TUESDAY, May 25 (HealthDay News) -- While antiplatelet drug response is clearly linked to the CYP2C19*2 polymorphism, the gene's presence does not explain most instances of poor antiplatelet response, even with other clinical factors taken into account, according to research published in the June 1 issue of the Journal of the American College of Cardiology.
Willibald Hochholzer, M.D., of the Herz-Zentrum Bad Krozingen in Germany, and colleagues studied 760 patients undergoing coronary stent placement following clopidogrel loading doses. The researchers used optical aggregometry to determine residual platelet aggregation prior to discharge, and regression analysis to assess the predictive value of the existence of the CYP2C19*2 polymorphism and baseline clinical variables for insufficient antiplatelet response to clopidogrel.
The researchers found that CYP2C19*2 carrier status was an independent predictor for insufficient antiplatelet response to clopidogrel (odds ratio [OR], 2.74). Other predictors for insufficient response were diabetes mellitus (OR, 1.75), body mass index (OR, 1.06), and age (OR, 1.03). However, the regression model including all these variables could only explain 11.5 percent of the antiplatelet response, with the CYP2C19*2 carrier status explaining only 5.2 percent.
"Our current data, despite confirming the strong impact of the CYP2C19 loss-of-function polymorphism on antiplatelet effect of clopidogrel, suggest that genotyping for CYP2C19 is insufficient for clinical decision-making without platelet function testing. Addition of clinical variables could not fully correct this shortcoming. Thus, our study does not suggest that, in patients critically dependent on adequate platelet inhibition, genotyping alone or in combination with clinical factors can replace phenotyping of platelet function," the authors write.
Abstract
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