Background: Clopidogrel’s ability to inhibit platelet function determined its clinical usefulness. The
role of CYP2C19*2 genotype on antiplatelet treatment is recently under question. Arterial wall properties and inflammation
are key players in atherosclerosis development. Hence, we evaluated the impact of CYP2C19*2 genetic
polymorphism on endothelial function, arterial stiffness and inflammation in coronary artery disease (CAD)
patients receiving clopidogrel treatment.
Methods and Results: In this study we enrolled 408 consecutive patients with stable CAD under dual antiplatelet
therapy (clopidogrel 75mg/day, aspirin 100mg/day), 30 days after percutaneous coronary intervention. Measurement of flow-mediated
dilation (FMD) of the brachial artery was used to evaluate endothelial function. Carotid-femoral pulse wave velocity (PWV) and augmentation
index (AIx) was measured to estimate arterial stiffness. Real time polymerase chain reaction was used for the genotyping of
CYP2C19*2. Levels of tumor necrosis factor alpha (TNF-a) and interleukin 6 (IL-6) were measured with ELISA. We found no difference
in basic clinical and demographic characteristics nor in FMD, PWV, AIx and inflammatory status (p=NS for all) between CYP2C19
homozygotes for the wild type; carriers of reduced function allele and homozygotes for the reduced function allele.
Conclusion: CYP2C19*2 loss of action polymorphism causes no impact on vascular function and inflammatory status in stable CAD patients
receiving clopidogrel treatment.