Chapter 9 Myocardial Infarction and Ischemia, II Non–ST Segment Elevation and Non–Q Wave Syndromes
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Myocardial infarction (MI) may be associated with abnormal Q waves associated with the typical progression of ST segment elevation myocardial infarction (STEMI) and T wave inversions described in Chapter 8. In many cases, however, myocardial ischemia (with or without actual infarction) may be limited primarily to the subendocardium (inner layer) of the ventricle, often associated with ST segment depressions, rather than primary ST elevations.
How can subendocardial ischemia occur without transmural ischemia or infarction? The subendocardium is particularly vulnerable to ischemia because it is most distant from the coronary blood supply and closest to the high pressure of the ventricular cavity. This inner layer of the ventricle can become ischemic while the outer layer (epicardium) remains normally perfused with blood.
The most common ECG change with subendocardial ischemia is ST segment depression (Fig. 9-1). The ST depression may be limited to the anterior leads (I, aVL, and V1 to V6) or to the inferior leads (II, III, and aVF), or it may be seen more diffusely in both groups of leads. As shown in Figure 9-1, the ST segment depression with subendocardial ischemia has a characteristic squared-off shape. (ST segment elevation is usually seen in lead aVR.)
Recall from Chapter 8 that acute transmural ischemia produces ST segment elevation, a current of injury pattern. This results from epicardial injury. With pure subendocardial ischemia, just the opposite occurs; that is, the ECG shows ST segment depression (except in lead aVR, which often shows ST elevation).
In summary, myocardial ischemia involving primarily the subendocardium usually produces ST segment depression, whereas acute ischemia involving the epicardium usually produces ST elevation. This difference in the direction of the injury current vector is depicted in Figure 9-2.
Figure 9-2 A, With acute subendocardial ischemia the electrical forces (arrows) responsible for the ST segment are deviated toward the inner layer of the heart, causing ST depressions in lead V5, which faces the outer surface of the heart. B, With acute transmural (epicardial) ischemia, electrical forces (arrows) responsible for the ST segment are deviated toward the outer layer of the heart, causing ST elevations in the overlying lead.
ECG Changes with Angina Pectoris
The term angina pectoris refers to transient attacks of chest discomfort caused by myocardial ischemia. Angina is a symptom of coronary artery disease. The classic attack of angina is experienced as a dull, burning, or boring substernal pressure or heaviness. It is typically precipitated by exertion, stress, exposure to cold, and other factors, and it is relieved by rest and nitroglycerin.
Many (but not all) patients with classic angina have an ECG pattern of subendocardial ischemia, with ST segment depressions seen during an attack. When the pain disappears, the ST segments generally return to the baseline. (Fig. 9-3 shows ST depressions during a spontaneous episode of angina.)
Figure 9-3 A, Marked ST depressions are seen in lead V4 of the ECG from a patient who complained of chest pain while being examined. B, Five minutes later, after the patient was given sublingual nitroglycerin, the ST segments have reverted to normal, with relief of angina.
The ECGs of some patients with angina do not show ST depressions during chest pain. Consequently, the presence of a normal ECG does not rule out underlying coronary artery disease. However, the appearance of transient ST depressions in the ECG of a patient with chest pain is a very strong indicator of myocardial ischemia.
Exercise (Stress) Testing and Coronary Artery Disease
Many patients with coronary artery disease have a normal ECG while at rest. During exercise, however, ischemic changes may appear because of the extra oxygen requirements imposed on the heart by exertion. To assist in diagnosing coronary artery disease, the cardiologist can record the ECG while the patient is being exercised under controlled conditions. Stress electrocardiography is usually performed while the patient walks on a treadmill or pedals a bicycle ergometer. The test is stopped when the patient develops angina, fatigue, or diagnostic ST changes or when the heart rate reaches 85% to 90% of a maximum predetermined rate predicted from the patient’s age. This approach is known as submaximal testing.
Figure 9-4A is the normal resting ECG of a patient, whereas Figure 9-4B shows the marked ST depressions recorded while the patient was exercising. The appearance of ST segment depressions constitutes a positive (abnormal) result. Most cardiologists accept horizontal or downward ST depressions of at least 1 mm or more, lasting at least 0.08 sec (two small boxes) as a positive (abnormal) test result (see Fig. 9-4B). ST depressions of less than 1 mm (or depressions of only the J point) with a rapid upward sloping of the ST segment are considered a negative (normal) test response (Fig. 9-5).
Figure 9-4 A, Baseline rhythm strip from the very positive (abnormal) exercise test of a patient with coronary artery disease. B, Notice the marked ST depressions with increased heart rate.
Figure 9-5 Lead V5 shows physiologic ST segment depression that may occur with exercise. Notice the J junction depression (arrow) with sharply upsloping ST segments.
(From Goldberger AL: Myocardial Infarction: Electrocardiographic Differential Diagnosis, 4th ed. St. Louis, Mosby, 1991.)
The finding of prominent ischemic ST changes, with or without symptoms, occurring at a low level of activity is particularly ominous. Sometimes, these changes will be associated with a drop in blood pressure. These findings may indicate severe three-vessel coronary disease and sometimes high-grade obstruction of the left main coronary artery.
Exercise electrocardiography is often helpful in diagnosing coronary artery disease. However, like all tests, it may give both false-positive and false-negative results. For example, up to 10% of men without evidence of coronary obstructions and an even higher percentage of normal women may have false-positive exercise tests.
False-positive tests (defined here as ST depressions without obstructive coronary disease) can also be seen in patients who are taking digitalis and in patients who have hypokalemia, left ventricular hypertrophy (LVH), ventricular conduction disturbances, or a Wolff-Parkinson-White pattern (see Chapter 12).
False-negative tests can occur despite the presence of significant underlying coronary artery disease. Therefore, a normal (“negative”) exercise test does not exclude coronary artery disease. The diagnostic accuracy of exercise tests may be increased in selected patients by simultaneous imaging studies, using echocardiography or nuclear medicine scans. Pharmacologic stress testing, an important related topic, lies outside the scope of this text.
In summary, subendocardial ischemia, such as occurs with typical angina pectoris (and as may be elicited with stress testing), often produces ST segment depressions in multiple leads.
“Silent” Myocardial Ischemia
A patient with coronary artery disease may have episodes of myocardial ischemia without angina, hence the term silent ischemia. Silent ischemia is sometimes detected during exercise testing. Ambulatory ECG (Holter) monitoring is the most useful way of assessing silent myocardial ischemia (see Chapter 3). The 24-hour ECG monitoring of patients with coronary artery disease reveals a surprisingly high frequency of ST depressions not associated with angina. This important topic is discussed again later in this chapter.
If ischemia to the subendocardial region is severe enough, actual infarction may occur. In such cases the ECG may show more persistent ST depressions instead of the transient depressions seen with reversible subendocardial ischemia.