High on-clopidogrel platelet reactivity: genotyping can help to optimize antiplatelet treatment.

摘要

Clopidogrel is a thienopyridine prodrug that must be converted into an active metabolite to target the platelet ADP P2Y_(12) receptor. The pharmacodynamic response to clopidogrel exhibits considerable interindividual variability, part of which is dependent on genetic factors. About 20% of patients have decreased biological responsiveness to clopidogrel with a higher risk of cardiovascular events [1]. Two genetic factors that contribute to limit the efficacy of clopidogrel have been identified in healthy volunteers.