3 reflecting the “resolution phase” of posterior infarction.

Fig. 2.9 Top panel is an enlargement of Vl to V3 shown in Fig. 2.8. Bottom panel was obtained from a photograph of the top panel but it was printed upside down. Note: (1) Pathological Q waves and deeply inverted T waves in Vl to V3 in the bottom panel. These are the ECG abnormalities which would have been seen in an oesophageal lead ECG, if it had been done in this patient. (2) The tall R and tall T waves in V, to V, in the top panel represent reciprocal changes of the pathological Q wave and the deeply inverted T wave respectively in the oesophageal lead ECG.

18

SUBENDOCARDIAL (NON-Q WAVE) INFARCTION In subendocardial infarction, only the inner half of the myocardium is involved. The clinical history of patients with subendocardial infarction and those with transmural infarction is similar. However, the ECG diagnosis of subendocardial infarction is not as precise as that for transmural infarction, since similar changes may occur in stable angina (i.e. angina induced by exercise or emotion) or unstable angina. The diagnosis of subendocardial infarction must therefore be based on the clinical history, together with ECG and biochemical abnormalities. In patients with subendocardial infarction, no pathological Q waves or elevated ST segments are seen. Instead, there are either deep and symmetrically inverted arrowheadT waves which are usually associated with ST segment depression (Fig. 2.10), or ST segment depression occurring alone. Unlike angina pectoris, these ECG abnormalities are usually persistent and may last for several hours or days. There is also an associated rise in the levels of the serum markers of acute myocardial infarction.

SUBENDOCARDIAL INFARCTION Fig. 2.10 Diagram showing ECG pattern of subendocardial infarction. Note deep and symmetrically inverted arrowhead T wave (T).

Figure 2.11 is the ECG of a 65-year-old woman with subendocardial infarction showing deep and symmetrically inverted arrowhead T waves and ST segment depression in leads V2 to V6, 11, I11 and aVF. Coronary angiography showed severe narrowing of the proximal left anterior descending artery. In this patient, the T wave inversion persisted for 3 years. She then suffered another attack of acute myocardial infarction. The ECG recorded at that time showed that all the previously inverted T waves had become upright (Fig. 2.12). This phenomenon of inverted T waves becoming upright during an episode of acute myocardial ischaemia is termed “pseudo-normalization”of the T wave.

19

Fig. 2.11 Subendocardial infarction. ECG of a 65-year-old woman with acute subendocardial infarction. Note: (1) Deep and symmetrically inverted T waves with ST segment depression in V2 to v,,f 11,111 and aVF. ( 2 ) Axis of about - 45’ reflecting left anterior hemiblock. Coronary angiography showed severe narrowing of the proximal left anterior descending artery.

I

111

aV R

aV L

aV F

Fig. 2.12 The ECG shown in Fig. 2.11 remained unchanged for 3 years. The patient then suffered another attack of acute myocardial infarction. This ECG was recorded at that time and it shows that all the deeply inverted T waves have become upright - “pseudo-normalization” of the T waves. Ventricular ectopic beats are seen in V1, V3 and vf,.

Figure 2.13 is the ECG recorded from another patient with subendocardial infarction and it shows very marked ST segment depression (downsloping and horizontal type) in multiple leads.

20

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... ....

......

.

~-

.~

I

I

I1

v1

111

aVF

aV L

V6

v2

Fig. 2.13 Subendocardial infarction. The patient was a 54-year-old man who presented with severe chest pain and cardiogenic shock. Note that there is very deep depression of the ST segments (downsloping and horizontal) in multiple leads - Vz to V6, I, 11,111and aVF. The deepest ST segment depression (14 mm) is seen in V5 (arrowhead).

In recent years, some experts have suggested that the ECG differentiation of transmural and subendocardial infarction should be a b a n d ~ n e d They .~ opined that many patients showing Q waves do not have full thickness (i.e. transmural) myocardial infarction. Furthermore, many other patients showing ST-T wave changes do not have infarction which is limited to the inner half of the ventricular wall. Because of this, they proposed that the ECG diagnosis of myocardial infarction should be described as either “Q wave infarction” (i.e. presence of pathological Q waves), or “non-Q wave infarction” (i.e. absence of pathological Q waves but presence of STT wave changes). Nevertheless, it is important to note that Q wave infarctions, although not always transmural in pathology, are in general significantly larger than non-Q wave infarctions.

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V2

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v5

V6

Fig. 2.14 Reinfarction. The ECG is from a patient who had previously suffered an acute myocardial infarction. Top panel is his usual ECG which shows old, transmural anterior infarction as reflected by pathological Q waves in V2 to V4 and loss of R wave voltage with T wave inversion in V4 to Vs. The bottom panel was recorded soon after he suffered a reinfarction and shows ST segment elevation in V, to V4, deepening of the T wave inversion in V4 to v g , deepening of the Q wave and loss of R wave in V4 and a further decrease in the height of the R waves in v5 and vg.

21

REINFARCTION A frequent clinical problem is the diagnosis of reinfarction in a patient who had previously suffered a myocardial infarction and now complains of chest pain. In this situation, it is important to compare the present ECG with those recorded in the recent past. If the current ECG shows new ST segment elevation, new Q waves or new T wave inversion, then most likely reinfarction has occurred. In addition, the serum markers of acute myocardial infarction will be elevated. Figure 2.14 shows an example of reinfarction.

CHRONIC ISCHAEMIC HEART DISEASE The hallmark ECG abnormality of chronic ischaemic heart disease is ST segment depression. Normally, the ST segment is isoelectric and blends smoothly and imperceptibly with the ascending limb of the T wave. In the J type or junctional ST segment depression, there is depression of the proximal part of the ST segment beginning at its junction with the QRS complex. The slope of the ST segment is upwards and its distal part merges gently and imperceptibly with the T wave (B in Fig. 2.15). J type ST segment depression may be present in normal subjects and is not significant unless it is very marked and its upward slope is so gradual as to appear nearly horizontal.

B

D

C

E

Fig. 2.15 Diagram showing the different types of ST segment depression indicated by arrows. (A) Isoelectric ST segment. (B) Junctional or J type. ( C ) Mirror image of the pass sign (/) “digitalis effect”. (D) Horizontal. (E) Downsloping (Sagging).

22

Figure 2.16 is an ECG showing J type ST segment depression in a 34-year-old man with atypical chest pain during treadmill exercise stress testing. C in Fig. 2.15 shows a type of ST segment depression which resembles a mirror image of the pass sign (v). This ECG finding, termed the “digitalis effect”, is seen in patients who have been given digitalis and is not a sign of digitalis toxicity. Figure 2.17 shows the ECGs of a patient recorded before and during digoxin administration. The other 2 types of STsegment depression shown in Fig. 2.15 are horizontal (plane depression) in D, and downsloping (sagging depression) in E. They are both abnormal and are seen in ischaemic heart disease. Before an ST segment depression is regarded as significant, it should be at least 1 mm in depth. In horizontal ST segment depression, there is, in addition, a sharp angle between the ST segment and the proximal limb of the T wave. This sharp angle ST-T junction is sometimes one of the earliest signs of coronary artery disease. It may be present even though the ST segment is not depressed. In this situation, the ST segment appears to hug the baseline giving an appearance of “horizontality” (Fig. 2.18).

Fig. 2.16 The ECGs (top and bottom panels) were recorded during treadmill exercise stress testing in a 34-year-old man. Top panel was recorded at rest and the bottom panel soon after exercise, in the recovery period. Arrowheads indicate J type ST segment depression.

23

V4

v5

V6

v5

V6

Fig. 2.17 “Digitalis effect”. Top panel was recorded in a patient before and bottom panel after the administration of digoxin. Note ST segment depression resembling the mirror image of the pass sign (/) in the bottom panel (arrowheads).

Fig. 2.18 “Horizontality” of the ST segment in a 62-year-old man with coronary artery disease which was confirmed by coronary angiography. Top panel was recorded at rest and is normal Bottom panel was recorded 15 minutes after the termination of an attack of chest pan. Note the sharp angle (arrow) between the ST segments and the proximal limbs of the T waves and

24

In a patient with stable angina, the ST segment depression is transient and is frequently present only during chest pain. If the history is typical of angina but the resting ECG is normal, the diagnosis of ischaemic heart disease cannot be excluded. Figures 2.19 and 2.20 show the ECGs of a patient with angina pectoris when he was having chest pain and when he was free of chest pain respectively.

I

v2

Vl

Zk'IiEE

aVL

aVF

VS

V6

v3

V4

Fig. 2.19 ECG was recorded in a patient with angina pectoris during an episode of chest pain. Note: ( 1 ) Marked horizontal ST segment depression in Vz, I and I1 (arrowhead in V2), (2) Marked downsloping ST segment depression in V3 to v6 (arrowhead in V3) associated with U wave inversion (arrow in V3),

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Fig. 2.20 Normal ECG recorded from the same patient whose ECG is shown in Fig. 2.19 during a pain-free period.

25

EXERCISE STRESS TEST In patients who are suspected of suffering from coronary artery disease but who have a normal resting ECG, an exercise ECG stress test should be done. This test may reveal ECG abnormalities (usually associated with angina) during exercise. In most laboratories or clinics, treadmill exercise stress test is performed using the Bruce protocol.1° Figure 2.21 is the treadmill exercise stress test ECG in a patient with angina and a normal resting ECG. During exercise, chest pain and marked ST segment depression were induced. Subsequent coronary angiography showed severe triple vessel disease. Figure 2.22 is the treadmill exercise stress test ECG of an asymptomatic 63-year-old woman. It shows marked, horizontal ST segment depression in multiple leads. No chest pain was noted during the test. Subsequent coronary angiography showed triple vessel disease (Figs. 2.24 and 2.25) indicating that the ST segment depression which was seen during the exercise stress test was indeed a reflection of “silent myocardial ischaemia”. After coronary artery bypass surgery was performed, the repeat treadmill exercise stress test ECG was normal, indicating an absence of myocardial ischaemia as a result of successful myocardial revascularization (Fig. 2.23). In recent years, Holter ambulatory ECG monitoring has also been frequently used to detect ST segment abnormalities, especially for the diagnosis of “silent myocardial ischaemia” and Prinzmetal’s angina.

RESTING

HYPERVENT

1

IMMEDIATE PE

8 MIN PE

26

10 MIN

PE

12 MIN PE

Fig. 2.21 Treadmill exercise stress testing in a 52-year-old man with angina pectoris. The patient experienced chest pain during Stage I of the Bruce exercise stress test protocol and the test was stopped. ECG was recorded using a modified V 5 lead. The resting ECG and that recorded after hyperventilation (HYPERVENT) are both normal. There is 3 mm ST segment depression (arrowhead) in Stage I. The following changes are seen in the post-exercise (PE) period. (1) Horizontal ST segment depression (arrowhead) and U wave inversion (arrow) in the immediate phase. (2) Downsloping ST segment depression (arrowhead) at 3 minutes. (3) Deeply inverted T wave (arrow) at 4 minutes. (4)“Horizontality” of the S T segment (arrowhead) and flat T wave at 10 minutes. ( 5 ) Normal ECG at 12 minutes.

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Fig. 2.22 12-lead ECG was recorded during treadmill exercise stress testing in a 63-year-old asymptomatic woman with familial hypercholesterolaemia. It shows the following: (i) The heart rate is about 15O/minute. (ii) Marked ST segment depression in V3 to v6, 11, 111 and aVF. The ST segment depression in V4 to v6 is horizontal and is about 2 mm deep (arrowheads in V5and V6). In the absence of chest pain, the ST segment depression could be interpreted as representing a false positive result. However, subsequent coronary angiogram revealed triple vessel disease (Figs. 2.24 and 2.25), thus indicating that the ST segment depression was truly a reflection of “silent myocardial ischaemia”

aVF

VI v2

v3

v5

V6

Fig. 2.23 12-lead ECG recorded at peak exercise during treadmill exercise stress testing in the same patient whose ECG is shown in Fig. 2.22, after successful coronary artery bypass surgery. It is now completely normal, indicating an absence of myocardial ischaemia.

27

Fig. 2.24 Left coronary angiogram (lateral view) in the same patient whose ECGs are shown in Figs. 2.22 and 2.23. Arrowhead indicates a discrete 99% stenosis of the left anterior descending artery (LAD). The circumflex artery is absent and was found to be totally occluded at operation. The patient’s right coronary angiogram is shown in Fig. 2.25.

Fig. 2.25 Right coronary angiogram in the left anterior oblique view. Arrowhead indicates a 50% discrete stenosis of the midright coronary artery (RCA).

28

UNSTABLE ANGINA Unstable angina is defined as a clinical syndrome which is between stable angina and acute myocardial infarction, with a wide variety of severity and presentation. In the more severe form, the patient presents with chest pain at rest and ST segment depression and/or T wave inversion in the ECG (Fig. 2.26). Pathological Q waves and elevated ST segments are not seen and the serum CK and CKMB levels are not elevated.

v1 v2

@ v3

VS

V6

Fig. 2.26 ECG of a 75-year-old woman with unstable angina recorded during an episode of chest pain occurring at rest. Note: (1) Marked ST segment depression in V2 to Vs (arrowheads in V3 and V4). (2) Tall P wave in I1 (“Ppulmonale”) reflecting co-existing chronic lung disease. (3) Complete right bundle branch block.

