To understand your question you must understand what a myocardial infarction is.
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. 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 reperfusio is more effective in salvaging the myocardium than decreasing oxygen demand.
The onset of acute Q-wave myocardial infarction 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 These misnomers have been replaced by the terms Q-wave infarction and nonQ-wave infarction for transmural and nontransmural infarction, respectively.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 reperfusion.
3. Peak plasma CK levels are reached on an average of 12 to 13 h after onset of symptoms, indicating early washout of the enzyme, as opposed to about 27 h after Q-wave infarction.
4. Reperfusion-induced contraction necrosis is extremely common, as it is in patients who undergo early reperfusion induced by thrombolytic therapy
5. Acute mortality rates are around 2 to 3 percent, compared with 10 percent for Q-wave infarction.
6. The complications are minimal compared with those after a Q-wave infarction.
7. Finally, the long-term prognosis is characterized by recurrent episodes of reinfarction, so that after about 2 years, survival is the same as that after Q-wave infarction.
Quite often with the initial heart attack
over half of the patients have significant obstructive atherosclerosis in only one vessel. However, in a recent study two fifths of the patients with acute myocardial infarction
had angiographic evidence of multiple complex coronary plaques, which were associated with a less favorable in-hospital course. The presence of these plaques with complex morphologic features is the angiographic hallmark of unstable coronary syndromes and correlates with pathologic plaque and thrombus
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