The relationship between smoking intensity and subclinical cardiovascular injury: The Multi-Ethnic Study of Atherosclerosis (MESA)

Mahmoud Al Rifai, Andrew P. DeFillippis, John W. McEvoy, Michael E. Hall, Ana Navas Acien, Miranda R. Jones, Rachel Keith, Hoda S. Magid, Carlos J. Rodriguez, Graham R. Barr, Emelia J. Benjamin, Rose Marie Robertson, Aruni Bhatnagar, Michael J. Blaha

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Background and aims Modern tobacco regulatory science requires an understanding of which biomarkers of cardiovascular injury are most sensitive to cigarette smoking exposure. Methods We studied self-reported current smokers from the Multi-Ethnic Study of Atherosclerosis. Smoking intensity was defined by number of cigarettes/day and urinary cotinine levels. Subclinical cardiovascular injury was assessed using markers of inflammation [high-sensitivity C-reactive protein (hsCRP), interleukin 6 & 2 (IL-2 & IL-6), tumor necrosis factor alpha (TNF-α)], thrombosis (fibrinogen, D-dimer, homocysteine), myocardial injury (troponin T; TnT), endothelial damage (albumin: creatinine ratio), and vascular function [aortic & carotid distensibility, flow-mediated dilation (FMD)]. Biomarkers were modeled as absolute and percent change using multivariable-adjusted linear regression models adjusted for cardiovascular risk factors and smoking duration. Results Among 843 current smokers, mean age was 58 (9) years, 53% were men, 39% were African American, mean number of cigarettes per day was 13 (10), and median smoking duration was 39 (15) years. Cigarette count was significantly associated with higher hsCRP, IL-6 and fibrinogen (β coefficients: 0.013, 0.011, 0.60 respectively), while ln-transformed cotinine was associated with the same biomarkers (β coefficients: 0.12, 0.04, 5.3 respectively) and inversely associated with aortic distensibility (β coefficient: −0.13). There was a limited association between smoking intensity and homocysteine, D-dimer, and albumin:creatinine ratio in partially adjusted models only, while there was no association with IL-2, TNF-α, carotid distensibility, FMD, or TnT in any model. In percent change analyses, relationships were strongest with hsCRP. Conclusions Smoking intensity was associated with early biomarkers of CVD, particularly, markers of systemic inflammation. Of these, hsCRP may be the most sensitive.

Original languageEnglish (US)
Pages (from-to)119-130
Number of pages12
JournalAtherosclerosis
Volume258
DOIs
StatePublished - Mar 1 2017
Externally publishedYes

Fingerprint

Atherosclerosis
Smoking
C-Reactive Protein
Wounds and Injuries
Biomarkers
Tobacco Products
Cotinine
Interleukin-6
Homocysteine
Fibrinogen
Interleukin-2
Dilatation
Albumins
Linear Models
Creatinine
Inflammation
Troponin T
African Americans
Tobacco
Blood Vessels

Keywords

  • Cigarette smoking
  • Endothelial damage
  • Inflammation
  • Myocardial injury
  • Smoking intensity
  • Thrombosis
  • Tobacco regulatory science
  • Vascular dysfunction

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Al Rifai, M., DeFillippis, A. P., McEvoy, J. W., Hall, M. E., Acien, A. N., Jones, M. R., ... Blaha, M. J. (2017). The relationship between smoking intensity and subclinical cardiovascular injury: The Multi-Ethnic Study of Atherosclerosis (MESA). Atherosclerosis, 258, 119-130. https://doi.org/10.1016/j.atherosclerosis.2017.01.021

The relationship between smoking intensity and subclinical cardiovascular injury : The Multi-Ethnic Study of Atherosclerosis (MESA). / Al Rifai, Mahmoud; DeFillippis, Andrew P.; McEvoy, John W.; Hall, Michael E.; Acien, Ana Navas; Jones, Miranda R.; Keith, Rachel; Magid, Hoda S.; Rodriguez, Carlos J.; Barr, Graham R.; Benjamin, Emelia J.; Robertson, Rose Marie; Bhatnagar, Aruni; Blaha, Michael J.