29

PRINZMETAL’S ANGINA Prinzmetal’s angina or variant angina is quite uncommon and is due to vasospasm of the coronary arteries which are either normal or are mildly or severely diseased. Such patients, unlike those with stable angina, usually experience chest pain spontaneously, especially in

II

I

Ill

aV R

aV L

aVF

Fig. 2.27 Prinzmetal’s angina in a 52-year-old man. ECG was recorded during a spontaneous attack of chest pain occurring at rest. Note: ( 1 ) ST segment elevation in I, I1 and aVL. (2) Reciprocal ST segment depression in 111, aVR, aVF and V1 to V3. (3) Deep T wave inversion in v4 to vg.

I

II

II I

aVR

aV L

Fig. 2.28 This ECG was recorded several minutes after Fig. 2.27, at a time when the chest pain had been relieved following sublingual glyceryl trinitrate administration. Note: (1) ST segments are now isoelectric. (2) Widespread, deep T wave inversion.

30

aV F

the early hours of the morning. The ECG recorded during an attack of chest pain will show elevated ST segments in certain leads, with reciprocal ST segment depression in the opposite leads, thus resembling very closely the “hyperacute phase” of transmural myocardial infarction. However, unlike acute myocardial infarction, the ECG quickly becomes normal when the chest pain subsides either spontaneously or following sublingual glyceryl trinitrate administration (Figs. 2.27,2.28 and 2.29). Cardiac arrhythmias such as frequent ventricular ectopic beats, ventricular tachycardia, ventricular fibrillation and atrioventricular (AV) block may all be encountered during an attack of Prinzmetal’s angina (Fig. 2.30).

I

I1

II I

V1

v2

v3

aV R

aV L

aV F

v5

Fig. 2.29 This ECG was recorded about 30 minutes after Fig. 2.27 and is essentially normal except for flat or isoelectric T waves in multiple leads. Coronary angiography showed severe triple vessel disease.

Fig. 2.30 Ventricular bigeminy during an attack of Prinzmetal’s angina. This ECG and Fig. 2.27 were recorded from the same patient. Note: ( 1 ) Elevated ST segment (arrowheads). (2) Ventricular ectopic beats (E) occurring in bigeminy.

31

U WAVE INVERSION In recent years, the importance of U wave inversion as a specific ECG marker of heart disease such as ischaemic, hypertensive and myocardial disease has been re-emphasized (Figs. 2.31,3.8 and 3.17). In ischaemic heart disease, U wave inversion is usually associated with ST segment depression (Fig. 2.19). However, it may rarely be the sole abnormality. Figure 2.32 was recorded in a 50-year-old man with stable angina. It shows isolated U wave inversion in leads V2 and V3. Subsequent coronary angiography showed critical stenosis of the proximal left anterior descending artery. In ischaemic heart disease patients showing U wave inversion in the mid- or left praecordial leads, the coronary arteries which are stenosed are nearly always the left main coronary artery or the left anterior descending artery. l1

A

6

C

Fig. 2.31 Diagram showing: (A) Normal upright U wave (arrowhead). (B) IsolatedU wave inversion (arrowhead). (C) U wave inversion (arrowhead) associated with ST segment depression (arrow).

I

II

111

aVR

aV L

aVF

Fig. 2.32 Isolated U wave inversion in a 50-year-old man with stable angina pectoris. U wave inversion, without ST segment depression, is seen in V2 and V3 (arrowheads). The axis is about -40' reflecting left anterior hemiblock. Coronary angiography showed a 99% narrowing of the proximal left anterior descending artery.

32

VENTRICULAR ECTOPIC BEATS The polarity of the T wave in ventricular ectopic beats is opposite to that of the QRS complex. It is therefore inverted when the ventricular complex shows a predominant R wave, and upright when it shows a predominant S wave. The ST segment blends smoothly and imperceptibly with the T wave whose 2 limbs are asymmetrical (Fig. 2.33). The following deviations in the morphology of the ventricular ectopic beat suggest underlying ischaemic or myocardial disease: (1) Deep and symmetrically inverted arrowhead T wave (Fig. 2.34); (2) T wave polarity identical to that of the qRS complex; (3) presence of a q wave in a ventricular ectopic beat with a predominant R or Rs complex (Fig. 2.35).

