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Effect of Smoking on Outcomes of Primary PCI in Patients With STEMI

Smoking is a well-established risk factor for ST-segment elevation myocardial infarction (STEMI); however, once STEMI occurs, smoking has been associated with favorable short-term outcomes, an observation termed the “smoker’s paradox.” It has been postulated that smoking might exert protective effec...

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Bibliographic Details
Published in:Journal of the American College of Cardiology 2020-04, Vol.75 (15), p.1743-1754
Main Authors: Redfors, Björn, Furer, Ariel, Selker, Harry P., Thiele, Holger, Patel, Manesh R., Chen, Shmuel, Udelson, James E., Ohman, E. Magnus, Eitel, Ingo, Granger, Christopher B., Maehara, Akiko, Kirtane, Ajay J., Généreux, Philippe, Jenkins, Paul L., Ben-Yehuda, Ori, Stone, Gregg W.
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Language:English
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Summary:Smoking is a well-established risk factor for ST-segment elevation myocardial infarction (STEMI); however, once STEMI occurs, smoking has been associated with favorable short-term outcomes, an observation termed the “smoker’s paradox.” It has been postulated that smoking might exert protective effects that could reduce infarct size, a strong independent predictor of worse outcomes after STEMI. The purpose of this study was to determine the relationship among smoking, infarct size, microvascular obstruction (MVO), and adverse outcomes after STEMI. Individual patient-data were pooled from 10 randomized trials of patients with STEMI undergoing primary percutaneous coronary intervention. Infarct size was assessed at median 4 days by either cardiac magnetic resonance imaging or technetium-99m sestamibi single-photon emission computed tomography. Multivariable analysis was used to assess the relationship between smoking, infarct size, and the 1-year rates of death or heart failure (HF) hospitalization and reinfarction. Among 2,564 patients with STEMI, 1,093 (42.6%) were recent smokers. Smokers were 10 years younger and had fewer comorbidities. Infarct size was similar in smokers and nonsmokers (adjusted difference: 0.0%; 95% confidence interval [CI]: −3.3% to 3.3%; p = 0.99). Nor was the extent of MVO different between smokers and nonsmokers. Smokers had lower crude 1-year rates of all-cause death (1.0% vs. 2.9%; p 
ISSN:0735-1097
1558-3597
1558-3597
DOI:10.1016/j.jacc.2020.02.045