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For nearly a decade, it has been appreciated that 1) thrombotic occlusion of an epicardial coronary artery is usually the proximate cause of acute myocardial infarction; 2) after sudden and sustained total occlusion of such a vessel, the course of myocardial necrosis is generally rapid and relentless (in most cases, the process is completed within 3 or 4 hours of the coronary occlusion, in 6 hours at a maximum); 3) infarct size is a critical determinant of left ventricular function; and 4) left ventricular function, in turn, is the most important determinant of early (in-hospital) and long-term (postdischarge) survival. Major efforts have been devoted to the development of techniques designed to interfere with the sequence of events summarized above. Considerable attention has been directed to achieving timely reperfusion of occluded coronary arteries to interrupt the infarction with the hope that the resultant limitation of infarct size will improve ventricular function and thereby patient survival.1 Many techniques to achieve reperfusion have been used, including emergency coronary artery bypass surgery, emergency percutaneous transluminal coronary angioplasty (PTCA), and the intracoronary and intravenous administration of a variety of thrombolytic agents; the last of these approaches is particularly attractive because its simplicity makes it applicable to a large proportion of patients with acute myocardial infarction. In some instances, combinations of these techniques, such as intravenous thrombolytic therapy followed by PTCA, have been used. These efforts to treat acute myocardial infarction have been notably successful, as reflected in an improvement in survival noted in controlled randomized trials.2-6 Also, the absolute mortality rates achieved in some recent trials of reperfusion therapy (3-5%) are far lower than those noted previ-

Myocardial reperfusion, limitation of infarct size, reduction of left ventricular dysfunction, and improved survival. Should the paradigm be expanded?