I

Fig. 2.33 “Benign” ventricular ectopic beats in a normal individual. Note the following characteristics of the ectopic beats. (1) The ST segments merge gently with the proximal limbs of the T waves. ( 2 )The T waves are opposite in polarity to the R waves or the S waves and their 2 limbs are asymmetrical. These features are best seen in the ventricular ectopic beats (E) in I1 and 111.

33

Fig. 2.34 This ECG is an enlargement of V3 in Fig. 2.12. Note deep and symmetrically inverted arrowhead T wave of the ventricular ectopic beat (E).

Fig. 2.35 ECG of a patient who had previously suffered a transmural myocardial infarction. Although the rS complex of the sinus beat is essentially normal except for a slightly coved ST segment, the ventricular ectopic beat (E) shows a pathological Q wave (arrowhead) indicating an old, transmural myocardial infarction.

Sometimes, the sinus beat immediately following either a ventricular or a supraventricular ectopic beat shows certain changes such as T wave inversion, ST segment depression or U wave inversion which are not present in the sinus beats preceding the ectopic beat (Figs. 2.36 and 5.13). All these changes suggest underlying ischaemic or myocardial disease. The postextrasystolic T wave changes have been termed by Levine as “poor man’s Master’s test”, since they indicate cardiac disease and the patient may thus be spared the cost of a formal exercise stress test.’* However, some investigators have suggested that post-extrasystolic T wave inversion is not specific for cardiac disease, claiming that it is also seen quite commonly in normal individ~a1s.l~ In the author’s experience, however, marked postextrasystolic T wave inversion is associated with ischaemic or myocardial disease in most instances.

34

Fig. 2.36 Post-extrasystolic T wave inversion. Note the inverted T wave (arrow) in the first postextrasystolic sinus beat. (E = ventricular ectopic beat).

ELECTROCARDIOGRAPHIC DIFFERENTIAL DIAGNOSIS OF ISCHAEMIC HEART DISEASE On the other side of the coin, there are many non-coronary causes of ST-T wave abnormalities. Table 2.1 lists the conditions which may produce ST segment depression and

TABLE 2.1* NON-CORONARY CAUSES OF ST-T WAVE ABNORMALITIES PHYSIOLOGICAL RACE, ADOLESCENCE PHARMACOLOGICAL DIGITALIS, ANTI-DEPRESSANT DRUGS PATHOLOGICAL CARDIAC VENTRICULAR HYPERTROPHY, MYOCARDITIS, CARDIOMYOPATHY EXTRA CARDIAC HYPOKALAEMIA, HYPOTHYROIDISM, INTRACRANIAL HAEMORRHAGE

ARTEFACTUAL FAULTY MACHINE (*Adapted from D Short. Br Heart J 1969; 31: 531-537 and withpermissionfforn the BMJ Publishing Group)

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T wave abnormalities which may mimic ischaemic heart disease.I4 They must be excluded before myocardial ischaemia is diagnosed. Most of these abnormalities will be discussed in the next chapter.

ATRIAL INFARCTION Atrial infarction is reported to occur in about 17% of patients with infarction involving the ventricular myocardium in necropsy studies. However, in clinical practice, ECG evidence of atrial infarction is much less frequently encountered. The main ECG abnormality in atrial infarction is elevation of the PR segment as shown in Fig. 2.37.

1: -1; i 7;I ii 1

jI jj

: ; 1 : : :. . ., .. .. ..... , I:.:: . . . . , -. . . . . . . . . . . . .. .. . . ,. . . .... . . . . .. . . -. . . .

Fig. 2.37 Atrial infarction in a 70-year-old woman. Note: (1) Elevated PR segments in 11, I11 and aVF (arrowheads) reflecting atrial infarction. (2) Pathological Q waves, elevated ST segments and T wave inversion in 111 and aVF reflecting acute, transmural inferior infarction.

REFERENCES 1. Deedwania PC, Carbajal EV. Silent myocardial ischaemia. Arch Intern Med 1991; 151: 2373. 2. Source: The Singapore Myocardial Infarction Registry, Ministry of Health, Singapore. 3. Schamroth L. The 12 Lead Electrocardiogram. Blackwell Scientific Publications, Oxford, 1st ed., 1989; p. 145. 4. Fisch C. Electrocardiography. In Heart Disease edited by E Braunwald, W B Saunders Company, Philadelphia, 5th ed., 1997; p. 129. 5. Chou TC. Electrocardiography in Clinical Practice. WB Saunders Company, Philadelphia, 4th ed., 1996; p. 181. 6. Shah PK, Berman DS. Implications of precordial ST segment depressions in acute inferior myocardial infarction. Am J Cardioll981; 48: 1167.

