Plaque rupture and/or endothelial damage lead to exposure of von Willebrand factor (VWF) and collagen which facilitate the adhesion of circulating platelets via glycoprotein (GP) GPIb-IX-V and integrin α₂β₁, respectively, to the damaged vessel wall. This process activates the platelets and leads to a conformational change of a second integrin α_IIbβ₃ 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 the risk for adverse outcome as a result of the hemostatic process. In the last five years, there has been a rapid accumulation of literature concerning the relationship between genetic variations in platelet glycoproteins and risk for coronary heart disease. In this study, we have presented a comprehensive review of the impact of platelet receptor polymorphisms and thrombotic risk.