OasisLMS

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Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor is standard of care following percutaneous coronary intervention (PCI), however, contemporary practice continues to rely heavily on one-size-fits-all antiplatelet strategies, despite well-established interpatient variability in platelet response and clinical risk. 

A major contributor to this variability is genetic polymorphism of the CYP2C19 enzyme, which governs clopidogrel activation. Approximately one-third of patients undergoing PCI carry loss of function CYP2C19 alleles, placing them at increased risk for high on treatment platelet reactivity and ischemic complications when treated with clopidogrel. Conversely, more potent P2Y12 inhibitors provide consistent platelet inhibition across genotypes but are associated with higher bleeding risk, particularly in patients who would otherwise respond adequately to clopidogrel. Bleeding avoidance is as critical as ischemic prevention in optimizing PCI outcomes.

Recent studies demonstrate that genotype-guided antiplatelet strategies can reduce ischemic events in CYP2C19 loss of function allele carriers without increasing bleeding risk, while allowing safe deescalation to clopidogrel in noncarriers. Join a multidisciplinary panel of experts to discuss the clinical challenges of DAPT in PCI, evidence for gene-guided therapy, and case-based strategies for implementing rapid genetic testing.

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