n the United States alone, approximately one million patients experience an acute myocardial infarction (AMI) annually with an acute mortality ranging from 5 to 30% followed by a substantial mortality in the first few years following discharge. Nonetheless, approximately 25 years of intensive coronary care have had a major beneficial impact on the outcome of AMI. The initial focus was on the identification and treatment of "primary malignant arrhythmias," followed by advances in the diagnosis and treatment of the mechanical complications of acute infarction.
We are now in the era of "myocardial salvage." The primary thrust was aimed at reducing myocardial oxygen demands (MV02) , followed by a recent shift toward acute reperfusion as the most effective approach toward reducing infarct size. The hypothesis that a reduction in MV02 could possibly salvage myocardium and reduce the incidence of lifethreatening arrhythmias was the impetus behind the numerous trials of beta-blocking agents in AMI during the 1970s and early 1980s, which showed a decline in early mortality of approximately 15 to 20% [1]. More recently, the calcium-blocking agents have been the subject of several trials, which examined their effects on mortality and indices of infarct size. To date, however, there has been no convincing evidence that calcium-blocking agents administered during the early phase of acute infarction or during "impending infarction" reduce mortality (see below).
In 1980, Dewood and colleagues demonstrated that total coronary artery occlusion due to thrombus was present in approximately 80% of patients with evolving MI presenting with ST segment elevation [2]. Understandably, these and other observations from the animal laboratory provided the stimulus for clot lysis Address for correspondence and reprint requests: Bernard J. Gersh,