The glycoprotein IIIa gene polymorphism and the risk of myocardial infarction

The hemostatic platelet response of an individual may be influenced by the genetic profile of the platelet membrane glycoprotein (GP) receptors. The GP IIIa, as a part of von Willebrand factor and fibrinogen receptor, plays a central role in platelet aggregation. Polymorphism in GP IIIa has been extensively studied for its association with myocardial infarction or coronary artery diseases. To date, the role of GP IIIa polymorphism in genetic susceptibility to thrombotic disease still remains controversial. The results of case-control association studies vary, even with the same ethnic background, and the association was hardly found in studies with larger sample size, suggesting publication-bias toward positive findings. In meta-analysis, the GP IIIa Pl(A2) allele carriers did not show increased risk for myocardial infarction compared with Pl(A1/A1) homozygotes. The functional studies also showed conflicting results. In conclusion, GP IIIa Pl(A1/A2) polymorphism does not seem to have a major role either in determining the individual variance of platelet function or the risk of myocardial infarction according to the currently available data. Therefore, the genotype determination of GP IIIa Pl(A1/A2 )polymorphism may not be useful for risk assessment of myocardial infarction at this time. Nevertheless, the author can not completely exclude its possible role in coronary thrombosis after angioplasty or sudden cardiac death. Thus, further evaluation in larger prospective or multicenter studies is required to elucidate the role of GPs in cardiovascular system.