Key result
Smoking was not associated with improved myocardial salvage or a lower risk of MACE at 12 months after adjusting for baseline risk factors (HR 0.71; 95% CI 0.36-1.38; P=0.31).
Why the study?
Does smoking improve myocardial salvage, reduce myocardial damage, or improve clinical outcomes in STEMI patients undergoing PPCI?
Population
727 consecutive patients with ST-elevation myocardial infarction reperfused within 12 hours after symptom…
Comparison
Current smoking (admission smoking status) vs Non-smoking
Design
Cohort
Follow-up
12 months
Authors
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No association after adjustment cautions against invoking the smoker's paradox in STEMI; leaves open residual confounding in observational data.
Cohort (n=727)
Yes
Does smoking improve myocardial salvage, reduce myocardial damage, or improve clinical outcomes in STEMI patients undergoing PPCI?
Hazard Ratio: 0.71 (95% CI 0.36–1.38)
Absolute Event Rate: 3.8% vs 8.2%
p-value: p=0.31
Smoking is not associated with improved myocardial salvage or reduced irreversible damage in STEMI patients undergoing PPCI, and the apparent 'smoker's paradox' for clinical outcomes is explained by baseline risk differences.
Reinstadler et al. (2016) conducted a cohort in ST-elevation myocardial infarction (STEMI) (n=727). Smoking vs. Non-smokers was evaluated on Major adverse cardiac event (MACE) at 12 months (HR 0.71, 95% CI 0.36-1.38, p=0.31). Smoking was not associated with improved myocardial salvage or a lower risk of MACE at 12 months after adjusting for baseline risk factors (HR 0.71; 95% CI 0.36-1.38; P=0.31).
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