Over the past several years, it has become evident that not all patients respond optimally to standard dosing of the antiplatelet medication clopidogrel. With the aid of pharmacogenetics research, polymorphisms in the CYP2C19 gene (*2, *3, *4, *5,*6, *7, *8) have been linked with the poor conversion of clopidogrel to its active metabolite and reduced clopidogrel efficacy. Poor response to clopidogrel therapy as evidenced by high platelet reactivity, particularly after stent implantation, has been linked with an increase in major adverse cardiac events. Intermediate and poor metabolism of clopidogrel can potentially be overcome with additional loading doses and higher maintenance doses, or switching to alternative antiplatelet medications. We suggest that the use of genotyping for guiding patient-specific pharmacotherapy is more useful and practical for clopidogrel than for warfarin but interpretation of the testing results can be difficult. To this end, a model for interpretation of pharmacogenetic testing results is proposed. Additionally, point-of-care testing, such as a P2Y12 inhibition assay, can reveal the percentage of platelet inhibition following clopidogrel dosing and is a tool that can be used to achieve optimal clopidogrel dosing.
Keywords: Antiplatelet, clopidogrel, CYP2C19, diagnostics, genetic testing, personalized medicine, pharmacogenetics, polymorphisms, pharmacotherapy, P2Y12 inhibition assay, polymorphism, bioactivation, pharmacogenetic assay, international normalized ratio (INR), myocardial infarction, warfarin, prasugrel, ticagrelor, regimen, Food and Drug Administration, International Normalized Ratio, Non steroidal anti-inflammatory drug, Transient ischemic attack
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