Chapter 11 Myocardial Ischemia, Injury, and Infarction

J. Willis Hurst, MD

 [Ventricular Electrocardiography © 1991, 1998 J. Willis Hurst, MD]

 Section 11.1 Myocardial Ischemia, Myocardial Injury, and Myocardial Infarction

 A mismatch of coronary artery blood flow and myocardial oxygen requirements produces myocardial damage. This is usually discussed in terms of a myocardial oxygen supply which is inadequate to meet myocardial oxygen demands. Two mechanisms are responsible for this condition: coronary artery blood flow may be impeded by chronically narrowed coronary arteries, with a mismatch occurring when there is an increased myocardial requirement for oxygen; or when the already narrowed coronary arteries become more acutely narrowed by coronary artery thrombosis, coronary spasm, or both. The disease most commonly responsible for the mismatch is coronary atherosclerosis, but many other causes are listed later in this chapter.

 The electrocardiographic consequences of the mismatch are ischemia, injury, and a myocardial dead zone. In the context of the mismatch, T wave abnormalities indicate myocardial ischemia, ST segment abnormalities indicate myocardial injury, and Q wave abnormalities indicate a myocardial dead zone. The electrophysiological mechanisms responsible for these abnormalities are discussed in Chapter 6 and throughout this chapter.

 The electrocardiographic abnormalities produced by the mismatch are determined by the intensity of the myocardial hypoxia, the duration and the locations of the hypoxia in the myocardium, as well as the coexistence of other heart disease. Electrocardiographic abnormalities secondary to myocardial hypoxia are almost always due to damage to the left ventricle, although the right ventricle and atria may also be damaged.

 Severe myocardial ischemia, including infarction, may not produce electrocardiographic abnormalties. This fact must be emphasized repeatedly. The antithesis to this is that many other disease processes may produce electrocardiographic abnormalities suggesting myocardial ischemia, injury, or dead zone. Under these circumstances, the electrocardiographic abnormalities are referred to as pseudoinfarctions. The conditions causing pseudoinfarctions will be discussed later; they must be remembered to prevent the possibility of a grave diagnostic error.

 Section 11.2 T Wave Abnormalities (Ischemia)

 The T wave abnormalities related to hypoxia may be located predominantly in the endocardial or epicardial area. Endocardial ischemia tends to be localized or generalized, whereas epicardial ischemia tends to be localized to specific areas of the ventricular myocardium. Myocardial ischemia usually occurs in the left ventricle, including the septum, but it may also occur in the right ventricle. A T wave abnormality may be the only sign of infarction and such infarctions are referred to as T wave infarctions (see later discussion).

 Section 11.3 ST Segment Abnormalities (Injury)

 The ST segment abnormalities related to hypoxia may be located predominantly in the endocardial or epicardial area. Endocardial injury tends to be generalized, and epicardial injury tends to be localized to specific areas of the ventricular myocardium. Like myocardial infarction, myocardial injury usually occurs in the left ventricle, including the septum, but it may also occur in the right ventricle.

 Section 11.4 Q Wave Infarction (Dead Zone)

 Myocardial damage may be sufficiently severe to cause the death of myocytes, which removes electrical forces from certain areas of the heart.[1] When this occurs, the electrical forces generated by the diametrically opposite side of the heart will dominate the electrical field. This may create abnormal Q waves in the electrocardiogram. Such abnormalities usually occur in the left ventricle, but may also occasionally involve the right ventricle. The myocardial damage responsible for the Q wave abnormality is located predominately in the endocardial area, and diminishes in magnitude as it approaches the epicardium. It is sometimes referred to as a transmural infarction. It seems proper, however, to discontinue the use of the term "transmural infarction" because abnormal Q waves may occur with an infarct that is not transmural;[1] the electrocardiogram is more accurately referred to as showing a Q wave infarction. Areas of injured and ischemic tissue surround the dead zone; they are usually located predominantly in the epicardial areas of the myocardium.

 Abnormal Q waves due to myocardial infarction are shown in Figure 6.7, along with the ST and T wave abnormalities. Whereas a mean initial 0.04-second QRS vector is used to represent the infarcted area, it must be emphasized that a Q wave may be abnormal even when its duration is less than 0.04 second. In such cases, the identification of an abnormality depends on determination of the relationship of the initial QRS forces to the subsequent QRS forces.

 Section 11.5 Non-Q Wave Infarction

 The term "subendocardial infarction" has fallen into disrepute. For many years, I have asked hundreds of individuals to describe their criteria for subendocardial infarction. The criteria varied greatly from one individual to another. I discovered that the criteria being used were "made up," and seemed to be "hand-me-downs of misinformation." Many of the persons who used the term had no notion of the pathophysiological mechanism involved in the process they described.

 In the past those using the term "subendocardial infarction" usually applied it to an electrocardiogram that showed the development of ST and T wave abnormalities without the development of abnormal Q waves. Although this approaches the truth, it misses the mark in that there are several reasons why abnormal Q waves may not appear in the electrocardiograms of many patients with myocardial infarction (Table 11.1). Note that a transmural infarction may be present, yet the electrocardiogram may not reveal abnormal Q waves. Consequently, it is more accurate to refer to such an infarction as a non-Q wave infarction than to presume that the infarction is located in the subendocardial area.

 There is one circumstance in which it seems proper to use the term "subendocardial infarction": when subendocardial injury persists for hours, it is often the first stage of a generalized subendocardial infarction. This type of infarct, one could argue, should be referred to as a "generalized endocardial infarction." The pathophysiology is often different from that of a spontaneous infarction associated with epicardial injury. Persistent subendocardial injury may occur when a patient with significant coronary atherosclerosis develops hypotension. It is especially likely in a patient with coronary atherosclerosis complicated by left ventricular hypertrophy and elevated left ventricular diastolic pressure, as may occur with severe aortic valve stenosis. Accordingly, patients with significant coronary atherosclerosis and aortic stenosis, hypertension, or aortic regurgitation are at greater risk for generalized subendocardial injury and subendocardial infarction. Recognized by an abnormal and persistent ST segment vector directed away from the centroid of the left ventricle, subendocardial injury may last for several hours, during which time a generalized endocardial infarction may develop. This, however, often gives way to the usual electrocardiographic signs of non-Q wave infarction.

 Section 11.6 Electrocardiographic Abnormalities Due to Myocardial Ischemia, Injury, and Myocardial Dead Zone

 The electrocardiographic characteristics of myocardial ischemia, injury, and abnormal Q waves of myocardial dead zone are listed in Table 11.2. Examples are shown in Figures 11.1 through 11.18.
 
 
Click to zoom Figure 11.1
This electrocardiogram was recorded from a 55-year-old patient with an acute inferolateral and posterior myocardial infarction. The heart rate is 72 complexes per minute, with a lower atrial rhythm. The duration of the QRS complex is 0.09 second and the duration of the QT interval is 0.36 second.
P waves: The mean P vector is directed superiorly; this signifies that atrial excitation originates in the lower portion of the atrium rather than in the sinus node.

 QRS complex: The mean QRS vector is directed about -35° to the left. It is parallel with the frontal plane, whereas normally, it would be directed more posteriorly. The mean initial 0.04-second QRS vector is directed about -85° to the left. This is abnormal since the vector should be inferior to a horizontally-directed mean QRS vector. The mean initial 0.04-second QRS vector has an abnormal anterior direction, producing tall R waves in leads V1 and V2. It is directed away from the inferolateral and posterior portion of the left ventricle.

 ST segment: The mean ST segment vector is huge. It is directed toward the epicardial injury located in the inferior, slightly posterior, and lateral portion of the left ventricle.

 T waves: The mean T vector is enormous. It may represent generalized endocardial ischemia in that it is directed toward the centroid of the left ventricle. The mean T vector, during this hyperacute phase, has not yet become directed away from the epicardial area of the inferior, posterior, and lateral portion of the left ventricle.

 A.The frontal plane projections of the mean P, mean initial 0.04-second QRS, mean QRS, mean ST, and mean T vectors.

 B. The spatial orientation of the mean P vector. It indicates a lower atrial rhythm because it is directed superiorly. The P waves are barely visible in the precordial leads; this makes it difficult to determine the degree of anterior or posterior deflection of the mean P vector. It is likely that all of the precordial electrode positions are near the transitional pathway for the mean P vector.

 C.The spatial orientation of the mean QRS vector. Note the course of the transitional pathway in the precordial leads.

 D.The spatial orientation of the mean initial 0.04-second QRS vector. It is abnormally directed anteriorly, superiorly, and away from the inferolateral and posterior portion of the left ventricle. It is the major cause of abnormal left axis deviation of the mean QRS vector. Leads V4, V5, and V6 are near the transitional pathway for the mean initial 0.04-second vector. Accordingly, the predicted deflections related to the mean initial 0.04-second vector do not fit the actual deflections shown in leads V4, V5, and V6 (see previous discussions of discrepancies between predicted and actual deflections).

 E.The spatial orientation of the mean ST vector. Note the course of the transitional pathway in the precordial leads. The mean ST vector is directed toward epicardial injury in the inferolateral and posterior portions of the left ventricle.

