ABSTRACT
Formation of platelet thrombi at the sites of ruptured atherosclerotic plaques is responsible for the majority of acute ischemic events in coronary, cerebral, and peripheral arteries. Platelet activation with exposure of phosphotidyl serine is also believed to play a role in some venous thrombotic disorders. In vitro assays demonstrating reduced platelet function correlate with mild (e.g., platelet secretion defects) and severe (e.g., Glanzmann thrombasthenia) clinical bleeding. More recently, there has been an increasing awareness of the prothrombotic risk of platelet hyperreactivity in normal subjects and those with coronary artery disease (1). This hemostasis-thrombosis heterogeneity in the population may be linked to the well-known interindividual variation in ex vivo measures of platelet reactivity. Although there may be acquired and technical explanations for interindividual variation in platelet phenotypes, there is strong evidence that heritability contributes to this variation (2,3). These genetic effects are consistent with an increasing number of reports of platelet gene polymorphisms that show associations with clinical outcomes and laboratory assays of platelet function (4-14).
