This term refers to the death of a certain segment of the heart muscle (myocardium), usually the result of a focal complete blockage in one of the main coronary arteries or a branch thereof. The main cause of myocardial infarction is atherosclerosis in the coronary arteries. Refer to figure 70 for the pathogenesis of myocardial infarction. This event results in impaired contractility of the heart muscle within seconds, and is initially restricted to the affected segment. The myocardial ischemia or infarction begins in the endocardium (the inner lining of the heart) and spreads to the epicardium (the outer lining of the heart). Irreversible heart damage will occur if the blockage is complete for at least 15-20 minutes. Irreversible damage occurs maximally in the area at risk, and when the occlusion is maintained for 4-6 hours. Most of the damage occurs in the first 2-3 hours. Restoration of flow within the first 4-5 hours is associated with salvage of the heart muscle, but the salvage is greater if flow is restored in the first 1-2 hours. A major determinant of death and illness is the size of the infarct. Increasing the oxygen supply to the involved site of blockage by coronary reperfusion (angioplasty, figures 52, 53, 54, 55, 56b, stents, figures 95a,95b, atherectomy, see figures 56a, 56c) is more effective in salvaging the myocardium than decreasing oxygen demand. The onset of acute Q-wave myocardial infarction (see figure 94 for normal EKG with a normal Q-wave, which is sharply inscribed, narrow in time of inscription and small in depth compared to the abnormal acute Q-wave type in myocardial infarction, which is deeper and wider in inscription time) occurs commonly in the morning hours shortly after arising, when there is increasing adrenergic activity, as well as increased blood fibrinogen levels and increased platelet (blood cell) adhesiveness. Non Q wave infarction does not show this circadian rhythm.
The traditional concept that myocardial infarctions can be classified as transmural or nontransmural on the basis of the presence or absence of Q waves is misleading, since autopsy studies have demonstrated convincingly that pathologic Q waves may be associated with nontransmural infarction and may be absent with transmural infarction. These misnomers have been replaced by the terms Q-wave infarction and nonQ-wave infarction for transmural and nontransmural infarction, respectively. The evolution of a non-Q-wave infarction is charcterized by a lack of development of an abnormal Q wave and by the appearance of reversible ST-T-wave changes with ST depression that usually returns to normal over a few days, but occasionally is permanent. Differentiation between these two types of infarctions has become entrenched, since there are major differences in their pathogenesis, clinical manifestations, treatment, and prognosis. The initiating events in the pathogenesis of Q-wave and non-Q-wave infarction are thought to be identical, namely, coronary occlusion induced by thrombus superimposed on a plaque together with vasoconstriction. There is considerable evidence, however, to indicate that in non-Q-wave infarction, early spontaneus reperfusion occurs, the mechanism of which remains uncertain. In contrast, in Q-wave infarction, the coronary occlusion is sustained at least for a long enough period to result in extensive necrosis. One explanation for early spontaneous reperfusion is the lack of sustained vasoconstriction, which may contribute to ocusion. The evidence supporting the existence of early spontaneous reperfusion in non-Q-wave infarction is as follows: 1. Coronary angiographic studies performed in the early hours after onset show that only 20-30% of patients have complete coronary occlusion of the infarct-related vessels;but for Q-wave infarction it is about 80 to 90%.
2. Infarct size is routinely much less than observed with Q wave infarction, which is consistent with salvage by early...
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