Key result
Current smokers treated with ADP-P2Y12 receptor inhibitors had significantly lower residual platelet reactivity compared to nonsmokers (MD -25.70; 95% CI -38.81 to -12.60; p=0.0001).
Why the study?
The influence of smoking on platelet ADP-P2Y12 receptor inhibitors lacked consistency across existing original studies.
Does smoking improve platelet inhibition in patients with acute coronary syndrome and/or stent deployment treated with ADP-P2Y12 receptor inhibitors?
Population
16 296 patients with ACS and/or stent deployment across 12 studies
Comparison
Current smokers vs nonsmokers
Design
Systematic review and meta-analysis
Authors
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Smoking may enhance P2Y12 inhibitor response; reinforces the smoker's paradox and supports smoking-stratified analyses in future trials.
Meta-Analysis (n=16,296)
Does smoking improve platelet inhibition in patients with acute coronary syndrome and/or stent deployment treated with ADP-P2Y12 receptor inhibitors?
Mean Difference: -25.7 (95% CI -38.81–-12.6)
p-value: p=0.0001
Current smokers exhibit significantly lower residual platelet reactivity in response to clopidogrel compared to nonsmokers, which may help explain the differential clinical outcomes observed in large-scale trials.
Liu et al. (2019) conducted a meta-analysis in Acute coronary syndrome and/or stent deployment (n=16,296). Cigarette smoking vs. Nonsmokers was evaluated on P2Y12 reaction unit (PRU) value measured by VerifyNow P2Y12 assay (MD -25.70, 95% CI -38.81 to -12.60, p=0.0001). Current smokers treated with ADP-P2Y12 receptor inhibitors had significantly lower residual platelet reactivity compared to nonsmokers (MD -25.70; 95% CI -38.81 to -12.60; p=0.0001).