Cigarette Smoking and Cardiovascular Events: Role of Inflammation and Infclinical Atherosclerosis from the Multiethnic Study of Atherosclerosis

John W. McEvoy, Michael J. Blaha, Andrew P. Defilippis, Joao A.C. Lima, David A. Bluemke, W. Gregory Hundley, James K. Min, Leslee J. Shaw, Donald M. Lloyd-Jones, R. Graham Barr, Matthew J. Budoff, Roger S. Blumenthal, Khurram Nasir*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

41 Scopus citations

Abstract

Objectives-To examine the contemporary effect of smoking in a multiethnic sample, and to explore the respective contributions of inflammation and infclinical atherosclerosis to the cardiovascular consequences of smoking. Approach and Results-We studied 6814 participants free of cardiovascular disease and coronary heart disease (CHD) from the Multiethnic Study of Atherosclerosis. Smoking status and cumulative exposure were determined by self-report and confirmed by urinary cotinine. Multivariable Cox regression was used to estimate the association between smoking parameters and all-cause cardiovascular disease, all-cause CHD, and hard CHD events. We further adjusted for high-sensitivity C-reactive protein and coronary artery calcium (CAC) in hierarchical Cox models. We identified 3218 never smokers, 2607 former smokers, and 971 current smokers. Median follow-up was 10.2 years. Compared with never smokers, adjusted hazard ratios in current smokers were 1.7 (95% confidence interval, 1.3-2.2) for all-cause cardiovascular disease, 1.6 (1.1-2.1) for all-cause CHD, and 1.7 (1.2-2.4) for hard CHD. Similarly, among current smokers, hazard ratios were higher in the 4th versus 1st quartile of pack-years (eg, all-cause CHD hazard ratio=2.7 [1.1-6.6]). Both CAC>100 and high-sensitivity C-reactive protein ≥3 mg/L identified higher relative risk among current smokers (eg, all-cause CHD hazard ratio of 3.0 [1.5-6.0, compared with CAC=0] and 2.6 [1.4-4.8, compared with high-sensitivity C-reactive protein <2 mg/L], respectively). However, CAC was a stronger mediator of events and adversely modified the effect of smoking on events (eg, P-interaction=0.02 for hard CHD). Compared with never smokers, former smokers (median cessation interval=22 years) had similar adjusted hazard for events. Conclusions-In this multiethnic cohort, current smoking and cumulative exposure remain important modifiable determinants of cardiovascular disease. Both high-sensitivity C-reactive protein ≥3 mg/L and, particularly, CAC>100 identified high-risk smokers who may benefit from more intensive smoking-cessation efforts.

Original languageEnglish (US)
Pages (from-to)700-709
Number of pages10
JournalArteriosclerosis, thrombosis, and vascular biology
Volume35
Issue number3
DOIs
StatePublished - Mar 1 2015

Keywords

  • coronary artery disease
  • inflammation
  • smoking

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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