TY - JOUR
T1 - The relationship between smoking intensity and subclinical cardiovascular injury
T2 - The Multi-Ethnic Study of Atherosclerosis (MESA)
AU - Al Rifai, Mahmoud
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.
N1 - Funding Information:
Research reported in this work was supported by grant number 5P50HL120163 from the National Heart, Lung, and Blood Institute (NHLBI) and FDA Center for Tobacco Products (CTP).
Publisher Copyright:
© 2017 Elsevier B.V.
PY - 2017/3/1
Y1 - 2017/3/1
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
UR - http://www.scopus.com/inward/record.url?scp=85013647958&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85013647958&partnerID=8YFLogxK
U2 - 10.1016/j.atherosclerosis.2017.01.021
DO - 10.1016/j.atherosclerosis.2017.01.021
M3 - Article
C2 - 28237909
AN - SCOPUS:85013647958
SN - 0021-9150
VL - 258
SP - 119
EP - 130
JO - Atherosclerosis
JF - Atherosclerosis
ER -