In: Atherosclerosis, Vol. 258, 01.03.2017, p. 119-130.

Research output: Contribution to journalArticle

Al Rifai, M, DeFillippis, AP, McEvoy, JW, Hall, ME, Acien, AN, Jones, MR, Keith, R, Magid, HS, Rodriguez, CJ, Barr, GR, Benjamin, EJ, Robertson, RM, Bhatnagar, A & Blaha, MJ 2017, 'The relationship between smoking intensity and subclinical cardiovascular injury: The Multi-Ethnic Study of Atherosclerosis (MESA)', Atherosclerosis, vol. 258, pp. 119-130. https://doi.org/10.1016/j.atherosclerosis.2017.01.021
Al Rifai, Mahmoud ; DeFillippis, Andrew P. ; McEvoy, John W. ; Hall, Michael E. ; Acien, Ana Navas ; Jones, Miranda R. ; Keith, Rachel ; Magid, Hoda S. ; Rodriguez, Carlos J. ; Barr, Graham R. ; Benjamin, Emelia J. ; Robertson, Rose Marie ; Bhatnagar, Aruni ; Blaha, Michael J. / The relationship between smoking intensity and subclinical cardiovascular injury : The Multi-Ethnic Study of Atherosclerosis (MESA). In: Atherosclerosis. 2017 ; Vol. 258. pp. 119-130.
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abstract = "Background and aims Modern tobacco regulatory science requires an understanding of which biomarkers of cardiovascular injury are most sensitive to cigarette smoking exposure. Methods We studied self-reported current smokers from the Multi-Ethnic Study of Atherosclerosis. Smoking intensity was defined by number of cigarettes/day and urinary cotinine levels. Subclinical cardiovascular injury was assessed using markers of inflammation [high-sensitivity C-reactive protein (hsCRP), interleukin 6 & 2 (IL-2 & IL-6), tumor necrosis factor alpha (TNF-α)], thrombosis (fibrinogen, D-dimer, homocysteine), myocardial injury (troponin T; TnT), endothelial damage (albumin: creatinine ratio), and vascular function [aortic & carotid distensibility, flow-mediated dilation (FMD)]. Biomarkers were modeled as absolute and percent change using multivariable-adjusted linear regression models adjusted for cardiovascular risk factors and smoking duration. Results Among 843 current smokers, mean age was 58 (9) years, 53{\%} were men, 39{\%} were African American, mean number of cigarettes per day was 13 (10), and median smoking duration was 39 (15) years. Cigarette count was significantly associated with higher hsCRP, IL-6 and fibrinogen (β coefficients: 0.013, 0.011, 0.60 respectively), while ln-transformed cotinine was associated with the same biomarkers (β coefficients: 0.12, 0.04, 5.3 respectively) and inversely associated with aortic distensibility (β coefficient: −0.13). There was a limited association between smoking intensity and homocysteine, D-dimer, and albumin:creatinine ratio in partially adjusted models only, while there was no association with IL-2, TNF-α, carotid distensibility, FMD, or TnT in any model. In percent change analyses, relationships were strongest with hsCRP. Conclusions Smoking intensity was associated with early biomarkers of CVD, particularly, markers of systemic inflammation. Of these, hsCRP may be the most sensitive.",
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AU - DeFillippis, Andrew P.

AU - McEvoy, John W.

AU - Hall, Michael E.

AU - Acien, Ana Navas

AU - Jones, Miranda R.

AU - Keith, Rachel

AU - Magid, Hoda S.

AU - Rodriguez, Carlos J.

AU - Barr, Graham R.

AU - Benjamin, Emelia J.

AU - Robertson, Rose Marie

AU - Bhatnagar, Aruni

AU - Blaha, Michael J.

