Tailored Thienopyridine therapy: no urgency for CYP2C19 genotyping.

Between 20% and 50% of cardiovascular patients treated with clopidogrel,an anti-p2y12 drug,display high on-treatment platelet reactivity (htpr) and are not adequately protected from major adverse cardiovascular events (mace). despite a minor influence of the cyp2c19*2 genetic variant on the pharmacodynamic response to clopidogrel (5% to 12%) and a limited or absent value for predicting stent thrombosis and mace,this latter polymorphism is currently considered an important candidate to tailor anti-p2y12 therapy during percutaneous coronary intervention. seven studies have examined the value of cyp2c19*2 for predicting htpr in comparison to a specific pharmacodynamic assay (vasp assay). overall,the summarized sensitivity of the cyp2c19*2 genotype for predicting htpr was 37.6% (95% ci: 32.2 to 43.3%),yielding a negative likelihood ratio of only 0.77 (95% ci: 0.68 to 0.86) which confirms its limited value as a routine clinical aid. a tailored anti-p2y12 treatment strategy restricted to cyp2c19*2 carriers may be of some help,but this restrictive approach leaves out noncarriers with htpr. as for platelet function testing,there is currently no convincing data to support that using cyp2c19*2 genotyping as a tailored anti-p2y12 treatment would be an effective strategy and there is no urgency for cyp2c19 genotyping in clinical practice. strategies incorporating genotyping,phenotyping,and clinical data in a stratified and sequential approach may be more promising.