BackgroundReperfusion strategies have led to a substantial improvement in the prognosis of patients with acute myocardial infarction (AMI). However, the beneficial effect of successful restoration of epicardial coronary flow on myocardial salvage may be offset by inadequate tissue perfusion, a condition referred to as the "no-reflow phenomenon". The mechanism responsible for the no-reflow phenomenon is uncertain and is likely multifactorial. Due to the potential for thrombus formation and release of vasoactive substances, it has been suggested that platelets may play a major role in the dissociation of epicardial artery recanalization and tissue-level reperfusion. However, the role of platelets in reperfusion injury remains to be determined. Similarly, although data exist that inhibition of the platelet glycoprotein â…¡b/â…¢a receptor prevents abrupt re-occlusion after PCI procedures and improves TIMI flow rates in AMI patients, the ability of glycoprotein â…¡b/â…¢a inhibitor to enhance flow at the microvascular level after coronary reperfusion has not been determined. Objectives1. To assess the ability of platelet inhibition and inactivation with tirofiban for...
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