ABSTRACT
INTRODUCTION Antithrombotic and antiplatelet therapy is central to successful percutaneous treatment of ST-segment elevation myocardial infarction (STEMI). Rupture of atherosclerotic plaque exposes the subendothelial matrix and leads to platelet adhesion, activation, and ultimately platelet aggregation into a flow-limiting platelet-fibrin plug (1). Various agonists including thromboxane A2, thrombin, collagen, norepinephrine, and adenosine diphosphate stimulate platelet activation. Regardless of the initial source of activation, the final pathway of platelet aggregation requires cross-linking of platelets by fibrinogen and von Willebrand factor through binding glycoprotein (GP) IIb/IIIa receptors on the surface of adjacent platelets (1).
