Key result
Genetic variation in CYP2C19 activity substantially influences short- and long-term antithrombotic effects of clopidogrel.
CYP2C19 genetic polymorphisms significantly influence the antiplatelet response to clopidogrel, highlighting the potential need for prediction models incorporating genotyping to individualize antithrombotic therapy.
May support CYP2C19 genotyping to guide clopidogrel therapy; leaves open prospective trials before practice change.
Increasing evidence for the role of pharmacogenetics in treatment resistance to the antiplatelet agent clopidogrel has been gained during the last years. Apart from CYP2C19 genetic polymorphisms, nongenetic factors, particularly drug-drug interactions, age and other clinical characteristics influence the interindividual variability in clopidogrel response to varying degrees. The present article reviews the so far accumulated evidence on the role of pharmacogenetic traits influencing CYP-activity as determinants of the antiplatelet response to clopidogrel, and its clinical implications. The genetic variation in CYP2C19 activity seems to influence short- and long-term antithrombotic effects of clopidogrel to a substantial extent. Prediction models for clopidogrel non-responsiveness that include CYP2C19 genotyping together with relevant non-genetic risk factors are needed to be verified for their potential benefit in individualization of antithrombotic therapy.
No takes yet. Share an insight, caveat, or question.
Dahl et al. (2010) conducted a review in Clopidogrel treatment resistance. CYP2C19 genetic polymorphisms was evaluated. Genetic variation in CYP2C19 activity substantially influences short- and long-term antithrombotic effects of clopidogrel.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: