Following percutaneous coronary intervention (PCI), dual antiplatelet therapy (DAPT) with aspirin and an inhibitor of the platelet adenosine diphosphate P2Y12 receptor (P2Y12) is standard care to reduce the occurrence of stent thrombosis and ischemic events. For many years, clopidogrel has been the most commonly used P2Y12 inhibitor for patients with an acute coronary syndrome (ACS) and those undergoing PCI. However, platelet function studies have revealed variability in the response to clopidogrel, with 20% to 40% of patients having persistent, high on-treatment platelet reactivity.1 This attenuated pharmacodynamic response in some patients is partly explained by genetic variants of CYP2C19, the gene that encodes the CYP2C19 liver enzyme responsible for metabolizing clopidogrel (a prodrug) to its active form. Variants in the CYP2C19 gene that reduce its activity (loss-of-function [LOF] variants) result in diminished activation of clopidogrel and reduced antiplatelet efficacy.
Moliterno DJ, Smyth SS, Abdel-Latif A. CYP2C19 Genotyping to Guide Antiplatelet Therapy After Percutaneous Coronary Interventions: One Size Rarely Fits All. JAMA. 2020;324(8):747–749. doi:10.1001/jama.2020.13094
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