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7. Wong CK, Freedman SB, Bautovich G, et al. Mechanism and significance of precordial ST segment depression during inferior myocardial infarction associated with severe narrowing of the dominant right coronary artery. Am J Cardiol 1993; 71:1025. 8. Reddy GV, Schamroth L. The electrocardiology of right ventricular myocardial infarction. Chest 1986; 90: 756. 9. Phibb B. “Transmural” versus “subendocardial” myocardial infarction: an electrocardiographic myth. J A m Coll Cardiol 1983; 1: 561. 10. Faris J, McHenry P, Stephen N. Concepts and applications of treadmill exercise testing and exercise electrocardiogram. Am Heart J 1978; 95: 102. 11. Gerson MC, McHenry PL. Resting U wave inversion as a marker of stenosis of the left anterior descending coronary artery. Am JMed 1980; 69: 545. 12. Levin HD, Lown B, Streeper RB. The clinical significance of post-extrasystolic T wave changes. Circulation 1952; 6: 358. 13. Engel TR. Postextrasystolic T wave changes and angiographic coronary disease. Br Heart J 1977; 39: 371.

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CHAPTER 3

MISCELLANEOUS CONDITIONS

NORMAL VARIANT In 1954, Grusin from South Africa described certain distinctive ECG patterns which differed from the usual ECGs seen in the white population, but which were apparently quite common amongst the blacks.’ In his description, pattern I showed deeply inverted T waves (especially in the praecordial leads) simulating subendocardial infarction (Fig. 3.1). This pattern is very rare in the normal Asian population. In contrast, pattern 11, which is also known as the early repolarization syndrome or pattern, is seen in approximately 30% of young healthy males of Indian, Chinese and Malay ethnic rigi in.^.^ Here, there is elevation of the ST segment, concave upwards. The T wave is tall and asymmetrical with a gently sloped ascending limb and a sharp descending limb ending in a prominent U wave. These changes are most prominent in the mid- and left praecordial leads V2 to Vg. The QRS voltages in the left praecordial leads are also increased (Figs. 3.1 and 3.2). Unlike the “hyperacute phase” of transmural myocardial infarction, there is no reciprocal ST segment depression. It is important to recognize the early repolarization pattern because it may be mistaken for the “hyperacute phase” of transmural myocardial infarction, acute pericarditis, left ventricular hypertrophy and hyperkalaemia. The points of differentiation will be discussed in the sections below.

A

NORMAL

GRUSIN

I

GRUSIN

II

B

--TL-

A --T

--+

--

Fig. 3.1 Diagram showing normal ECG pattern and the Grusin pattern I and pattern I1 (early repolarization syndrome) normal variants. A = right praecordial lead, B = left praecordial lead.

Fig. 3.2 Early repolarization syndrome in a 61-year-old asymptomatic man. Note: (1) The ST segments are elevated (concave upwards) in Vz to V6 (arrowhead in V4) and they merge with very tall T waves (T = 17 mm in V4) . (2) Rightward displacement of the transition zone resulting in a positive QRS complex in V3. (3) Tall R waves in V4 to Vg.

39

ACUTE PERICARDITIS In acute pericarditis, there is widespread elevation of the ST segments (concave upwards). Frequently, ST segment depression is present only in lead aVR and the ST segment is isoelectric in lead aVL (Fig. 3.3). This is because in acute pericarditis, the ST segment vector in the frontal plane is directed towards lead 11, resulting in maximum ST segment elevation in this lead, isoelectric ST segment in lead aVL, and ST segment depression in lead aVR.4 In contrast, in the “hyperacute phase” of transmural, inferior myocardial infarction, the maximum ST segment elevation is very often in lead 111. Maximal elevation of the ST segment in lead 11, together with widespread ST segment elevation in the praecordial leads, also help to distinguish acute pericarditis from acute, transmural myocardial infarction and the early repolarization pattern. A further point of distinction between acute pericarditis and the early repolarization pattern is that the height of the T waves in the former is normal, whereas it is considerably increased in the latter. As a result of this, the ST/T ratio (i.e. the height of ST segment elevation divided by the amplitude of the T wave) in lead V6 and other left praecordial leads is >0.25 in acute pericarditis, and