 F.The spatial orientation of the mean T vector. Note that the transitional pathway cannot be identified in the precordial leads, making it impossible to identify how far anteriorly the vector is directed. The T wave is about the same size in V1 as in V6, suggesting that the mean T vector is directed about 30° to 45° anteriorly. The hyperacute mean T vector is probably due to endocardial ischemia. At a later stage of myocardial infarction, it would be directed away from epicardial ischemia in the inferolateral and posterior region of the left ventricle.

 Summary: This electrocardiogram shows abnormalities of the mean initial 0.04-second QRS vector, the mean ST vector, and the mean T vector that are characteristic of an early stage of inferolateral and posterior myocardial infarction. The direction of the mean ST vector suggests, but does not prove, that obstruction of the circumflex coronary artery is the culprit.

 From Hurst JW, Woodson GC Jr: Atlas of Spatial Vector Electrocardiography. New York: Blakiston, 1952, p. 123. (Copyright held by JW Hurst) 

Click to zoom Figure 11.2
This electrocardiogram, showing inferior myocardial infarction, was recorded from a 52-year-old man with chest pain. He gave a history of previous myocardial infarction. Coronary arteriography revealed 61% occlusion of the left anterior descending artery beyond its first branch, 41% occlusion of the first diagonal branch, and 16% occlusion of the left circumflex coronary artery.

 The rhythm is normal, and the heart rate is 75 complexes per minute. The PR interval is 0.16 second. The duration of the QRS complex is 0.08 second, and the duration of the QT interval is 0.36 second.

P waves: The P waves are normal.

 QRS complex: The mean QRS vector is directed about -18° to the left, and parallel with the frontal plane; normally, it should be directed slightly posteriorly. The

 mean initial 0.04-second QRS vector is abnormal; it is directed about -55° to the left, away from the inferior portion of the left ventricle. It is parallel with the frontal plane. Normally, it should be inferior to a horizontally-directed mean QRS vector.

 T waves: The mean T vector is large, and directed away from an area of epicardial ischemia located in the inferior portion of the left ventricle. It shows an abnormal shift to the left of the horizontal mean QRS vector. Normally, the mean T vector would also be inferior to a horizontally directed mean QRS vector.

 A.The frontal plane projections of the mean QRS, mean initial 0.04-second QRS, and mean T vectors.

 B.The spatial orientation of the mean QRS vector. Note the course of the transitional pathway in the precordial leads. The mean ORS vector is more anteriorly directed than it is normally.

 C. The spatial orientation of the mean initial 0.04-second QRS vector. Note the course of the transitional pathway in the precordial leads. The mean initial 0.04-second QRS vector is directed away from a dead zone in an inferior portion of the left ventricle.

 D. The spatial orientation of the mean T vector. Note that the transitional pathway cannot be identified in the precordial leads. The T wave in lead V1 is much smaller than in lead V6. Accordingly, the mean T vector is directed about 20° to 30° anteriorly.

 Summary: The mean initial 0.04-second QRS vector is directed away from a dead zone in the inferior portion of the left ventricle. The mean T vector points away from the area of epicardial ischemia in the inferior portion of the left ventricle. Coronary arteriography revealed a significant obstruction in the left anterior descending coronary artery after its first branch. This type of infarction is usually caused by obstruction of the right coronary arteries. On rare occasions, as in this patient, it can be caused by obstruction of a "wraparound" left anterior descending artery.[4]

Click to zoom Figure 11.3
This electrocardiogram was recorded from a 59-year-old woman with an acute inferoposterior myocardial infarction. She had previously undergone coronary bypass surgery, and underwent coronary arteriography following unstable angina pectoris. This revealed that the vein grafts to the left anterior descending and right coronary arteries were closed. The circumflex coronary artery was totally obstructed, and the left anterior descending coronary artery was 60% occluded. There were three sequential obstructions in the right coronary artery, the most severe being a 90% occlusion. The patient was given tissue plasminogen activator (tPA), which resulted in a marked decrease in the size of the ST segment vector. Intravenous nitroglycerin and heparin were administered, and coronary bypass surgery was performed the following day.

 The heart rate is 48 complexes per minute; sinus bradycardia is present. The PR interval is 0.18 second. The duration of the QRS complex is 0.12 second, and the duration of the QT interval is 0.40 second.

P waves: The P waves are normal.

 QRS complex: The duration of the QRS complex is 0.12 second. The mean QRS vector is directed about +118° inferiorly, and about 45° anteriorly. The mean terminal 0.04-second QRS vector is directed to the right and slightly anteriorly; this signifies right bundle branch block.

 ST segment: The mean vector representing the ST segment is directed +120° inferiorly and slightly posteriorly. When there is uncomplicated right bundle branch block, the mean T and ST vectors should be directed to the left and posteriorly, opposite the mean QRS vector. In this case of complicated right bundle branch block, the mean ST segment vector is directed inferiorly and posteriorly, toward an area of epicardial myocardial injury in the inferior and posterior portion of the left ventricle.

 T waves: The mean T vector is directed about +90° inferiorly, and markedly posteriorly. This probably represents early endocardial ischemia of the inferoposterior portion of the left ventricle. It is likely that this vector will, at a later time, be directed away from an area of inferior and posterior epicardial ischemia.

 A. The frontal plane projections of the mean QRS, mean ST vector, and mean T vectors.

 B. The spatial orientation of the mean QRS vector. The features are characteristic of right bundle branch block.

 C. The spatial orientation of the mean ST vector.

 D. The spatial orientation of the mean T vector.

 Summary: The abnormalities in this electrocardiogram can be used to illustrate several points. They indicate the way in which the ST segment and early T wave abnormalities of inferoposterior infarction can be identified in the presence of right bundle branch block. The mean vectors representing the ST and T abnormalities of uncomplicated right bundle branch block should be directed opposite the mean QRS vector of right bundle branch block. Such is not the case in this patient with complicated right bundle branch block. The mean ST and T vectors are abnormal as the result of an inferior-posterior infarction. The ST segment abnormality almost disappeared following the use of tPA, indicating the lysis of a clot.

Click to zoom Figure 11.4
This electrocardiogram was recorded from a 58-year-old man with an inferolateral myocardial infarction and stable angina pectoris. He had a history of two previous myocardial infarctions requiring bypass surgery in 1980. He had class 2 to 3 stable angina pectoris (Canadian Cardiovascular Society Classification). A coronary arteriogram made in June 1983 showed 100% occlusion of the left anterior descending artery, distal to the first septal perforator. The first diagonal branch and the circumflex coronary arteries were 100% occluded. The bypass grafts were patent. The ejection fraction was 58%. The distal right coronary artery was normal. The apex and inferior apical areas of the myocardium were noncontractile, and the inferior basal area showed a moderate decrease in contractility.

 The rhythm is normal and the heart rate is 107 complexes per minute. The PR interval is 0.16 second. The duration of the QRS complex is 0.10 second, and that of the QT interval is 0.32 second.

P waves: The P waves are normal.

 QRS complexes: The QRS complexes are abnormal. The mean QRS vector is directed at -100° superiorly, and about 60° posteriorly. The mean initial 0.04-second QRS vector is directed at -85° superiorly and about 30° anteriorly, away from an inferoposterior dead zone (see later discussion).

 T waves: The T waves are abnormal. The mean T vector is directed about +5° in the frontal plane, and 85° to 90° anteriorly. It is directed away from an area of epicardial ischemia located in the posterior portion of the left ventricle.

 A. The frontal plane projections of the mean QRS, mean initial 0.04-second QRS, and mean T vectors.

 B. The spatial orientation of the mean QRS vector. Note that the QRS complexes are all negative in the precordial leads. The QRS complex in lead V1 is more negative than it is in lead V6; accordingly, the mean QRS vector is directed at least 60° posteriorly.

 C. The spatial orientation of the mean initial 0.04-second QRS vector. It is directed superiorly and anteriorly, away from the inferoposterior and lateral portions of the left ventricle. The transitional pathway for the mean initial 0.04-second vector is located near electrode positions V5 and V6. Accordingly, the diagram, which is constructed using a rigid format, does not match the actual deflections of the mean initial 0.04-second vector as reflected in leads V5 and V6 (see previous discussions).

 D.The spatial orientation of the mean T vector. It is directed anteriorly at 85° to 90°, so that the T wave is isoelectric in lead V6, and upright in all other precordial leads; it is directed away from an area of epicardial injury in the posterior portion of the left ventricle.

 Summary: This electrocardiogram illustrates the presence of an inferior posterior dead zone and a posterior area of epicardial ischemia. These abnormalities could be due to two separate infarcts or a single infarct that is located in the proper area of the left ventricle.

Click to zoom Figure 11.5
This electrocardiogram, showing inferolateral infarction, was taken from a 78-year-old man with a history of myocardial infarction and angina pectoris occurring at rest.

 The rhythm is normal, and the heart rate is 75 complexes per minute. A coronary arteriogram revealed 60% occlusion of the third marginal branch of the left circumflex coronary artery.

 The PR interval is 0.13 second. The duration of the QRS complex is 0.08 second, and the duration of the QT interval is 0.40 second.

P waves: The P waves are normal.

 QRS complex: The mean QRS vector is directed -50° to the left and about 45° posteriorly. The mean initial 0.04-second QRS vector is directed 40° to the left, and parallel with the frontal plane. It is directed away from the inferior portion of the left ventricle. The marked left axis deviation is due to the inferior infarction.

 ST segment: The mean ST vector is directed toward an inferior area of epicardial injury.

 T waves: The mean T vector is directed away from an inferior-posterior area of epicardial ischemia.

 A.The frontal plane projections of the mean QRS, mean initial 0.04-second QRS, mean ST, and mean T vectors.

 B. The spatial orientation of the mean QRS vector. Note the course of the transitional pathway in the precordial leads.

 C. The spatial orientation of the mean initial 0.04-second QRS vector. It points away from an inferior area of the left ventricle. Note the course of the transitional pathway in the precordial leads.

 D. The spatial orientation of the mean ST vector. All precordial electrode positions are located near the transitional pathway for the mean ST vector.

 E. The spatial orientation of the mean T vector. Note the course of the transitional pathway in the precordial leads. The V4, V5, and V6 electrode positions are located near the transitional pathway for the mean T vector. Because of this, the diagram, based on a rigid format, does not match the deflections. Note that the T waves are inverted in leads V5 and V6, whereas the diagram suggests that they would be upright (see discussion of discrepancies between actual and predicted deflections earlier in this chapter).

 Summary: The mean initial 0.04-second QRS vector is directed away from an inferior left ventricular dead zone, and the mean ST segment vector points toward the same area. The mean T vector points away from an inferoposterior area of left ventricular epicardial ischemia. Note that the culprit artery was the third marginal branch of the circumflex coronary artery.

Click to zoom Figure 11.6
This electrocardiogram was recorded from an 89-year-old man with an inferior myocardial infarction. He had class 2 to 3 angina pectoris (Canadian

 Cardiovascular Society Classification), a history of three infarctions, and systemic hypertension. He was receiving digoxin for heart failure. Coronary bypass surgery had been performed in 1976, and arteriography performed at that time revealed 90% obstruction of the left main coronary artery, 80% obstruction of the left anterior descending coronary artery, 80% obstruction of the circumflex coronary artery, and 100% obstruction of the right coronary artery. The inferior portion of the left ventricle was akinetic.

 The rhythm is normal and the heart rate is 68 complexes per minute. The PR interval is 0.16 second. The duration of the QRS complex is 0.09 second, and that of the QT interval is 0.39 second.

P waves: The mean P vector is directed +85° inferiorly, and slightly posteriorly. The second halves of the P waves in leads V1 and V2 suggest a left atrial abnormality. The P waves are not definitely abnormal.

 U waves: The U waves are large in leads V2 and V3.

 QRS complexes: The QRS complexes are abnormal. The mean QRS vector is directed about +8° in the frontal plane and about 30° posteriorly. The total 12-lead QRS amplitude is greater than 124mm, and the QRS amplitude in lead V5 is greater than 25mm. The mean initial 0.04-second QRS vector is directed -70° to the left, about 10° posteriorly, and abnormally to the left of a horizontal mean QRS vector. This is due to a dead zone in the inferior portion of the left ventricle.

 ST segment: The mean ST (early T) vector is directed +150° to the right and parallel with the frontal plane. This is probably due to the digitalis medication.

 T waves: The mean late T vector is directed +85° inferiorly, and 85° anteriorly.

 A. The frontal plane projections of the mean QRS, mean initial 0.04-second QRS, mean ST (early T), and mean late T vectors.

 B. The spatial orientation of the mean QRS vector. Note the course of the transitional pathway in the precordial leads.

 C. The spatial orientation of the mean initial 0.04-second QRS vector. The electrode positions for leads V2, V3, and V4 are all near the transitional pathway for the mean 0.04-second vector.

 D. The spatial orientation of the mean ST (early T) segment vector.

 E. The spatial orientation of the mean late T vector. The abnormal anterior direction is not due to digitalis because the vector is directed about 115° anterior to the mean QRS vector. This wide QRS-T angle is due either to left ventricular hypertrophy or left ventricular ischemia.

 Summary: This electrocardiogram exhibits evidence of an inferior dead zone, posterior ischemia, and a digitalis effect.

Click to zoom Figure 11.7
This electrocardiogram was recorded in the intensive care unit from a 59-year-old man who had just undergone coronary bypass surgery. The previous electrocardiogram showed inferior infarction. The coronary arteriogram showed 100% occlusion of the left anterior descending coronary artery after its first branch, 79% occlusion of the first diagonal branch, 59% occlusion of the mid and 57% occlusion of the distal portion of the circumflex coronary artery, and 95% occlusion of the distal portion of the right coronary artery. The ejection fraction was 40%, and there was anterobasal and anterior mild hypokinesis, apical, septal, and posterolateral moderate hypokinesis, and inferoapical inferior akinesis. The conduction abnormality shown in this electrocardiogram was not present prior to coronary bypass surgery; it was observed for only a few hours after surgery.

 The rhythm is normal and the heart rate is 90 complexes per minute. The PR interval is 0.16 second. The duration of the QRS complex is 0.14 second and the QT interval is 0.44 second.

P waves: The P waves are normal.

 QRS complexes: The QRS duration is 0.14 second. The mean QRS vector is directed +160° to the right and about +35° anteriorly, signifying complicated right bundle branch block. The mean initial 0.04-second QRS vector is abnormal; it is directed -70° superiorly and anteriorly. The anterior direction of the vector could be caused by a true posterior infarction or right ventricular hypertrophy. In this patient, the anterior direction of the vector was transient; it persisted for only a few hours, ruling out right ventricular hypertrophy. The leftward deviation of the vector is due to inferior infarction because it was present throughout the period of observation. However, its anterior direction changed, suggesting a posterior area of "stunned" myocardium. The orientation of the mean terminal 0.04-second QRS vector was also transient. It is directed +135° to the right and parallel with the frontal plane, suggesting left posterior-inferior division block and right bundle branch block.

 ST segment: The mean ST vector is directed +100° inferiorly and slightly posteriorly, in the direction of the epicardial injury in the inferior portion of the left ventricle.

 T waves: The mean T vector is directed +30° in the frontal plane, and about 35° posteriorly, away from an area of anterior left ventricular epicardial ischemia.

 A. The frontal plane projections of the mean QRS, mean initial 0.04-second QRS, mean terminal 0.04-second QRS mean ST, and mean T vectors.

 B. The spatial orientation of the mean QRS vector.

 C. The spatial orientation of the mean initial 0.04-second QRS vector.

 D. The spatial orientation of the mean terminal 0.04-second QRS vector. It is directed so far to the right that right bundle branch block alone does not account for it.

 E. The spatial orientation of the mean ST vector.

 F. The spatial orientation of the mean T vector.

 Summary: This unusual electrocardiogram reveals signs of inferoposterior

 infarction. The leftward and slightly anterior direction of the mean initial 0.04-second QRS vector is due to an inferoposterior dead zone. Its anterior direction may be due to an area of temporarily "stunned" posterior myocardium.

 The mean terminal 0.04-second QRS vector is abnormal, owing to transient right bundle branch block; it is directed so far to the right and anteriorly that additional, transient posterior-inferior division block should be considered. The mean T vector indicates anterior epicardial ischemia. The cause of the transient conduction disturbance in this patient is related to ischemia or hypothermia which may have occurred during bypass surgery. There may be many different explanations for these transient electrocardiographic abnormalities, but those given here seem plausible in this patient.

Click to zoom Figure 11.8
This electrocardiogram was recorded from a 59-year-old hypertensive man with angina pectoris and a history of inferior myocardial infarction. The coronary arteriogram revealed 100% occlusion of the left anterior descending coronary artery beyond its first branch, 100% occlusion of the distal portion of the left circumflex coronary artery, and 100% occlusion of the third marginal branch of the circumflex coronary artery.

 The rhythm is normal and the heart rate is 78 complexes per minute. The PR interval is 0.20 second. The duration of the QRS complex is 0.08 second and the duration of the QT interval is 0.36 second.

P waves: The P waves are normal.

 QRS complex: The mean QRS vector is directed at 0° in the frontal plane and about 50° to 60° posteriorly. The mean initial 0.04-second QRS vector is directed about -50° to the left and to an undetermined degree anteriorly. The mean initial 0.04-second QRS vector is abnormal for two reasons: it is superior to a horizontally directed mean QRS vector, and the spatial angle between the initial 0.04-second QRS vector and the mean QRS vector is greater than 60°. This vector is directed away from a dead zone located in the inferior and slightly posterior portion of the left ventricle.

 T waves: The mean T vector is directed at +60°, and at least 45° anteriorly (the T wave amplitude in leads V1 and V6 is about equal). The QRS-T angle is abnormal because it is greater than 90°.

 A. The frontal plane projections of the mean QRS, mean 0.04-second QRS, and mean T vectors.

 B. The spatial orientation of the mean QRS vector. Note the course of the transitional pathway in the precordial leads.

 C. The spatial orientation of the mean initial 0.04-second QRS vector. Note the difficulty in identifying the transitional pathway in the precordial leads. One can assume, however, that the vector has a moderately anterior orientation.

 D. The spatial orientation of the mean T vector. Note the difficulty in identifying the transitional pathway in the precordial leads. One can assume that the mean T vector is directed about 45° anteriorly, because the size of the T waves is about equal in leads V1 and V6.

