Current but not past smoking increases the risk of cardiac events: Insights from coronary computed tomographic angiography

Rine Nakanishi; Daniel S. Berman; Matthew J. Budoff; Heidi Gransar; Stephan Achenbach; Mouaz Al-Mallah; Daniele Andreini; Filippo Cademartiri; Tracy Q. Callister; Hyuk Jae Chang; Victor Y. Cheng; Kavitha Chinnaiyan; Benjamin J.W. Chow; Ricardo Cury; Augustin Delago; Martin Hadamitzky; Jörg Hausleiter; Gudrun Feuchtner; Yong Jin Kim; Philipp A. Kaufmann; Jonathon Leipsic; Fay Y. Lin; Erica Maffei; Gianluca Pontone; Gilbert Raff; Leslee J. Shaw; Todd C. Villines; Allison Dunning; James K. Min

doi:10.1093/eurheartj/ehv013

Current but not past smoking increases the risk of cardiac events: Insights from coronary computed tomographic angiography

Rine Nakanishi, Daniel S. Berman, Matthew J. Budoff, Heidi Gransar, Stephan Achenbach, Mouaz Al-Mallah, Daniele Andreini, Filippo Cademartiri, Tracy Q. Callister, Hyuk Jae Chang, Victor Y. Cheng, Kavitha Chinnaiyan, Benjamin J.W. Chow, Ricardo Cury, Augustin Delago, Martin Hadamitzky, Jörg Hausleiter, Gudrun Feuchtner, Yong Jin Kim, Philipp A. KaufmannJonathon Leipsic, Fay Y. Lin, Erica Maffei, Gianluca Pontone, Gilbert Raff, Leslee J. Shaw, Todd C. Villines, Allison Dunning, James K. Min

Department of Internal Medicine

Research output: Contribution to journal › Article › peer-review

32 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	1031-1040
Number of pages	10
Journal	European heart journal
Volume	36
Issue number	17
DOIs	https://doi.org/10.1093/eurheartj/ehv013
Publication status	Published - 2015 May 1

Bibliographical note

Funding 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.

Funding Information:
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.

Publisher Copyright:
© 2015 Published on behalf of the European Society of Cardiology.

All Science Journal Classification (ASJC) codes

Cardiology and Cardiovascular Medicine

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10.1093/eurheartj/ehv013

Cite this

Nakanishi, R., Berman, D. S., Budoff, M. J., Gransar, H., Achenbach, S., Al-Mallah, M., Andreini, D., Cademartiri, F., Callister, T. Q., Chang, H. J., Cheng, V. Y., Chinnaiyan, K., Chow, B. J. W., Cury, R., Delago, A., Hadamitzky, M., Hausleiter, J., Feuchtner, G., Kim, Y. J., ... Min, J. K. (2015). Current but not past smoking increases the risk of cardiac events: Insights from coronary computed tomographic angiography. European heart journal, 36(17), 1031-1040. https://doi.org/10.1093/eurheartj/ehv013

@article{ab0940047f8141e29afffdf4de39e145,

title = "Current but not past smoking increases the risk of cardiac events: Insights from coronary computed tomographic angiography",

abstract = "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.",

author = "Rine Nakanishi and Berman, {Daniel S.} and Budoff, {Matthew J.} and Heidi Gransar and Stephan Achenbach and Mouaz Al-Mallah and Daniele Andreini and Filippo Cademartiri and Callister, {Tracy Q.} and Chang, {Hyuk Jae} and Cheng, {Victor Y.} and Kavitha Chinnaiyan and Chow, {Benjamin J.W.} and Ricardo Cury and Augustin Delago and Martin Hadamitzky and J{\"o}rg Hausleiter and Gudrun Feuchtner and Kim, {Yong Jin} and Kaufmann, {Philipp A.} and Jonathon Leipsic and Lin, {Fay Y.} and Erica Maffei and Gianluca Pontone and Gilbert Raff and Shaw, {Leslee J.} and Villines, {Todd C.} and Allison Dunning and Min, {James K.}",

note = "Funding 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{\textquoteright} 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{\textquoteright} 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{\textquoteright} 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. Funding Information: 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. Publisher Copyright: {\textcopyright} 2015 Published on behalf of the European Society of Cardiology.",

year = "2015",

month = may,

day = "1",

doi = "10.1093/eurheartj/ehv013",

language = "English",

volume = "36",

pages = "1031--1040",

journal = "European heart journal",

issn = "0195-668X",

publisher = "Oxford University Press",

number = "17",

}

Nakanishi, R, Berman, DS, Budoff, MJ, Gransar, H, Achenbach, S, Al-Mallah, M, Andreini, D, Cademartiri, F, Callister, TQ, Chang, HJ, Cheng, VY, Chinnaiyan, K, Chow, BJW, Cury, R, Delago, A, Hadamitzky, M, Hausleiter, J, Feuchtner, G, Kim, YJ, Kaufmann, PA, Leipsic, J, Lin, FY, Maffei, E, Pontone, G, Raff, G, Shaw, LJ, Villines, TC, Dunning, A & Min, JK 2015, 'Current but not past smoking increases the risk of cardiac events: Insights from coronary computed tomographic angiography', European heart journal, vol. 36, no. 17, pp. 1031-1040. https://doi.org/10.1093/eurheartj/ehv013

TY - JOUR

T1 - Current but not past smoking increases the risk of cardiac events

T2 - Insights from coronary computed tomographic angiography

AU - Nakanishi, Rine

AU - Berman, Daniel S.

AU - Budoff, Matthew J.

AU - Gransar, Heidi

AU - Achenbach, Stephan

AU - Al-Mallah, Mouaz

AU - Andreini, Daniele

AU - Cademartiri, Filippo

AU - Callister, Tracy Q.

AU - Chang, Hyuk Jae

AU - Cheng, Victor Y.

AU - Chinnaiyan, Kavitha

AU - Chow, Benjamin J.W.

AU - Cury, Ricardo

AU - Delago, Augustin

AU - Hadamitzky, Martin

AU - Hausleiter, Jörg

AU - Feuchtner, Gudrun

AU - Kim, Yong Jin

AU - Kaufmann, Philipp A.

AU - Leipsic, Jonathon

AU - Lin, Fay Y.

AU - Maffei, Erica

AU - Pontone, Gianluca

AU - Raff, Gilbert

AU - Shaw, Leslee J.

AU - Villines, Todd C.

AU - Dunning, Allison

AU - Min, James K.

N1 - Funding 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. Funding Information: 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. Publisher Copyright: © 2015 Published on behalf of the European Society of Cardiology.

PY - 2015/5/1

Y1 - 2015/5/1

N2 - 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.

AB - 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.

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JF - European heart journal

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ER -

Current but not past smoking increases the risk of cardiac events: Insights from coronary computed tomographic angiography

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