Platelet activation plays a pivotal role in the pathogenesis of acute coronary syndromes, strokes and other thrombophilic diseases. Atheromatous plaque rupture changes the shear forces of blood flowing over the injured vessel surface and also exposes collagen as well as other prothrombotic factors (9-11). As the initial hemostatic event, platelets become activated and cover the injured surface. Following platelet activation highly active substances like adenosine diphosphate (ADP) and thromboxane A2 (TxA2) are released from the platelet to promote and recruit further platelet aggregation to the injury site (12). If this process proceeds unabated, as it often does in atherosclerotic diseases, the vessel becomes occluded and infarction may follow.