 Summary: This interesting electrocardiogram is included to make a single point: the clinician should not assume that the QRS-T angle abnormality is due to inferior infarction. Even though the direction of the mean initial 0.04-second QRS vector indicates an inferoposterior infarction, the QRS-T angle indicates another abnormality; it does not conform to the changes expected with such an infarct. The QRS-T angle is abnormal owing to either an early stage of left ventricular systolic pressure overload due to hypertension, or posterior-superior epicardial ischemia of obstructive coronary disease.

Click to zoom Figure 11.9
This electrocardiogram, showing a tall R wave in lead V1 secondary to a true posterior infarction, was recorded from a 75-year-old man. The patient had unstable angina pectoris for 2 months. A coronary arteriogram made on June 9, 1988, revealed 79% obstruction of the left anterior descending coronary artery beyond the first septal perforator. The first diagonal branch was 52% obstructed, and the proximal right coronary artery was 66% obstructed. The circumflex coronary artery was normal, and the third marginal branch and left posterior descending coronary arteries were absent. The ejection fraction was 65% to 70%. Coronary bypass surgery was performed on June 13, 1988.

 The heart rhythm is normal and the heart rate is 75 complexes per minute. The PR interval is 0.17 second. The duration of the QRS complex is 0.07 second and the duration of the QT interval is 0.38 second.

P waves: The P waves are normal.

 QRS complex: The mean QRS vector is directed about +65° to the right, and

 10° anteriorly; this is abnormal. The mean initial 0.04-second QRS vector is directed about +45° to the right and about 40° anteriorly. It is impossible to determine how far anteriorly it is directed, because the initial forces are positive in all of the precordial leads. The fact that the R wave in lead V1 is almost as large as that in lead V6 indicates that the initial 0.04-second QRS vector is directed moderately anteriorly. This is due to a dead zone located in the true posterior portion of the left ventricle. Right ventricular hypertrophy could cause this, but the frontal plane orientations of the mean QRS and initial 0.04-second QRS vectors rule against such a view.

 T waves: The T waves are normal. The mean T vector is directed +30° in, and parallel with, the frontal plane.

 A. The frontal plane projections of the mean QRS, mean initial 0.04-second QRS, and mean T vectors.

 B. The spatial orientation of the mean QRS vector.

 C. The spatial orientation of the mean initial 0.04-second QRS vector.

 D. The spatial orientation of the mean T vector.

 Summary: This electrocardiogram illustrates three points: first, hasty inspection of the tracing could lead the observer to conclude that it was normal, whereas the patient actually had severe coronary disease. Second, the tracing also illustrates how a true posterior infarction can produce tall R waves in leads V1 and V2 because the initial 0.04-second QRS vector is directed anteriorly to an abnormal degree. There are no abnormal Q waves in the tracing; they would be found in a recording made from the patient's back. This figure also illustrates that the location of an infarction does not always signify which coronary artery has the greatest chronic obstruction. In this patient, the greatest obstruction was in the left anterior descending coronary artery, which was not responsible for the electrocardiographic abnormalities.

Click to zoom Figure 11.10 (I)
These electrocardiograms, showing the development of a right ventricular infarction, were recorded from a 51-year-old man. He had an anterior infarction in August 1988. A coronary arteriogram made at that time revealed total obstruction of the first diagonal coronary artery and the left anterior descending coronary artery after the first septal perforator. The patient had coronary bypass surgery the same month. He developed recurrent ventricular tachycardia that could not be controlled with drugs, including amiodarone. Electrophysiologic testing with endocardial mapping and possible endocardial surgical resection was planned. It seemed wise to make a coronary arteriogram prior to these procedures in order to determine whether myocardial ischemia might be responsible for the patient's arrhythmia.

 The arteriogram was made on November 29, 1988. Unfortunately, the procedure precipitated severe dissection of the right coronary artery, which became completely occluded. The patient was transferred to Emory University Hospital where percutaneous transluminal coronary angioplasty was unsuccessful; the proximal portion of the right coronary artery became completely obstructed. These events made it possible to study the evolution of a right ventricular myocardial infarction occurring in the presence of a former anteroseptal myocardial infarction. The patient responded to the specific treatment for right ventricular infarction.

I. This electrocardiogram was recorded at 7:24 pm on November 29, 1988, after coronary arteriography, at which time a severe dissection of the right coronary artery occurred. It shows the previous anteroseptal infarction due to total occlusion of the left anterior descending artery.

 The rhythm is normal; there are 72 complexes per minute. The duration of the PR interval is 0.17 second. The duration of the QRS complex is 0.09 second and that of the QT interval is 0.37 second.

 P waves: The P waves are normal.

 QRS complex: The mean QRS vector is directed at 0° in the frontal plane. It is directed at about 20° to 30° posteriorly, and the mean initial 0.04-second vector is directed about 20° posteriorly -- a little more than it should be for this particular mean QRS vector.

 T waves: The mean T vector is directed at 0° in the frontal plane, and 80° posteriorly, away from an area of anterior epicardial ischemia.

 A. The frontal plane projections of the mean QRS, mean initial 0.04-second QRS, mean ST segment, and mean T vectors.

 B-D. The spatial orientations of the mean QRS, mean initial 0.04-second QRS, and mean T vectors, respectively.

Click to zoom Figure 11.10 (II)
This electrocardiogram was recorded at 11:46 pm, after an attempted angioplasty to open the totally occluded right coronary artery. A more proximal portion of this vessel became completely obstructed, at which time the electrocardiogram showed evidence of right ventricular infarction.

 The rhythm is normal. There are 80 complexes per minute. The duration of the PR interval is 0.20 second. The duration of the QRS complex is 0.10 second, and the duration of the QT interval is 0.36 second.

P waves: The P waves are normal, although the mean P vector is a little more posteriorly directed than in the tracing shown in Figure 11.10 (1)

 QRS complex: The mean QRS vector is directed +45° inferiorly, and 15° posteriorly. The mean initial 0.04-second QRS vector is directed a little more to the left than it was in Figure 11.10 (I); this may be due to a new inferior dead zone.

 ST segment: The mean ST vector is huge. It is directed about +130° to the right, and 40° to 60° anteriorly. This is characteristic of epicardial injury associated with inferior and right ventricular infarction.

 T waves: The mean T vector shows a markedly posterior direction. It is difficult to identify the frontal plane projection of the mean T vector, but the T waves are definitely inverted in leads V1 through V5. The vector is directed away from an area of anterior epicardial ischemia.

 A. The frontal plane projections of the mean QRS, mean initial 0.04-second QRS, mean ST, and mean T vectors.

 B-E. The spatial orientations of the mean QRS, mean initial 0.04-second QRS, mean ST, and mean T vectors, respectively.

 Summary: The unusual electrocardiogram shown in part II exhibits abnormalities characteristic of right ventricular infarction. Tracing I shows an anteroseptal infarction. Tracing II followed coronary angioplasty which was performed to open the right coronary artery which became occluded after coronary artery dissection associated with arteriography. The mean ST segment vector is directed to the right and anteriorly in tracing II. A tracing made from V3R would show an elevated ST segment. When one is able to diagram spatially oriented vectors, it is not necessary to record right precordial leads such as V3R. The direction of the mean ST segment vector is a better indicator of the culprit artery than that of the mean initial 0.04-second QRS or the mean T vector.

Click to zoom Figure 11.11
This electrocardiogram was recorded from a 47-year-old man with anterolateral myocardial infarction. He had a history of angina pectoris at rest. A coronary arteriogram revealed 100% obstruction of the left anterior descending coronary artery beyond its first branch, and 75% occlusion of the right posterior descending artery. The right ventricular branch of the right coronary artery was missing.

 The rhythm is normal and the heart rate is 88 complexes per minute. The PR interval is 0.20 second. The duration of the QRS complex is 0.09 second, and the duration of the QT interval is 0.35 second.

P waves: The P waves are severely notched in leads I and II. The duration of the P wave is 0.14 second. The mean P vector (Pm) is directed at +60° in, and parallel with, the frontal plane. The abnormalities may be due to a localized lesion in the atria, perhaps indicating atrial infarction. The first deflection of what appears to be a P wave could be a U wave, but careful study of several deflections suggests that it is the first part of a notched P wave.

 QRS complex: The duration of the QRS complex is 0.09 second. The mean QRS vector is directed about +115 to the right, and about 15° posteriorly. The mean initial 0.04-second QRS vector is directed about +130° to the right, and parallel with the frontal plane. This produces the abnormal Q waves in leads V5 and V6, and is responsible for the rightward deviation of the mean QRS vector. The small R waves seen in leads V2, V3, and V4 are less than 0.04-second in duration, and it is likely that the transitional pathway for the mean initial 0.04-second portion of the QRS complexes is near electrode positions V2, V3, and V4.

 ST segment: The mean ST vector is directed -50° to the left, and about 10° anteriorly, toward an area of anterolateral epicardial injury.

 T waves: The mean T vector is directed about +45° to the right and 10° anteriorly.

