ABSTRACT
Rationale for antiplatelet therapy Experiments in animal models and autopsy studies have demonstrated the primary involvement of platelets during thrombus formation and plugging of microvasculature (11,12). Increased expression of platelet surface molecules and heightened platelet reactivity have been demonstrated in patients with ACS and during PCI (2,13,14). High platelet reactivity has been associated with stent thrombosis, restenosis, inflammation, myocardial infarction (MI), and other ischemic events (15-22). Platelet activation and high platelet reactivity have also been associated with diabetes, hypertension, and hyperlipidemia (23-25). Therefore, the rationale for antiplatelet therapy is to prevent the development of occlusive thrombus formation, to arrest the procoagulant activity and inflammatory processes, to promote disaggregation of platelets, and finally to facilitate the reperfusion of occluded blood vessels. The determination of optimal platelet inhibition is dependent on the degree of ischemic risk and is counterbalanced by the risk of bleeding.
