Many antiplatelet therapies are prodrugs that require metabolic activation.\u00a0 It has been hypothesized that smoking may activate this metabolic conversion for some antiplatelets (i.e. clopidogrel) more than others (i.e. prasugrel and ticagrelor).\u00a0 In this systematic review and meta-analysis, the authors identified 9 randomized controlled trials of clopidogrel, prasugrel, or ticagrelor which examined outcomes among subgroups of smokers and non-smokers.\u00a0 In the studies of clopidogrel, smokers on clopidogrel saw a 25% reduction in the primary composite outcome of cardiovascular death, MI, and stroke compared with patients in the control group (RR 0.75, 95% CI 0.67 \u2013 0.83).\u00a0 However, in non-smokers there was only an 8% reduction in the primary end point (RR 0.92, 95% CI 0.87 \u2013 0.98).\u00a0 Similarly, greater risk reduction was observed for smokers on ticagrelor or prasugrel when compared to clopidogrel while risk reduction was similar for all three drugs in non-smokers.<\/p>\n
Conclusion: <\/strong><\/p>\n It is unclear if the relative effect of antiplatelet therapies in smokers simply reflects differences in baseline clinical risk or differences in the metabolic activation of antiplatelet drugs.\u00a0 Study of antiplatelet therapies stratified by patient cardiovascular disease risk may provide further insight.<\/p>\n