Effect of aspirin on myocardial ischemia

Abstract

The clinical manifestations of coronary artery disease (CAD) are consequences of myocardial ischemia and infarction. Myocardial ischemia may result from increased myocardial oxygen demand as occurs with exercise or from a primary reduction in blood supply to the myocardium via spasm of a coronary artery. Recently, myocardial ischemia has been shown to occur despite the absence of increases in workload or the presence of spasm. 1 The etiology of these episodes is unclear, but in a dog model, Foils et al 2 have shown that transient acute decreases in coronary blood flow occur when platelet aggregates obstruct a stenotic segment of a coronary artery. Treatment with aspirin eliminates these episodes. If patients with CAD also have intermittent obstruction by platelet aggregates, treatment with aspirin might be expected to be beneficial. The elegant experimental model of Folts et al is difficult to reproduce in patients. The direct measurement of coronary blood flow is impossible in ambulatory subjects; therefore, an indirect measure of myocardial ischemia is necessary. In addition, aspirin is not likely to affect myocardial oxygen mismatches resulting from exertion or arterial spasm, but if these other causes of ischemia are treated, it may be possible to unmask the effect of aspirin. This study evaluates the effect of aspirin on myocardial ischemia as quantitated by ambulatory Holter monitoring of ST-segment shifts in patients with known CAD who are concurrently treated with β blockers, nitrates and calcium antagonists.