Cigarette Smoking Is Associated With a Dose-Response Effect in Clopidogrel-Treated Patients With Diabetes Mellitus and Coronary Artery Disease

Abstract

Cigarette smoking is associated with a dose-response effect on clopidogrel-induced antiplatelet effects and lower rates of HPR in diabetes mellitus patients.

Mechanisms of Coronary Thrombosis in Cigarette Smoke Exposure

“…54,55 Smokers also have higher P 2 Y 12 expression in platelet lysates than nonsmokers. 56 Platelet activation and recruitment are partly regulated by products of the endothelium, including PGI 2 and NO.…”

Effect of Smoking Status on Clinical Outcome and Efficacy of Clopidogrel in Acute Coronary Syndrome

“…26 The present analysis demonstrated a reduced benefit from clopidogrel therapy in non-smokers, in agreement with the Desai et al and Ueno et al studies. 11, 27 The present results indicate that cigarette smoking modifies the beneficial effect of clopidogrel on clinical outcome. Clopidogrel, a PCI, thus excluding patients who were not eligible for coronary revascularization.…”

The impact of smoking on clinical efficacy and pharmacodynamic effects of clopidogrel: a systematic review and meta-analysis

“…The percentage of current smokers varied more apparently from 10% to 70%. Conventional light transmittance aggregometry (LTA) is endorsed as a better standard for OPR measurement and has been the most widely adopted method, as is the case in our review that nine studies (69.2%) implemented it 19 20 36 37 40 41 43–45. For the two studies using both LTA and the VerifyNow P2Y 12 assay,20 36 only the results by LTA were pooled to avoid duplicate summation.…”

“…In 8 (n=3260) of the 13 laboratory studies (n=6761), current smoking was associated with significantly enhanced pharmacodynamic effects of clopidogrel 19 20 35–39 44. The other five independent studies (n=3501) from two articles observed no significant interaction between smoking and OPR 21 45.…”

“…Although with low intensity of argumentation, the meta-analysis of cross-sectional studies is potentially capable of unmasking the underlying correlation. All studies were based on self-reported smoking status and intensity except one which relied on an objective approach of serum cotinine measurement 20. In six studies (46.2%), former smokers were not excluded or analysed separately, which could greatly affect the results 21 37 40–42 44.…”