Mechanisms contributing to precipitation of unstable angina and acute myocardial infarction: implications regarding therapy

Abstract

Clinical and autopsy studies indicate that most patients who present with unstable angina or an acute myocardial infarction (AMI) have significant underlying coronary atherosclerosis. This review discusses 4 mechanisms that may contribute to the precipitation of these acute ischemic clinical syndromes: progression of atherosclerosis, acute coronary thrombosis, coronary artery spasm, and platelet aggregation. Numerous clinical trials using thrombolytic agents early during AMI have shown the incidence of thrombosis to be at least 60%. Other studies suggest that platelet aggregation frequently contributes to the evolution of AMI from unstable angina and that spasm may occasionally play a similar role. The therapeutic implications of these mechanisms are also considered in light of their potential to restore coronary artery blood flow (vs conventional methods thought mainly to reduce myocardial oxygen demand) and thereby limit the infarct process. The role of vasodilators, thrombolytic agents, antiplatelet drugs and beta-adrenergic blocking drugs are discussed. Finally, therapeutic guidelines for the treatment of acutely ill patients are constructed that emphasize the need for a comprehensive yet time-efficient treatment strategy that uses nitrates, calcium channel-blocking drugs, streptokinase, heparin, aspirin and, in selected patients in an unstable condition, emergency percutaneous transluminal coronary angioplasty and coronary artery bypass grafting.