 A. The frontal plane projections of the mean P, mean QRS, mean initial 0.04-second QRS, mean ST, and mean T vectors.

 B. The spatial orientation of the mean QRS vector.

 C. The spatial orientation of the mean initial 0.04-second QRS vector. 

D. The spatial orientation of the mean ST vector. 

E. The spatial orientation of the mean T vector.

 Summary: This electrocardiogram reveals how anterolateral myocardial infarction can produce right axis deviation of the mean QRS vector. It also exemplifies how P waves may be altered in the setting of infarction. The P wave abnormality may be due to atrial infarction.

Click to zoom Figure 11.12
This electrocardiogram, showing anterolateral myocardial infarction, right bundle branch block, and left anterior-superior division block, was recorded from a 48-year-old man with angina pectoris at rest. He gave a history of myocardial infarction. A coronary arteriogram made when the patient was 51 years of age revealed 100% obstruction of the proximal portion of the left anterior descending coronary artery. The septum and inferoapical areas of the myocardium were akinetic. The ejection fraction was 20%.

 The rhythm is normal and the heart rate is 82 complexes per minute. The PR interval is 0.15 second. The duration of the QRS complex is 0.12 second and that of the QT interval is 0.34 second.

P waves: The mean P vector is directed at +30° in the frontal plane. When viewed in space, it is parallel with the frontal plane. P2 is abnormal at -0.06 mm/sec in lead V1, signifying a left atrial abnormality.

 QRS complex: The duration of the QRS complex is 0.12 second. The mean QRS vector is directed -85° to the left, .and parallel with the frontal plane. The deflections in leads V5 and V6 are actually negative, whereas the diagram indicates that the deflection recorded at V6 would be positive, and the deflection at V5 would be transitional. The lack of correspondence occurs because the electrodes at V5 and V6 record near the transitional pathway (see previous discussions). The mean terminal 0.04-second QRS vector is directed -100° to the left, and 15° anteriorly. This signifies, when the QRS duration is 0.12 second, the presence of right bundle branch block and left anterior-superior division block, which produces a tall R wave in lead V1, and left axis deviation of the mean QRS vector. The mean initial 0.04-second QRS vector is directed about -60° to the left, and about 80° posteriorly; this signifies an extensive anterior dead zone. The vector produced by left anterior-superior division block shows the direction of depolarization of the myocardium served by the left posterior-inferior division of the conduction system, and retrograde depolarization of that portion of the myocardium served by the left anterior-superior division.

 ST segment: The mean ST vector is directed about +75° to the right and 15° anteriorly, indicating extensive inferior, apical, and perhaps lower septal injury (review the abnormalities in the coronary arteriogram). The mean ST vector of this patient is not parallel with the mean T vector, as it should be when there is uncomplicated bundle branch block. It is directed toward an area of epicardial injury.

 T wave: The mean T vector is directed +120° to the right and about 10° posteriorly. This is caused by anterolateral epicardial ischemia.

 A. The frontal plane projections of the mean P, mean QRS, mean initial 0.04-second QRS, mean terminal 0.04-second QRS, mean ST, and mean T vectors.

 B. The spatial orientation of the mean QRS vector. 

C. The spatial orientation of the mean initial 0.04-second QRS vector. 

D. The spatial orientation of the terminal 0.04-second QRS vector.

 E. The spatial orientation of the mean ST vector. 

F. The spatial orientation of the mean T vector.

 Summary: This electrocardiogram is a good example of the development of right bundle branch block plus left anterior-superior division block due to an anterolateral myocardial infarction. These findings remind us that right bundle branch block does not prevent the identification of abnormal initial QRS forces caused by myocardial infarction. They also reveal how an extensive infarction can produce severe conduction defects. In this tracing, the direction of the initial 0.04-second QRS vector signifies myocardial infarction, as do the directions of the mean ST and T vectors.

Click to zoom Figure 11.13
This electrocardiogram was recorded from a 62-year-old man with an old anteroseptal myocardial infarction.

 The rhythm is normal, and the heart rate is 75 complexes per minute. The PR interval is 0.12 second. The duration of the QRS complex is 0.08 second and the QT interval is 0.36 second.

P waves: The P waves are normal.

 QRS complex: The mean QRS vector is directed 0° to the left and 20° posteriorly. The mean initial 0.04-second QRS vector is directed about +30° inferiorly and 30° posteriorly, it is posterior to the mean QRS vector, and signifies an anteroseptal dead zone.

 ST segment: The mean ST segment vector is directed +118° to the right and about 40° anteriorly; it signifies anterior epicardial injury.

 T waves: The mean T vector is directed about +88° inferiorly and about 30° posteriorly; it signifies anterior epicardial ischemia.

 A. The frontal plane projections of the mean QRS, mean initial 0.04-second QRS, mean ST, and mean T vectors.

 B. The spatial orientation of the mean QRS vector. Note that the transitional pathway courses between the electrode sites for V2 and V3.

 C. The spatial orientation of the mean initial 0.04-second QRS vector. Note the transitional pathway which courses between electrode sites V3 and V4.

 D. The spatial orientation of the mean ST vector.

 E. The spatial orientation of the mean T vector.

 Summary: This electrocardiogram illustrates the abnormalities associated with an anteroseptal myocardial infarction. Note that the mean initial 0.04-second QRS vector is posterior to the mean QRS vector; this arrangement produces the absent R wave in leads V1 and V2, and the Q followed by the R wave in lead V3.

 From Hurst JW, Woodson GC Jr: Atlas of Spatial Vector Electrocardiography. New York: Blakiston, 1952, p. 149. (Copyright held by JW Hurst)

Click to zoom Figure 11.14
This electrocardiogram, recorded from a hypertensive man, shows complicated left bundle branch block and extensive anterior epicardial ischemia and injury.

 The rhythm is normal, and the heart rate is 70 complexes per minute. The PR interval is 0.16 second. The duration of the QRS complex is 0.16 second, and that of the QT interval is 0.48 second in lead V2

P waves: The P waves are abnormal. The mean P vector (Pm) is directed +60° to the right, and 5° posteriorly. P2 is abnormal; the duration-amplitude product of the second half of the P wave is 0.07 mm/sec in lead V1, signifying a left atrial abnormality.

 QRS complex: The duration of the QRS complex is 0.16 second. The mean QRS vector is directed about +45° inferiorly, and about 60° posteriorly. The mean terminal 0.04-second QRS vector is directed about -30° to the left, and about 45° posteriorly, signifying left bundle branch block. Myocyte damage is undoubtedly present in addition to the conduction abnormality.

 ST segment: The mean ST segment vector is directed -160° to the left, and about 70° anteriorly; it is not parallel with the mean T vector, as it should be in uncomplicated bundle branch block. It is directed toward an area of anterior epicardial injury.

 T waves: The mean T vector is directed +90° to the right, and about 45° posteriorly. It is directed at least 115° posterior to the mean ST vector, away from an area of epicardial ischemia. It represents a primary T wave abnormality. Note that the T waves are positive (upright) in leads V5 and V6, whereas the diagram indicates that they would be negative (inverted). This lack of correspondence between the actual and predicted T waves arises because the electrodes at positions V4, V5, and V6 record from the area near transitioned pathway of the mean T vector (see previous discussions).

 A. The frontal plane projections of the mean QRS, mean terminal 0.04-second QRS, mean ST, and mean T vectors.

 B. The spatial orientation of the mean QRS vector. 

C. The spatial orientation of the mean terminal 0.04-second QRS vector. 

D. The spatial orientation of the mean ST vector. 

E. The spatial orientation of the mean T vector (see previous discussions).

 Summary: This electrocardiogram illustrates the presence of epicardial injury and ischemia in a patient with complicated left bundle branch block. Initial QRS abnormalities due to infarction may not be identified when there is left bundle branch block, but the ST and T changes of epicardial injury and ischemia can sometimes be identified in the presence of the block.

 From Hurst JW, Woodson GC Jr: Atlas of Spatial Vector Electrocardiography. New York: Blakiston, 1952, p. 181. (Copyright held by JW Hurst)

Click to zoom Figure 11.15
This electrocardiogram, showing extensive, acute apical epicardial injury associated with myocardial infarction, was recorded from a 52-year-old man. The coronary arteriogram showed 100% obstruction of the right coronary artery, 68% obstruction of the circumflex coronary artery, 50% occlusion of the first marginal coronary artery, and only 25% occlusion of the left anterior descending coronary artery, proximal to its left branch. The ejection fraction was 45%, and the inferior and posterolateral areas of the left ventricle were hypokinetic.

 The rhythm is normal, and the heart rate is 90 complexes per minute. The PR interval is 0.12 second. The duration of the QRS complex is 0.10 second, and that of the QT interval is 0.36 second.

P waves: The P waves are normal.

 QRS complex: The mean QRS vector is directed at +35° in the frontal plane and 15° posteriorly.

 ST segment: The mean ST vector is huge; it is directed about +60° inferiorly, and 15° posteriorly. The vector is due to extensive epicardial injury associated with myocardial infarction. The frontal plane direction of the mean ST vector could be produced by pericarditis. The size of the ST segment vector and its direction both indicate epicardial injury associated with apical myocardial infarction.

 T waves: The T waves are difficult to separate from the ST segment.

