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Cigarette smoking induces CYP1A2 and may, therefore, enhance the conversion of clopidogrel to its active metabolite. Until now, there were no reports of clopidogrel response to smoking status according to urine nicotine level.
We consecutively enrolled 100 patients treated with coronary stenting and administered 75mg clopidogrel as maintenance dose. All patients were allocated into current smokers (CS, n=50) and nonsmokers(NS, n=50) based on the questionnaire and results of nicotine urine stick test (NickCheckTM, Mossman associates, Blackstone, MA, USA). Platelet aggregation was assessed by the VerifyNow P2Y12 assay (accumetrics Inc., San Diego, California).
There was no significant difference of platelet reactivation unit (PRU) and platelet inhibition% (PI %) according to smoking status (CS vs NS; 48 ± 10 vs 59 ± 11 of PRU, 36 ± 23 vs 38 ± 20 of PI%, respectively, p>0.05). An analysis of variance demonstrated no significant differences of PRU and PI % in 3 groups (A group: urine nicotine level 0 vs B group:1 to 6 level vs C group: > 6 level; 180 ± 70 vs 192 ± 76 vs 182 ± 73 of PRU; 38 ± 20 vs 34 ± 21 vs 39 ± 24 of PI%, respectively, p>0.05). When 239 of PRU was regarded as the cut-off value of high post-treatment platelet reactivity (HPPR) - the predictive factor of future cardiovascular events, Old age (OR 17, p<0.001), the presence of peripheral vascular disease(OR 6, p=0.017), daily number of smoking cigarettes(OR 8.2, p=0.004) and smoking duration(OR 8.2, p= 0.004) were predictors of high platelet aggregation in univariate logistic regression analysis. But, in multivariate logistic regression analysis, there were not predictors of HPPR.
Nicotine level in urine and smoking status are not associated with platelet aggregation on the contrary to previous studies. Measurement of nicotine or its metabolites might be needed for the future studies of evaluating the relationship objectively between smoking and clopidogrel response.