Myocardial Ischemia and Infarction, Part II: Non-ST Segment Elevation and Non-Q Wave Syndromes


Myocardial infarction (MI) may be associated with the appearance of classic ST segment elevation MI (STEMI), usually followed by T wave inversions, as described in Chapter 9 . Q waves may appear in one or more of these leads. However, in many cases, myocardial ischemia (with or without actual infarction) presents with ST segment depressions rather than primary ST elevations. Q waves are less likely to develop in these cases and the most affected areas are likely to be in the inner (subendocardial) layers of the left ventricle. In contrast, severe ischemia involving the full thickness of the wall, including the outer (epicardial) zones is likely to result in ST segment elevations. As discussed later, non-ST elevation MI may also present without characteristic ST-T changes (with normal ST segments, or nonspecific ST-T changes). In some cases (e.g., Wellens’ syndrome), prominent T wave inversions without ST deviations are seen.

This chapter continues the discussion of acute coronary syndromes (ACS), as well as related conditions (e.g., takotsubo/stress cardiomyopathy syndrome; coronary vasospasm) that may be associated with electrocardiogram (ECG) changes usually attributed to atherosclerosis-based coronary occlusion. We then summarize the differential diagnosis of ST elevations, ST depressions and T wave inversions—the hallmark repolarization signatures of ischemia, followed by an overview of the ECG in acute and chronic ischemic heart disease.

Subendocardial Ischemia

How can subendocardial ischemia occur without transmural ischemia? The subendocardium is particularly vulnerable to ischemia because it is most distant from the epicardial coronary blood supply and closest to the high pressure of the ventricular cavity. Therefore the inner layers of the ventricle can become ischemic while the outer layer (subepicardium) remains normally perfused with blood.

The most common ECG change with predominant subendocardial ischemia is ST segment depression ( Fig. 10.1 ). The ST depressions may be limited to two or more of the anterior-lateral leads (I, aVL, and V 1 to V 6 ) or to the inferior leads (II, III, and aVF), or they may be seen more diffusely in both lead groups. As shown in Fig. 10.1 , the ST segment depressions most suggestive of subendocardial ischemia have a characteristic squared-off or downsloping shape.

Fig. 10.1, Predominantly subendocardial ischemia may produce ST segment depressions in multiple precordial and limb leads.

Recall from Chapter 9 that acute transmural ischemia produces ST segment elevations, more technically referred to as a current of injury pattern. This characteristic finding results primarily from an injury current generated by the epicardial/subepicardial layers of the ventricle. With pure subendocardial ischemia, just the opposite occurs; that is, multiple ECG leads (sometimes, anterior and inferior) show ST segment depressions, except lead aVR, which often shows ST elevations. a

a An important exception to the interpretation of diffuse ST depressions exclusively as a marker of subendocardial ischemia may occur with severe ischemia or actual MI because of left main coronary or very proximal left anterior descending blockage. In such cases, ST elevations in aVR and V 1 may be accompanied by diffuse ST depressions (see the next section in this chapter), likely reflecting a complex combination of transmural basal ischemia, primary subendocardial ischemia, and reciprocal changes.

To summarize: myocardial ischemia involving primarily the subendocardium usually produces ST segment depressions, whereas acute severe ischemia involving the epicardium/subepicardium and subendocardium produces ST elevations. This difference in the direction of the injury current vector is depicted in Fig. 10.2 .

Fig. 10.2, (A) With acute subendocardial ischemia the electrical forces ( arrows ) responsible for the ST segment are directed toward the inner layer of the heart, causing ST depressions in lead V 5 , which faces the outer surface of the heart. (B) With acute transmural (epicardial) ischemia, electrical forces ( arrows ) responsible for the ST segment are directed toward the outer layer of the heart, causing ST elevations in overlying leads.

ECG Changes with Angina Pectoris

The term angina pectoris (see Chapter 9 ) refers to bouts of chest discomfort caused by transient myocardial ischemia. Angina is a symptom of coronary artery disease. The “typical” episode is described as a dull, burning, or squeezing substernal pressure or heaviness, sometimes with radiation to the neck or jaw or down one or both arms. This symptom is often precipitated by exertion, emotional stressors, or exposure to cold and is relieved by rest and/or nitroglycerin.

Many (but not all) patients during episodes of classic angina have the ECG pattern attributable to subendocardial ischemia, with new or increased ST segment depressions. When the discomfort disappears, the ST segments generally return to the baseline, although there may be a lag between symptom relief and remittance of ECG findings. ( Fig. 10.3 shows ST depressions during a spontaneous episode of angina.)

Fig. 10.3, (A) Marked ST depressions are seen in lead V 4 of the ECG from a patient who complained acutely 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.

Clinicians should also be aware that some patients with angina do not show ST depressions during chest discomfort. Consequently, the presence of a normal ECG during an episode of angina-like chest discomfort does not rule out underlying coronary artery disease. However, the appearance of transient ST depressions in the ECG of a patient with characteristic anginal chest discomfort, or an “anginal-equivalent” such as dyspnea in some cases, 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. However, during exercise, ischemic changes may appear because of the extra oxygen requirements imposed on the heart by exertion and other stressors. Therefore to assist in diagnosing coronary artery disease, cardiologists often record the ECG while the patient exercises under controlled, closely monitored conditions. Stress electrocardiography is most often accomplished by having the patient walk on a treadmill or pedal a bicycle ergometer at increasing workloads. The test is stopped when the patient develops progressive angina, fatigue, dyspnea, or diagnostic ST changes or at the patient’s request. When symptoms or ST changes do not occur with exertion, the test is considered negative, especially if the heart rate reaches 85% or more (or some other predetermined target) of a maximum estimated rate, usually predicted from the patient’s age.

Fig. 10.4A shows the normal resting ECG of a patient, whereas Fig. 10.4B shows the marked ST depressions recorded while the same 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; 80 msec) as a positive (and potentially abnormal) test result (see Fig. 10.4B ). 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) or nondiagnostic ECG test response ( Fig. 10.5 ).

Fig. 10.4, (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 only modest increased heart rate.

Fig. 10.5, Lead V 5 shows physiologic ST segment depression that may occur with exercise. Notice the J junction depression ( arrow ) with sharply upsloping ST segments.

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. This combination of findings raises suspicion of severe three-vessel coronary disease and sometimes indicates high-grade stenosis of the left main coronary artery.

Exercise (stress) electrocardiography is often helpful in suggesting the presence of obstructive coronary artery disease in carefully selected patients. However, like virtually all medical tests, it yields 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 healthy 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 digoxin and in patients who have hypokalemia, left ventricular hypertrophy (LVH), ventricular conduction disturbances (i.e., left bundle branch block, Wolff–Parkinson–White preexcitation pattern), or ventricular paced rhythms. (See also Chapter 24 .)

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 using intravenous medications to increase the heart rate or promote coronary vasodilation in lieu of exercise is an important and related topic, but it lies outside the scope of this introductory text.

In summary, subendocardial ischemia, such as occurs with typical angina pectoris (or induced 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, which is the basis of the term silent ischemia. This important topic is discussed in Chapter 9 .

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