 A. The frontal plane projections of the mean QRS and mean ST vectors. 

B. The spatial orientation of the mean QRS vector. 

C. The spatial orientation of the mean ST vector.

 Summary: This electrocardiogram illustrates severe, extensive, epicardial injury associated with acute myocardial infarction. It also illustrates how the ST segment vector reflecting epicardial injury of infarction can, on rare occasions, mimic some of the features of pericarditis. Note that there are no reciprocal changes in the extremity leads in this tracing. An ST segment vector of the magnitude shown here almost never occurs with pericarditis. In this electrocardiogram, the ST segment vector is produced by apical infarction. It is most likely due to epicardial injury produced by occlusion of the circumflex and marginal coronary arteries, because the proximal portion of the left anterior descending artery revealed only 25% obstruction. The electrocardiographic abnormality decreased considerably, as did the patient's chest pain, following the injection of tissue plasminogen activator (tPA).

Click to zoom Figure 11.16
This electrocardiogram, showing extensive anterolateral myocardial infarction, was recorded from a 43-year-old man who suffered angina pectoris at rest. He gave a history of previous myocardial infarction. The coronary arteriogram performed 2 years later revealed 100% obstruction of the midportion of the left anterior descending coronary artery, 60% occlusion of the first diagonal branch, 40% obstruction of the first marginal branch and 20% occlusion of the distal right coronary artery. The anterior portion of the left ventricular wall was akinetic.

 The rhythm is normal, and the heart rate is 56 complexes per minute. The PR interval is 0.12 second. The duration of the QRS complex is 0.08 second, and that of the QT interval is 0.36 second.

P waves: The P waves are normal.

 QRS complex: The mean QRS vector is directed about +100° inferiorly, and parallel with the frontal plane. The electrode position for lead V6 is near the transitional pathway for the mean QRS vector. Therefore, the QRS complex predicted from the diagram would be resultantly negative whereas it is actually positive in the electrocardiogram. (The cause for this lack of fit is discussed in the section entitled "Comments Regarding the Diagrams Shown in this Chapter.") This abnormal, inferior orientation is the result of an anterolateral dead zone that has removed electrical forces from that region. The mean initial 0.04-second QRS vector is directed inferiorly and posteriorly for the same reason. The mean initial 0.02-second QRS vector is directed about +100° to the right, and the mean initial 0.04-second QRS vector is directed about +80° to the right. The remainder of the QRS complex, represented as mean vector, is directed far to the right. This identifies an abnormality of the early portion of the QRS loop, because this loop is, at first, directed to the right, then less to the right, and finally far to the right.

 T waves: The mean T vector is directed +140° to the right and parallel with the frontal plane. It is directed away from an area of extensive anterolateral epicardial ischemia.

 A. The frontal plane projections of the mean QRS, mean initial 0.04-second QRS, and mean T vectors. 

B. The spatial orientation of the mean QRS vector.

 C. The spatial orientation of the mean initial 0.04 second QRS vector.

 D. The spatial orientation of the mean T vector.

 Summary: This electrocardiogram illustrates how rightward deviation of the mean QRS vector can be produced by myocardial infarction. It also illustrates an abnormally directed mean initial 0.02-second QRS vector in relation to the mean initial 0.04 second QRS, and the mean QRS vectors. Normally, the initial QRS loop should be directed in a clockwise manner when the mean QRS vector is vertical. Here, it is initially directed to the right (mean 0.02-second vector), then less to the right (mean 0.04-second vector), and then far to the right.

Click to zoom Figure 11.17
This electrocardiogram, showing a non-Q wave infarction, was recorded from a 50-year-old woman. The patient had angina pectoris at rest, and gave a history of previous myocardial infarction. The coronary arteriogram revealed 37% obstruction of the proximal portion of the left anterior descending artery, and 90% obstruction of the left anterior descending coronary artery after its first branch.

 The rhythm is normal, and the heart rate is 75 complexes per minute. The duration of the PR interval is 0.20 second. The duration of the QRS complex is 0.07 second, and that of the QT interval is 0.36 second.

P waves: The P waves are normal.

 QRS complex: The mean QRS vector is large but normally directed. It is directed +60° inferiorly and 20° posteriorly. The total 12-lead QRS amplitude is 199mm. This suggests left ventricular hypertrophy, but other methods of examination would be needed to confirm this suspicion. The mean initial 0.04-second QRS vector is normal.

 T waves: The mean T vector is directed -95° superiorly and to the left, and 5° posteriorly, away from a large area of inferior, anterior, and lateral ischemia.

 A. The frontal plane projections of the mean QRS and mean T vectors. 

B. The spatial orientation of the mean QRS vector. 

C. The spatial orientation of the mean T vector.

 Summary: This electrocardiogram is abnormal owing to extensive inferior, anterior, and lateral epicardial ischemia. It illustrates a non-Q wave infarction. Formerly, some clinicians referred to this as a subendocardial infarction, this terminology is now in disrepute. It must be remembered that some Q wave infarcts are localized to the endocardium while others are actually transmural. Further, some T wave infarcts are actually transmural. It is more scientific to refer to either Q wave or non-Q wave infarcts.[1]

Click to zoom Figure 11.18
This electrocardiogram, showing anteroseptal infarction and left ventricular hypertrophy, was recorded from an 80-year-old man. The patient had congestive heart failure and experienced angina pectoris at rest. His systolic blood pressure was 170mmHg, and his diastolic blood pressure was 60mmHg. The coronary arteriogram revealed 90% obstruction of the left anterior descending coronary artery proximal to its first branch, and three lesions distal to the first branch.

 They constituted 50%, 40%, and 30% reductions in luminal diameter, respectively. There was a 40% obstruction in the first diagonal branch, a minor lesion in the left circumflex coronary artery, and 70% obstruction of the first marginal coronary artery. The left ventricular diastolic pressure was 20mmHg, and the ejection fraction was 36%. The anterior and apical areas of the left ventricle were akinetic and the inferior wall was hypokinetic.

 The heart rhythm is normal, and the heart rate is 64 complexes per minute. The duration of the PR interval is 0.20 second. The duration of the QRS complex is 0.08 second, and the duration of the QT interval is 0.35 second.

P waves: The P waves are normal.

 QRS complex: The mean QRS vector is directed at 0° in the frontal plane and 45° to 60° posteriorly. The mean initial 0.04-second QRS vector is directed about +50° inferiorly and about 45° posteriorly. The mean initial 0.01-second QRS vector is directed about +50° inferiorly and about 45° posteriorly, but the mean initial 0.02-second vector is directed about +50° inferiorly and about 30° posteriorly. This produces a notch on the S wave in lead V1, and a small Q wave followed by an R and then an S wave in leads V2 and V3. It identifies an initial abnormality of the QRS loop, and serves to emphasize that a Q wave need not be 0.04-second wide to signify infarction. The 12-lead QRS amplitude is greater than 180mm, suggesting the presence of left ventricular hypertrophy.

 ST segment: The mean ST vector is directed +120° inferiorly and about 20° anteriorly. It is relatively parallel with the mean T vector.

 T waves: The mean T vector is directed +120° inferiorly and about 20° anteriorly. The vector could be abnormal because of systolic pressure overload of the left ventricle.

 A. The frontal plane projections of the mean QRS, mean 0.01-second QRS, mean 0.02-second QRS, mean 0.04-second QRS, mean ST, and mean T vectors.

 B. The spatial orientation of the mean QRS vector.

 C. The spatial orientation of the mean initial 0.01-second QRS vector. Note that it is posterior to the 0.02-second vector.

 D. The spatial orientation of the mean initial 0.02-second QRS vector; note that it is anterior to the 0.01-second vector.

 E. The spatial orientation of the mean initial 0.04-second QRS vector; note that it is posterior to the 0.02-second vector.

 F. The spatial orientation of the mean ST vector; note that it parallels the mean T vector.

 G. The spatial orientation of the mean T vector.

 Summary: This electrocardiogram illustrates an anteroseptal myocardial infarction associated with left ventricular hypertrophy due to systolic pressure overload of the left ventricle secondary to hypertension. The direction of the initial 0.01-second QRS vector and its relationship to the mean initial 0.02-second and mean initial 0.04-second QRS vectors signify anteroseptal infarction. This creates the slur in the initial part of the S wave in lead V1, and the small Q wave followed by an R wave in leads V2 and V3. The directions of the mean ST and T vectors indicate left ventricular hypertrophy, but epicardial ischemia may play a role. First-degree atrioventricular block is present.

The etiologic considerations related to myocardial ischemia, myocardial injury, and development of a myocardial dead zone are: atherosclerotic coronary heart disease; atherosclerotic coronary heart disease plus coronary artery spasm; coronary spasm without obstructive coronary atherosclerosis; coronary embolism; coronary thrombosis without evidence of other disease; the antiphospholipid antibody syndrome; dissection of the coronary artery; coronary arteritis; Kawasaki's disease; trauma of the heart muscle or coronary artery; involvement of the coronary arteries with amyloid; and congenital anomalies of the coronary arteries.

 Section 11.7 Special Considerations

 Coronary artery spasm (Prinzmetal's angina or variant angina).

