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