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Abstract
There has been recent interest in treating acute myocardial infarction with coronary
reperfusion by fibrinolytic therapy. Experimental studies have shown that myocardial
infarct size can be reduced by coronary reperfusion. However, return of cardiac function,
high energy phosphate metabolism, and cardiac ultrastructure may be delayed within
tissue which is salvaged by coronary reperfusion. This postischemic ventricular dysfunction
is transient and has been termed the ‘stunned myocardium’ phenomenon. Although reperfused
infarcts are hemorrhagic, the hemorrhage is confined well within tissue which is already
necrotic and does not appear to exacerbate the extent of necrosis. Clinical trials
designed to assess the benefits of reperfusion for the therapy of acute myocardial
infarction should concentrate on long-term rather than short-term changes in cardiac
function.