 The electrocardiographic abnormalities associated with coronary artery spasm were first identified by Frank Wilson and Franklin Johnston in 1941,[2] and the clinical syndrome associated with it was described by Prinzmetal and associates in 1959.[3] Most patients with coronary spasm also have coronary atherosclerosis, although a few do not. The patient with chest discomfort due to coronary artery spasm exhibits transient electrocardiographic abnormalities that simulate those of an acute myocardial infarction. The mean ST vector is directed toward the area of epicardial injury. The mean T vector may be directed away from the area of epicardial ischemia, but the ST segment abnormality usually dominates the tracing. There may be abnormal but transient Q wave abnormalities, with the initial mean 0.04-second QRS vector being directed away from the transiently "dead" or "stunned" myocytes. Atrioventricular block and other arrhythmias may be present. These abnormalities occur with the usual infarction, but, when caused by transient coronary artery spasm, they disappear as chest discomfort subsides. The only other time this disappearance occurs is when thrombolytic therapy is successful in patients in whom thrombosis is superimposed on high-grade obstructive coronary atherosclerosis. In such cases, the electrocardiographic abnormalities and chest discomfort often subside as the clot is lysed. The electrocardiogram of a patient with coronary artery spasm is shown in Figure 11.19.
 
 
Click to zoom

  I

Figure 11.19 (I and II) (click image to zoom) These electrocardiograms were recorded from a 59-year-old male with Prinzmetal angina pectoris, who was experiencing repeated anterior chest discomfort at rest.
I. The top electrocardiogram was recorded at 10 am; the patient was having no chest pain at the time. The bottom electrocardiogram was recorded at 5 pm during an episode of chest pain. Note the high degree of atrioventricular block and marked ST segment displacement. The mean ST vector is directed inferiorly and posteriorly.

 II. This electrocardiogram was recorded at 6:15 pm the same day. It is similar to the one recorded at 9 am.

h Parts A-C illustrate the appearance (or absence) of the mean ST vector at 10 am, 5 pm, and 6:15 pm. Note that no ST vector was present at 10 am and 6:15 pm.

 Summary: Coronary arteriography revealed a discrete lesion (95% obstruction) in the right coronary artery. This series of electrocardiograms illustrates a patient with obstructive coronary disease who also had coronary artery spasm.

 From Hurst JW, King III SB, Walter PF, Friesinger GC, Edwards JE: Atherosclerotic coronary heart disease: angina pectoris, myocardial infarction, and other manifestations of myocardial ischemia, in Hurst JW (ed): The Heart Ed. 5. New York: McGraw-Hill, 1982, p. 1090. The electrocardiogram was originally provided by Dr. Joel Felner.

Exercise electrocardiography.

 There are many different protocols available for exercise electrocardiography. While I have used the Bruce protocol almost exclusively, I recognize that other techniques are equally good. An abnormal electrocardiographic response to exercise is said to be present when an arrhythmia, an abnormal ST segment displacement, or a T wave abnormality occurs. The ST segment displacement is more likely to indicate myocardial hypoxia than are the other abnormalities, and this displacement is usually due to generalized subendocardial injury. Accordingly, the mean ST segment is directed approximately opposite the mean QRS vector. An ST segment displacement of 1mm that continues horizontally for more than 0.08 second, or slopes downward, is more likely due to myocardial injury than is an ST segment displacement characterized by a displaced J point, but which rapidly ascends in an up-sloping manner. The predictive value of a positive electrocardiographic response, indicating injury due to myocardial ischemia, is about 80% in adult males and 50% in females under 45 years of age. The predictive value varies according to the amount of ST segment displacement during the test, and the duration of displacement after completion of the exercise.

 The lead system used for exercise electrocardiography does not permit determination of the spatial characteristics of the electrical forces responsible for the mean ST segment vector. Therefore, the details of this particular abnormality are not discussed here. Suffice it to say that ST segment displacement due to exercise can be caused by transient subendocardial injury, but as stated earlier, false positive tests also occur, especially in young women. While the causes of these false positive tests are usually unknown, they are likely to occur in hypokalemic patients or those receiving digitalis. Patients with ST segment displacement due to left ventricular hypertrophy, left bundle branch block, or ventricular pre-excitation may be exercised to determine if there is exercise-induced angina, but it is not possible to accurately interpret the electrocardiographic response.

 Section 11.8 Pseudoinfarction

 Several conditions produce electrocardiographic abnormalities that must be differentiated from those due to myocardial infarction. Such abnormalities are called pseudoinfarctions. The electrocardiographic abnormalities associated with pseudoinfarction are listed in Table 11.3 and the causes of pseudoinfarction are listed in Table 11.4. Electrocardiograms illustrating pseudoinfarction are shown in Figures 11.20 through 11.23
 
 
Click to zoom Figure 11.20
This electrocardiogram, illustrating an example of pseudoinfarction, was recorded from a 31-year-old man with Friedreich's ataxia.

 An atrial ectopic rhythm is present; the atrial rate is about 210 depolarizations per minute, and 2:1 atrioventricular block is also present. The ventricular rate is 105 depolarizations per minute, the duration of the QRS complex is 0.08 second, and the duration of the QT interval is 0.34 second.

 P waves: The shape of the P waves is abnormal; note the tall, narrow, sharp P waves in lead V1. This is probably due to an unusual atrial conduction defect.

 QRS complex: Although the QRS duration is only 0.08 second, there is evidence of a peculiar conduction defect within the ventricles. The mean QRS vector is directed -120° superiorly, and parallel with the frontal plane. The mean initial 0.04-second QRS vector is directed so that Q waves are recorded in leads I, II, III, and aVF. This could lead an observer to consider an inferior and lateral infarction. The mean terminal 0.04-second QRS vector is also directed about -120° superiorly, and more than 15° to 20° posteriorly.

 The exact type of conduction defect in this case cannot be determined. It is likely that the left anterior-superior division is involved, but diseases of the heart muscle responsible for the initial 0.04 second of the QRS complex may play a role. The 12-lead QRS amplitude is 69mm, indicating a low QRS voltage.

 T waves: It is difficult to determine the direction of the mean T vector because the P waves interrupt them. The vector seems to be directed slightly anteriorly.

 A. The frontal plane projections of the mean QRS, mean terminal 0.04-second QRS, and mean T vectors.

 B. The spatial orientation of the mean QRS vector.

 C. The spatial orientation of the mean terminal 0.04-second QRS vector.

 D. The spatial orientation of the mean T vector.

 Summary: This electrocardiogram exhibits peculiar P waves and peculiar QRS complexes due to the cardiomyopathy associated with Friedreich's ataxia. In this condition, the cardiac conduction system and myocytes are involved; note the extremely low QRS voltage. These ventricular abnormalities can produce an electrocardiogram that mimics that of myocardial infarction; hence the term "pseudoinfarction." Patients with dilated, hypertrophic, or restrictive cardiomyopathy may have electrocardiograms that exhibit pseudoinfarction.

Click to zoom Figure 11.21
This electrocardiogram, recorded from a 43-year-old man, illustrates a pseudoinfarction due to sarcoid of the heart. The patient had recurrent episodes of refractory ventricular tachycardia for which an internal defibrillator was installed.

 The heart rhythm is normal and the heart rate is 63 complexes per minute. The PR interval is 0.16 second. The duration of the QRS complex is 0.11 second, and that of the QT interval is 0.40 second.

P wave: The P waves are abnormal. In lead I, they are notched, and their duration is 0.12 second. The second half of the P wave vector (P2), representing left atrial depolarization, is directed about +30° inferiorly and about 30° posteriorly. Note that the second half of the P wave is isoelectric in lead lilt The amplitude duration product of last half of the P wave in V1 is greater than -0.03 mm/sec. These abnormalities suggest a left atrial abnormality.

 QRS complex: The mean QRS vector is directed about +20° to 30° inferiorly, and about 40° posteriorly. The mean initial 0.02-second QRS vector is directed +180° to the right, and 30° anteriorly. The mean initial 0.03-second QRS vector is directed about +130° to the right, and about 40° anteriorly. The "Q waves" seen in leads I, II, aVL, V4, V5, and V6 suggest lateral myocardial infarction.

 T waves: The mean T vector is directed -115° to -120° superiorly, and about 20° anteriorly. The vector is abnormal, suggesting lateral or generalized epicardial ischemia.

 A. The frontal plane projections of the mean QRS, mean 0.02-second QRS, mean 0.03-second QRS, and mean T vectors. 

B. The spatial orientation of the mean QRS vector. 

C. The spatial orientation of the mean initial 0.03-second QRS vector. 

D. The spatial orientation of the mean T vector.

 Summary: This tracing shows a pseudoinfarction due to sarcoid involving the myocardium. Certain neoplastic diseases, amyloid deposits, and many of the connective tissue diseases that involve the heart may produce abnormalities of pseudoinfarction in the electrocardiogram. Some of these diseases, such as amyloid and collagen diseases, may also involve the coronary arteries, and when they do, they may cause obstructive coronary disease and atrial myocardial infarction.

Click to zoom Figure 11.22
This tracing, showing the electrocardiographic abnormalities of the Wolff-Parkinson-White syndrome and atrial fibrillation (see diagram F), was recorded from a 35-year-old man. The abnormalities simulate myocardial infarction, and represent another common cause of pseudoinfarction.

