Abstract
Acute myocardial infarction is a common manifestation of ischemic heart disease and a leading cause of admission to the acute-care facilities in community and university hospitals. Although the great variations in clinical outcome in this disease are primarily related to the magnitude of acute myocardial loss, medical treatment directed at preservation of jeopardized myocardium has not appeared to result in substantial salvage,1 and the beneficial effects, if any, are probably related to effects on remote — possibly underperfused — myocardium. Myocardial necrosis is a consequence of a profound reduction in regional blood flow sustained for a long enough period to . . .