SINCE the advent of the coronary care unit (CCU) in 1962, the in-hospital mortality of patients with acute myocardial infarction has been notably reduced, predominantly because of better management of ventricular arrhythmias. Despite adequate antiarrhythmic therapy, there remains a 15% to 25% acute mortality that is related primarily to pump failure, a major determinant of which is the extent of myocardial damage (infarct size).
Postmortem studies have shown that patients dying of cardiogenic shock exhibit 40% or more destruction of the myocardium. Clearly, therapeutic efforts in the modern CCU must be directed toward reducing the extent of myocardial damage associated with myocardial infarction. Pioneering studies by Braunwald and others1 suggested that the development of myocardial damage is a dynamic event that can be favorably altered, notably by decreasing the imbalance between myocardial oxygen supply and demand. This provided the impetus for an area of research, namely, protection of ischemic myocardium,