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N2 - Background and aims Modern tobacco regulatory science requires an understanding of which biomarkers of cardiovascular injury are most sensitive to cigarette smoking exposure. Methods We studied self-reported current smokers from the Multi-Ethnic Study of Atherosclerosis. Smoking intensity was defined by number of cigarettes/day and urinary cotinine levels. Subclinical cardiovascular injury was assessed using markers of inflammation [high-sensitivity C-reactive protein (hsCRP), interleukin 6 & 2 (IL-2 & IL-6), tumor necrosis factor alpha (TNF-α)], thrombosis (fibrinogen, D-dimer, homocysteine), myocardial injury (troponin T; TnT), endothelial damage (albumin: creatinine ratio), and vascular function [aortic & carotid distensibility, flow-mediated dilation (FMD)]. Biomarkers were modeled as absolute and percent change using multivariable-adjusted linear regression models adjusted for cardiovascular risk factors and smoking duration. Results Among 843 current smokers, mean age was 58 (9) years, 53% were men, 39% were African American, mean number of cigarettes per day was 13 (10), and median smoking duration was 39 (15) years. Cigarette count was significantly associated with higher hsCRP, IL-6 and fibrinogen (β coefficients: 0.013, 0.011, 0.60 respectively), while ln-transformed cotinine was associated with the same biomarkers (β coefficients: 0.12, 0.04, 5.3 respectively) and inversely associated with aortic distensibility (β coefficient: −0.13). There was a limited association between smoking intensity and homocysteine, D-dimer, and albumin:creatinine ratio in partially adjusted models only, while there was no association with IL-2, TNF-α, carotid distensibility, FMD, or TnT in any model. In percent change analyses, relationships were strongest with hsCRP. Conclusions Smoking intensity was associated with early biomarkers of CVD, particularly, markers of systemic inflammation. Of these, hsCRP may be the most sensitive.

AB - Background and aims Modern tobacco regulatory science requires an understanding of which biomarkers of cardiovascular injury are most sensitive to cigarette smoking exposure. Methods We studied self-reported current smokers from the Multi-Ethnic Study of Atherosclerosis. Smoking intensity was defined by number of cigarettes/day and urinary cotinine levels. Subclinical cardiovascular injury was assessed using markers of inflammation [high-sensitivity C-reactive protein (hsCRP), interleukin 6 & 2 (IL-2 & IL-6), tumor necrosis factor alpha (TNF-α)], thrombosis (fibrinogen, D-dimer, homocysteine), myocardial injury (troponin T; TnT), endothelial damage (albumin: creatinine ratio), and vascular function [aortic & carotid distensibility, flow-mediated dilation (FMD)]. Biomarkers were modeled as absolute and percent change using multivariable-adjusted linear regression models adjusted for cardiovascular risk factors and smoking duration. Results Among 843 current smokers, mean age was 58 (9) years, 53% were men, 39% were African American, mean number of cigarettes per day was 13 (10), and median smoking duration was 39 (15) years. Cigarette count was significantly associated with higher hsCRP, IL-6 and fibrinogen (β coefficients: 0.013, 0.011, 0.60 respectively), while ln-transformed cotinine was associated with the same biomarkers (β coefficients: 0.12, 0.04, 5.3 respectively) and inversely associated with aortic distensibility (β coefficient: −0.13). There was a limited association between smoking intensity and homocysteine, D-dimer, and albumin:creatinine ratio in partially adjusted models only, while there was no association with IL-2, TNF-α, carotid distensibility, FMD, or TnT in any model. In percent change analyses, relationships were strongest with hsCRP. Conclusions Smoking intensity was associated with early biomarkers of CVD, particularly, markers of systemic inflammation. Of these, hsCRP may be the most sensitive.

KW - Cigarette smoking

KW - Endothelial damage

KW - Inflammation

KW - Myocardial injury

KW - Smoking intensity

KW - Thrombosis

KW - Tobacco regulatory science

KW - Vascular dysfunction

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