Aims We evaluated coronary artery disease (CAD) extent, severity, and major adverse cardiac events (MACEs) in never, past, and current smokers undergoing coronary CT angiography (CCTA). Methods and results We evaluated 9456 patients (57.1 ± 12.3 years, 55.5% male) without known CAD (1588 current smokers; 2183 past smokers who quit ≥ 3 months before CCTA; and 5685 never smokers). By risk-adjusted Cox proportional-hazards models, we related smoking status to MACE (all-cause death or non-fatal myocardial infarction). We further performed 1:1:1 propensity matching for 1000 in each group evaluate event risk among individuals with similar age, gender, CAD risk factors, and symptom presentation. During a mean follow-up of 2.8 ± 1.9 years, 297 MACE occurred. Compared with never smokers, current and past smokers had greater atherosclerotic burden including extent of plaque defined as segments with any plaque (2.1 ± 2.8 vs. 2.6 ± 3.2 vs. 3.1 ± 3.3, P < 0.0001) and prevalence of obstructive CAD [1-vessel disease (VD): 10.6% vs. 14.9% vs. 15.2%, P < 0.001; 2-VD: 4.4% vs. 6.1% vs. 6.2%, P = 0.001; 3-VD: 3.1% vs. 5.2% vs. 4.3%, P < 0.001]. Compared with never smokers, current smokers experienced higher MACE risk [hazard ratio (HR) 1.9, 95% confidence interval (CI) 1.4-2.6, P < 0.001], while past smokers did not (HR 1.2, 95% CI 0.8-1.6, P = 0.35). Among matched individuals, current smokers had higher MACE risk (HR 2.6, 95% CI 1.6-4.2, P < 0.001), while past smokers did not (HR 1.3, 95% CI 0.7-2.4, P = 0.39). Similar findings were observed for risk of all-cause death. Conclusion Among patients without known CAD undergoing CCTA, current and past smokers had increased burden of atherosclerosis compared with never smokers; however, risk of MACE was heightened only in current smokers.
Bibliographical noteFunding Information:
Conflict of interest: S.A. received support from Siemens and Bayer Schering Pharma and has consulted for Servier. D.A. has served on the Speakers’ Bureau of GE Healthcare. M.J.B. has consulted for GE Healthcare. F.C. received grant support from GE Healthcare and has served on the Speakers’ Bureau of Bracco, and has consulted for Servier. K.C. received grant support from Bayer Pharma. B.J.W.C. received research and fellowship support from GE Healthcare, research support from Servier, and educational support from TeraRecon. R.C. has served as a consultant for Astellas Pharma, GE Healthcare, and Novartis. J.H. received a research grant from Siemens Medical Systems. P.A.K. received research support from GE Healthcare. J.L. received research support from GE Healthcare and speakers’ bureau. G.P. received grant support from GE Healthcare and Heartflow. G.R. received grant support from Siemens and Bayer Pharma. A.D. was partially supported by Clinical Translational Science Center (grant UL1-RR024996). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
ResearchreportedinthispublicationwassupportedbytheHeartLungand Blood Institute of the National Institutes of Health (1R01HL115150). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. This research was supported by Leading Foreign Research Institute Recruitment Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future Planning (MSIP) (2012027176). This study was also funded, in part, by a generous gift from the Dalio Institute of Cardiovascular Imaging and the Michael Wolk Foundation.
© 2015 Published on behalf of the European Society of Cardiology.
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine