Abstract
The dual antiplatelet therapy of aspirin and clopidogrel is currently the standard therapy for patients with acute coronary syndrome (ACS). There has been accumulating evidence indicating presence of clopidogrel resistance or non-responders. Clopidogrel non-responders are associated with more ischemic events. Inhibition of platelet aggregation is reduced in non-responders. Because clopidogrel exhibits its antiplatelet effects through biotransformation to active metabolite by CYP2C19 in the liver, the reduced function of CYP2C19 is considered as the main reason for non-responders. This is supported by several observations that patients with CYP2C19 loss of function allele had more frequent ischemic events with reduced exposure to the active metabolite, and that more potent and consistent, a new antiplatelet agent, prasugrel, showed improved clinical outcomes compared with clopidogrel. There remains unclear whether or not antiplatelet strategy based on the genotyping or measurements of antiplatelet activity in each individual will improve clinical outcomes.
