期刊
CLINICAL PHARMACOLOGY & THERAPEUTICS
卷 109, 期 3, 页码 705-715出版社
WILEY
DOI: 10.1002/cpt.2039
关键词
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资金
- National Institutes of Health (NIH) part of the NIH IGNITE network [U01 HG007269, U01 HG007775, U01 HG007762]
- NIH part of the NIH Pharmacogenomics Research Network [T32 HG008958, K01 HL141690, U01 GM074492, U01 HL105198]
- University of Florida and its Clinical Translational Science Institute [UL1 TR000064, UL1 TR001427]
- NIH [UL1 TR002489, R01 HL092173, K24 HL133373, UL1 TR000165, UL1 TR0000005, U54 MD010723]
- Penn Center for Precision Medicine at the Perelman School of Medicine at the University of Pennsylvania
- Hugh Kaul Precision Medicine Institute at the University of Alabama, Birmingham
- University of Pittsburgh/UPMC Institute for Precision Medicine
- American Society of Health System Pharmacists
- American Heart Association [17MCPRP33400175]
The study found that the CYP2C19*17 allele did not significantly impact post-PCI prescribing decisions or clinical outcomes in genotype-guided antiplatelet therapy, suggesting limited clinical utility of the CYP2C19*1/*17 and *17/*17 genotypes in guiding antiplatelet therapy after PCI.
Genotyping forCYP2C19no function alleles to guide antiplatelet therapy after percutaneous coronary intervention (PCI) improves clinical outcomes. Although results for the increased functionCYP2C19*17allele are also reported, its clinical relevance in this setting remains unclear. A collaboration across nine sites examined antiplatelet therapy prescribing and clinical outcomes in 3,342 patients after implementation ofCYP2C19-guided antiplatelet therapy. Risk of major atherothrombotic and bleeding events over 12 months after PCI were compared across cytochrome P450 2C19 isozyme (CYP2C19) metabolizer phenotype and antiplatelet therapy groups by proportional hazards regression. Clopidogrel was prescribed to a similar proportion of CYP2C19 normal (84.5%), rapid (82.9%), and ultrarapid metabolizers (80.6%) (P = 0.360). Clopidogrel-treated normal metabolizers (20.4 events/100 patient-years; adjusted hazard ratio (HR) 1.00, 95% confidence interval (CI), 0.75-1.33,P = 0.993) and clopidogrel-treated rapid or ultrarapid metabolizers (19.1 events/100 patient-years; adjusted HR 0.95, 95% CI, 0.69-1.30,P = 0.734) exhibited no difference in major atherothrombotic events compared with patients treated with prasugrel or ticagrelor (17.6 events/100 patient-years). In contrast, clopidogrel-treated intermediate and poor metabolizers exhibited significantly higher atherothrombotic event risk compared with prasugrel/ticagrelor-treated patients (adjusted HR 1.56, 95% CI, 1.12-2.16,P = 0.008). When comparing clopidogrel-treated rapid or ultrarapid metabolizers to normal metabolizers, no difference in atherothrombotic (adjusted HR 0.97, 95% CI, 0.73-1.29,P = 0.808) or bleeding events (adjusted HR 1.34, 95% CI, 0.83-2.17,P = 0.224) were observed. In a real-world setting of genotype-guided antiplatelet therapy, theCYP2C19*17allele did not significantly impact post-PCI prescribing decisions or clinical outcomes. These results suggest theCYP2C19 *1/*17and*17/*17genotypes have limited clinical utility to guide antiplatelet therapy after PCI.
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