Key result
Smoking was an independent predictor of the composite endpoint of death, MI, or stroke (HR 1.8; 95% CI 1.3-2.5; P=0.001) in patients with complex CAD undergoing revascularization.
Why the study?
Some studies have suggested a smoker's paradox of neutral or favorable outcomes in smokers who developed CAD, especially MI.
Population
Patients with complex CAD undergoing revascularization with PCI or CABG in the SYNTAX trial
Comparison
Clinical outcomes compared according to smoking status
Design
Randomized controlled trial subanalysis
Follow-up
5-year follow-up
Authors
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Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“are sobering and emphasize that our efforts at smoking cessation for our patients with the most severe CAD need to be continuous, not myopically targeted only to the time of initial revascularization.”
“Abstinence from smoking may improve the outcomes achieved with coronary revascularization, and all patients undergoing PCI or CABG should be encouraged to stop smoking indefinitely before revascularization.”
“There is no question that there is a pharmacodynamic interaction of smoking with clopidogrel metabolism. Smoking enhances active metabolite generation and the resultant [pharmacodynamic] effect.”
Smoking was associated with worse post-revascularization outcomes; hypothesis-generating and requires RCTs before guiding cessation practice.
RCT
Hazard Ratio: 1.8 (95% CI 1.3–2.5)
p-value: p=0.001
Zhang et al. (2015) conducted an RCT in complex coronary artery disease (CAD). Smoking vs. Non-smoking was evaluated on composite endpoint of death/MI/stroke (HR 1.8, 95% CI 1.3-2.5, p=0.001). Smoking was an independent predictor of the composite endpoint of death, MI, or stroke (HR 1.8; 95% CI 1.3-2.5; P=0.001) in patients with complex CAD undergoing revascularization.
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