Abstract
Angiographic and pathological studies have established the causative role of coronary-artery thrombosis in acute transmural myocardial infarction.1 , 2 The rupture of atheromatous plaque leads to occlusive thrombosis, which produces myocardial ischemia, tissue necrosis, and loss of ventricular function. Thrombolytic therapy for acute myocardial infarction is based on the premise that dissolving the fibrin component of a coronary thrombus is necessary and sufficient for recanalization and that reflow may save myocardium that is at risk. The magnitude of the effect, however, appears to depend on timing, and late reopening of the artery may contribute to clinical benefit through mechanisms other than myocardial . . .