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).
Cohort (n=727)
Yes
Does smoking improve myocardial salvage, reduce myocardial damage, or improve clinical outcomes in STEMI patients undergoing PPCI?
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.
Hazard Ratio: 0.71 (95% CI 0.36–1.38)
Absolute Event Rate: 3.8% vs 8.2%
p-value: p=0.31
AIMS: There is evidence suggesting a positive effect of cigarette smoking on myocardial tissue reperfusion and clinical outcomes in patients with myocardial infarction ('smoker's paradox'). We aimed to evaluate the relationship of smoking with cardiac magnetic resonance (CMR)-determined myocardial salvage and damage as well as clinical outcomes in patients undergoing primary percutaneous coronary intervention (PPCI) for ST-elevation myocardial infarction (STEMI). METHODS AND RESULTS: This multicentre study included 727 consecutive STEMI patients reperfused within 12 h after symptom onset. CMR imaging parameters area at risk (AAR), infarct size (IS), myocardial salvage index (MSI), and microvascular obstruction (MVO) and intramyocardial haemorrhage (IMH) were compared according to admission smoking status. Major adverse cardiac event (MACE) rates at 12 months after infarction were compared between groups. Three hundred and thirty-nine (46.6%) patients were current smokers. There was no difference in the extent of AAR 35 (24-47) vs. 37 (27-49) % of left ventricular volume (LV), P = 0.10, IS 16 (8-25) vs. 17 (10-26) %LV, P = 0.21, MSI 53 (29-70) vs. 52 (34-71), P = 0.47, MVO 0 (0-1.7) vs. 0 (0-1.6) %LV, P = 0.91, or in the frequency of IMH (42 vs. 39%, P = 0.58) between smokers and non-smokers. Smokers had lower MACE (3.8 vs. 8.2%, P = 0.01) rates. However, adjustment for differences in baseline risk factors attenuated the association of smoking with MACE markedly (hazard ratio = 0.71, 95% confidence interval 0.36-1.38, P = 0.31). CONCLUSION: Smoking is not associated with PPCI efficacy (myocardial salvage) or irreversible myocardial damage in patients with STEMI. The lower MACE rate of smokers was entirely explained by differences in baseline risk characteristics, thus challenging the existence of a smoker's paradox.
Reinstadler et al. (Sun,) 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).