 The rhythm is normal in the 12-lead tracing, and the heart rate is 60 complexes per minute. The PR interval is about 0.12 second. The duration of the PR interval appears to be 0.16 second in some leads, but this is an illusion, because the electrical forces seen during the early part of the QRS complex are isoelectric in those leads. Note that the QRS complex appears to be about 0.10 second in lead II. However, when simultaneous leads are studied, it is apparent that the early QRS forces are perpendicular to lead axis II, producing a PR interval that falsely appears to be at least 0.16 second. The duration of the QRS complex is 0.14 second, and that of the QT interval is 0.48 second.

P waves: The P waves are normal, and the PR interval is short. Atrial fibrillation with a rapid ventricular rate is shown in diagram F.

 QRS complex: The mean QRS vector is directed about -50° to the left, and about 20° posteriorly. The mean initial 0.04-second QRS vector is directed -60° to the left and about 10° posteriorly, simulating the abnormality due to inferior infarction. Note the slurring of the initial portion of the QRS complexes; this is a classic delta wave. The delta wave is best seen in leads V1, V5, and V6.

 ST segment: The direction of the mean ST segment vector is about +145° inferiorly, and about 80° anteriorly.

 T waves: The direction of the mean T vector is about +110° inferiorly and about 60° anteriorly.

 A. The frontal plane projections of the mean QRS, mean initial 0.04-second QRS, mean ST, and mean T vectors.

 B. The spatial orientation of the mean QRS vector. 

C. The spatial orientation of the mean initial 0.04-second QRS vector.

 D. The spatial orientation of the mean ST vector.

 E. The spatial orientation of the mean T vector.

 F. This electrocardiogram was recorded during an episode of tachycardia. It shows atrial fibrillation with a high ventricular rate.

 Summary: The short PR interval (0.12 second) and the delta waves are characteristic of pre-excitation of the ventricles in a patient with the Wolff-Parkinson-White syndrome. The duration of the QRS complex in this patient is 0.14 second and also simulates left bundle branch block. However, the short PR interval and delta wave distinguish this type of electrocardiogram from one showing true left bundle branch block.

 The QRS duration may be as short as 0.10 second or as long as 0.18 second in patients with pre-excitation of the ventricles. In these cases, electrocardiograms may simulate anterior or inferior infarction. There is usually no other evidence of heart disease in patients with the Wolff-Parkinson-White syndrome, but the clinician is obligated to search for idiopathic ventricular hypertrophy, Ebstein's anomaly, and atrial septal defect, since these conditions occur with greater than average frequency in such patients.

 When atrial fibrillation occurs in a patient with a bypass tract, the ventricular rate may reach 220-280 complexes per minute.

Click to zoom Figure 11.23
This electrocardiogram shows a pseudoinfarction as well as right and left ventricular hypertrophy. The tracing was recorded from a 7-year-old boy with a large aortic septal defect.

 The rhythm is abnormal owing to lower atrial rhythm. Note that the mean P vector is directed -20° to the left and about 30° anteriorly. The heart rate is 110 complexes per minute. The PR interval is 0.12 second. The duration of the QRS complex is 0.08 second, and the duration of the QT interval is 0.36 second.

P waves: The mean P vector (Pm) is directed -20° to the left, and 30° anteriorly. The depolarization of the atria is abnormal because of an ectopic atrial rhythm.

 QRS complex: The mean QRS vector is directed about +90° inferiorly, and about 30° anteriorly. The QRS complexes recorded from leads V5 and V6 are from the area near the transitional pathway in this 7-year-old child (see previous discussions). The QRS amplitude is large; the QRS complexes are almost off the electrocardiographic paper in leads V3 and V4. Their direction and magnitude suggest right and left ventricular hypertrophy. The initial 0.02-second vector is large; it is directed about +120° inferiorly in the frontal plane, and 20° anteriorly. The size of this vector might be interpreted as being due to myocardial infarction.

 T waves: The mean T vector is directed +50° inferiorly, and about 15° posteriorly.

 A. The frontal plane projections of the mean P, mean QRS, mean initial 0.02-second QRS, and mean T vectors.

 B. The spatial orientation of the mean QRS vector.

 C. The spatial orientation of the mean initial 0.02-second QRS vector.

 D. The spatial orientation of the mean T vector.

 Summary: This patient with congenital heart disease had a large left-to-right shunt through an aortic septal defect. Diastolic pressure overload of both the left and right ventricles was undoubtedly present. The tracing shows an atrial ectopic rhythm and suggests left and right ventricular hypertrophy and lateral infarction (thought this is not present). This is a good example of the many types of congenital heart disease that exhibit pseudoinfarction on the electrocardiogram.

 From Cabrera E, Estes EH, Hellerstein HK: Case 40 in Hurst JW, Wenger NK (eds.): Electrocardiographic Interpretation. New York: McGraw-Hill, 1963, p. 217.

Section 11.9 Electrocardiographic Correlates

 Many patients with extensive coronary atherosclerosis have normal resting electrocardiograms, and as I have already stressed, there are multiple reasons why myocardial infarction may not be reflected in the electrocardiogram.

 It is not possible to accurately predict the ejection fraction of the left ventricle, or to predict abnormalities in the contractility of segments of the left ventricular wall, by studying the electrocardiogram. For example, a large initial QRS abnormality may be associated with normal contractility of the left ventricular wall, and poor contractility of the ventricular wall may be associated with normal QRS complexes in the electrocardiogram. One clinical point that should be emphasized is that congestive heart failure is usually associated with an abnormal electrocardiogram. The opposite is not true: an abnormal electrocardiogram need not be associated with congestive heart failure.

 The ability to predict the particular coronary artery that is obstructed and, therefore, responsible for an infarction, is fraught with difficulty. Before the advent of coronary arteriography, an effort was made to correlate the electrocardiographic abnormalities of myocardial infarction with autopsy data. It was then discovered that the location of an infarct determined by electrocardiography did not correlate perfectly with the abnormalities found at autopsy. One reason for this is that on the autopsy table, the orientation of the anatomic parts of the heart is not the same as within the thorax of a living patient. Recent studies using coronary arteriography have yielded more insight into this problem and, as indicated by the following discussion, the ability to predict the artery responsible for an infarct has improved, though it still remains relatively crude.

 The prediction of the culprit artery is more accurate when one uses the mean ST vector of an acute infarction, and less accurate when one uses the Q waves of an old infarction. Clearly, such a prediction does not indicate the severity of the disease in other vessels. It should also be emphasized that the prediction does not eliminate the need to estimate the risk of other coronary events through other techniques such as coronary arteriography, radionuclide testing, or exercise electrocardiography.

 The relationships between the electrocardiographic abnormalities of infarction and the culprit coronary arteries are discussed below:
 
 

Section 11.10 Comments Regarding the Diagrams Shown in This Chapter

 The reader will note that in some of the diagrams in this chapter, the actual electrocardiographic deflections do not match those that would be predicted by studying the spatial orientation of the vectors that have been drawn to represent them. For example, the T waves may be positive in leads V5 and V6 but the direction of the vector representing the T waves may be oriented so that negative T waves would be recorded in leads V5 and V6 (see Fig. 11.14). Whereas similar problems occur in several illustrations throughout the book, the diagrams shown in this chapter can serve as examples of a problem that deserves reemphasis (see discussion following the table of contents).

 The frontal plane direction of a mean vector can usually be determined without difficulty. This is true because the extremity lead electrodes are almost electrically equidistant from the heart, and the distance varies very little from one person to another. Consequently, a rigid display system changes little from one subject to another, and the hexaxial reference system is used to display the frontal plane projection of the vectors.

 The anterior and posterior directions of a vector are determined by studying the deflections in the precordial leads. There are several problems associated with this method, and an accurate, rigid display system cannot be created.

 The problems are as follows:
 
 

Owing to the aforementioned reasons, it is impossible for one to always determine, and then to display on a rigid replica of the chest, the exact number of degrees to which vector is anteriorly or posteriorly directed in the frontal plane. It is usually possible, in such cases, to identify several precordial electrode deflections in which there is no argument about polarity, and these deflections should be used to determine the anterior or posterior direction of the vector. Often, when the deflections in the other precordial leads do not match what was predicted, it is because these other electrodes record electrical impulses from near the transitional pathway for the vector.

 Whenever there is an apparent "lack of a fit" between the actual and the predicted deflections of an electrocardiogram, I have indicated such in the legend, and I refer the reader to this section and to the discussion following the table of contents for an appropriate explanation.
 
 

References

  1. Antaloczy Z, Barcsak J, Magyar E: Correlation of electrocardiologic and pathologic findings in 100 cases of Q wave and non-Q wave myocardial infarction. J Electrocardiol 21(4):331, 1988.
  2. Hurst JW: Coronary spasm as viewed by Wilson and Johnston in 1941. Am J Cardiol 57:1000, 1988.
  3. Prinzmetal M, Kennamer R, Merlis R, et al: Angina pectoris. I. A variant form of angina pectoris. Am J Med 27:375, 1959.
  4. Hurst JW, Pollak SJ, Brown CL, Lutz JF: Electrocardiographic signs suggesting inferior infarction associated with angiographic evidence of obstruction of the left anterior descending coronary artery or its branches. Emory Univ J Med 2(3):170, 1988.