Blood Platelets and Myocardial Infarction: Do Hyperactive Platelets Really Exist?

The existence of platelet ‘hyperreactivity’ as a trigger of acute vascular events has been postulated clinically for decades. However, the molecular nature of an intrinsically enhanced platelet function remained unknown. Recently, a possible explanation was provided in that several genetically determined variants of platelet glycoprotein receptors can be responsible for an increased thrombogenicity and thereby accelerate acute occlusive complications of arterial disease. Distinct polymorphisms within the genes of platelet membrane glycoprotein receptors can alter their antigenicity, regulate, at least in part, their expression levels on the platelet surface, and modify their functional properties with regard to ligand binding and adhesion activity. This review will focus on 2 essential platelet receptors, the integrins aIIbß3 and a2ß1, their polymorphisms, and their potential clinical impact of genetically determined receptor variants on cardiovascular disease. Moreover, the genotype- to-phenotype relation of relevant platelet receptor variants will be discussed, and an attempt is made to assess the interdependency of phenotype to disease.