ABSTRACT
Introduction 161 Mechanism of action and clinical efficacy of
antiplatelet drugs 161
References 168
Platelets are vital components of normal hemostasis and key participants in pathologic thrombosis by virtue of their capacity to adhere to injured blood vessels and to accumulate at sites of injury.1 Although platelet adhesion and activation can be viewed as a physiologic repair response to the sudden fissuring or rupture of an atherosclerotic plaque, uncontrolled progression of such a process through a series of self-sustaining amplification loops may lead to intraluminal thrombus formation, vascular occlusion, and transient ischemia or infarction. Currently available antiplatelet drugs interfere with some steps in the activation process, including adhesion, release, and/or aggregation,1 and have a measurable impact on the risk of arterial thrombosis that cannot be dissociated from an increased risk of bleeding.2
