Unstable angina appears to be caused by relatively brief, repetitive episodes of myocardial oxygen impairment secondary to platelet aggregation and dynamic vasoconstriction at sites of coronary stenosis and endothelial injury. With chronic endothelial injury, the accumulation of thromboxane A(2), serotonin, and other mediators may contribute to platelet aggregation and dynamic vasoconstriction. Aspirin acetylates the platelet enzyme, cyclooxygenase, thereby inhibiting the formation of thromboxane A(2). In certain patients with unstable angina, 1 to 4 aspirin tablets per day has proved beneficial in reducing the risk of myocardial infarction and death. Moreover, combining aspirin with a selected thrombolytic agent, such as streptokinase, appears to potentiate thrombolysis and further reduce mortality. Aspirin's toxicity to the gastrointestinal tract and its tendency to decrease vascular concentrations of prostacyclin, a local endothelial factor that hinders thrombogenesis and promotes endogenous vasodilation, are concerns when used in long-term treatment; for this reason, we do not recommend aspirin therapy for every patient with an acute coronary syndrome. We do, however, advocate such therapy for those with unstable angina and, in combination with selected thrombolytic interventions, for those with acute Q-wave myocardial infarctions in whom aspirin is not contraindicated.