Perspective:

This study suggests that smoking cessation resulted in reversal of the enhanced response to clopidogrel in smokers. At baseline, current smokers had significantly lower OPR compared with never smokers. Among those who were actively smoking at baseline, those who stopped smoking thereafter (quitters) showed an increase in OPR, in contrast to persistent smokers whose OPR did not change significantly at follow-up. Furthermore, there was a linear relationship between the amount of cigarette smoking and the antiplatelet effect of clopidogrel. The data should not be construed to mean that smoking improves the effectiveness of antiplatelet therapy. The slight increase in platelet inhibition has not been associated with improved outcomes, and is unlikely to offset the greatly increased risk of a thrombotic event from smoking. Further investigation is warranted to elucidate the true clinical implications of this phenomenon, but for now, smoking should be strongly discouraged.