ABSTRACT
Coagulation is a complex series of biochemical and cellular reactions that results in the polymerization of fibrin and formation of platelet/fibrin hemostatic plugs. In normal blood vessels, these interactions serve as the primary mechanism to control hemorrhage. However, when combined with vascular pathology of major arteries, such activation can result in thrombosis and life-threatening vascular occlusion (1,2). Platelets play a major role in mediating some of the earliest events of both hemostasis and thrombosis. Antiplatelet therapies have been anti-thrombotic targets and the source of effective therapies (3). Most of the antiplatelet drugs target platelet biochemical pathways. To date, only the glycoprotein IIb/IIIa (GPIIb/IIIa) antagonists have targeted platelet adhesion mechanisms and been approved for the treatment of acute coronary events (4-6). Although the GPIIb/IIIa antagonists have been shown to provide improved outcomes, their efficacy is complicated by bleeding at platelet-inhibitory doses. Over the past few years, increased interest has been directed toward other platelet adhesion mechanisms that might permit separation of platelet inhibition from bleeding. Two of these adhesion pathways, von Willebrand factor/GPIba (VWF/GPIba) and GPVI, will be discussed in this chapter (7).
