Genetic determinants of responsiveness to antiplatelet therapy

Antiplatelet drugs are well-established therapies for acute coronary syndromes and for the primary and secondary prevention of coronary artery disease, stroke, and peripheral vascular disease. However, wide interindividual variability exists in the degree of platelet suppression among patients treated with antiplatelet drugs, and many individuals develop atherothrombotic events while on therapy. Although many potential mechanisms may contribute to the response variation observed, there is accumulating evidence that polymorphisms of genes from multiple biologic pathways involved in platelet activation are at least partly responsible for variable platelet responsiveness and potentially responsible for clinical failure of antiplatelet therapy.