TY - JOUR
T1 - Effect of Smoking on Outcomes of Primary PCI in Patients With STEMI
AU - Redfors, Björn
AU - Furer, Ariel
AU - Selker, Harry P.
AU - Thiele, Holger
AU - Patel, Manesh R.
AU - Chen, Shmuel
AU - Udelson, James E.
AU - Ohman, E. Magnus
AU - Eitel, Ingo
AU - Granger, Christopher B.
AU - Maehara, Akiko
AU - Kirtane, Ajay J.
AU - Généreux, Philippe
AU - Jenkins, Paul L.
AU - Ben-Yehuda, Ori
AU - Stone, Gregg W.
N1 - Funding Information:
Dr. Patel has received grants from Bayer, Janssen, HeartFlow, and the National Heart, Lung, and Blood Institute; and has served as an advisor/consultant for AstraZeneca, Bayer, Janssen, and HeartFlow. Dr. Udelson has served on a trial steering committee for Abiomed; and has served as a consultant for Imbria Pharmaceuticals. Dr. Ohman has received research grants from Abiomed, Chiesi, and Portola; and has served as a consultant for Abiomed, Cara Therapeutics, Genentech, Imbria Pharmaceuticals, Impulse Dynamics, Janssen Pharmaceuticals, Medtronic, Medscape, Milestone Pharmaceuticals, and XyloCor Therapeutics. Dr. Granger has received research grants from AstraZeneca, the U.S. Food and Drug Administration, National Institutes of Health, GlaxoSmithKline, Medtronic, Novartis, Apple, Boehringer Ingelheim, Bristol-Myers Squibb/Pfizer, and Janssen; has served as a consultant for AstraZeneca, Espero, GlaxoSmithKline, Medtronic, Novartis, Boehringer Ingelheim, Boston Scientific, Bristol-Myers Squibb/Pfizer, Daiichi-Sankyo, Merck, Roche, Eli Lilly, The Medicines Company, and Janssen. Dr. Maehara has received grant support from and served as a consultant for Abbott Vascular and Boston Scientific; and has served as a consultant for Conavi Medical Inc. Dr. Kirtane has received institutional funding to Columbia University and/or Cardiovascular Research Foundation from Medtronic, Boston Scientific, Abbott Vascular, Abiomed, CSI, CathWorks, Siemens, Philips, and ReCor Medical. Dr, G?n?reux has received speaker fees from Abbott Vascular, Edwards Lifesciences, Medtronic, Tryton Medical Inc., Cardinal Health, and Cardiovascular Systems Inc.; has received consulting fees from Abbott Vascular, Boston Scientific, Cardiovascular Systems Inc., and Pi-Cardia; has received an institutional research grant from Boston Scientific; and has equity in SIG.NUM, SoundBite Medical Solutions Inc., Saranas, and Pi-Cardia. Dr. Stone has served as a consultant to Miracor, TherOx, and Abiomed. All other authors have reported that they have no relationships relevant to the contents of this paper. Harvey D. White, DSC, FACC, served as Guest Associate Editor for this paper.
Publisher Copyright:
© 2020 American College of Cardiology Foundation
Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 2020/4/21
Y1 - 2020/4/21
N2 - Background: 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. Objectives: The purpose of this study was to determine the relationship among smoking, infarct size, microvascular obstruction (MVO), and adverse outcomes after STEMI. Methods: 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. Results: 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 < 0.001) and death or HF hospitalization (3.3% vs. 5.1%; p = 0.009) with similar rates of reinfarction. After adjustment for age and other risk factors, smokers had a similar 1-year risk of death (adjusted hazard ratio [adjHR]: 0.92; 95% CI: 0.46 to 1.84) and higher risks of death or HF hospitalization (adjHR: 1.49; 95% CI: 1.09 to 2.02) as well as reinfarction (adjHR: 1.97; 95% CI: 1.17 to 3.33). Conclusions: In the present large-scale individual patient-data pooled analysis, recent smoking was unrelated to infarct size or MVO, but was associated with a worse prognosis after primary PCI in STEMI. The smoker's paradox may be explained by the younger age and fewer cardiovascular risk factors in smokers compared with nonsmokers.
AB - Background: 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. Objectives: The purpose of this study was to determine the relationship among smoking, infarct size, microvascular obstruction (MVO), and adverse outcomes after STEMI. Methods: 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. Results: 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 < 0.001) and death or HF hospitalization (3.3% vs. 5.1%; p = 0.009) with similar rates of reinfarction. After adjustment for age and other risk factors, smokers had a similar 1-year risk of death (adjusted hazard ratio [adjHR]: 0.92; 95% CI: 0.46 to 1.84) and higher risks of death or HF hospitalization (adjHR: 1.49; 95% CI: 1.09 to 2.02) as well as reinfarction (adjHR: 1.97; 95% CI: 1.17 to 3.33). Conclusions: In the present large-scale individual patient-data pooled analysis, recent smoking was unrelated to infarct size or MVO, but was associated with a worse prognosis after primary PCI in STEMI. The smoker's paradox may be explained by the younger age and fewer cardiovascular risk factors in smokers compared with nonsmokers.
UR - http://www.scopus.com/inward/record.url?scp=85082840441&partnerID=8YFLogxK
UR - https://www.mendeley.com/catalogue/77c763c3-a620-3884-99ba-eb21c3263141/
U2 - 10.1016/j.jacc.2020.02.045
DO - 10.1016/j.jacc.2020.02.045
M3 - Journal articles
C2 - 32299585
AN - SCOPUS:85082840441
SN - 0735-1097
VL - 75
SP - 1743
EP - 1754
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 15
ER -