Platelet receptor polymorphisms and thrombotic risk.

Plaque rupture and/or endothelial damage lead to exposure of von Willebrand factor and collagen which facilitate the adhesion of circulating platelets via glycoprotein Ib-IX-V and the integrin alpha2 beta1, respectively, to the damaged vessel wall. This process activates the platelet and leads to a conformational change of a second integrin alphaIIb beta3 that facilitates fibrinogen binding and platelet aggregation. Thrombin generated at the blood-plaque interface converts fibrinogen to fibrin, which stabilizes thrombus growth. Therefore, any genetic differences that might alter surface expression or activity of these receptors could influence risk for adverse outcomes as a result of the haemostatic process. In the last 5 years, there has been a rapid accumulation of the literature concerning the relationship between genetic variations in platelet glycoproteins and risk for coronary heart disease. In this chapter, we present a comprehensive review of the impact of platelet receptor polymorphisms and thrombotic risk.