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Impairment of left ventricular function is a major consequence of acute myocardial infarction. Several interventions have been proposed to reduce the extent of myocardial tissue undergoing necrosis after cornoracy artery occlusion. Therapy for patients with acute myocardial infarction has long relied on interventions aimed at reducing oxygen consumption, such as administration of β-blockers and nitrates. However, despite clinical evidence that these interventions can reduce mortality or prevent left ventricular dilatation, no clear benefit has been observed on left ventricular function. Over the past few years, treatment of acute myocardial infarction has radically changed. Availability of several thrombolytic agents has made reperfusion of ischemic myocardium a routine procedure. Early reperfusion has been shown to be the most powerful intervention to reduce infarct size and minimize left ventricular dysfunction in experimental preparations. Several clinical trials have also demonstrated that patients with acute myocardial infarction may greatly benefit from early thrombolysis. As this procedure is associated with improvement of global and regional left ventricular function and reduction in mortality. However, in spite of its obvious advantages, reperfusion might result in a paradoxical tissue damage that may blunt the net beneficial effect of restoring perfusion of ischemic myocardium. Reperfusion-mediated myocardial injury has been shown to occur in several experimental preparations and it has been proposed that generation of toxic oxygen metabolites at the moment of reflow is responsible for the occurrence of this phenomenon. Indeed, administration of free radical scavengers may significantly reduce the extent of reperfusion injury and improve contractile recovery in experimental preparations. If reperfusion injury is proven to occur in patients with acute myocardial undergoing thrombolytic therapy, new avenues for the therapy of such patients might be opened by interventions aimed at minimizing this phenomenon.