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

被引:66
|
作者
Al Rifai, Mahmoud [1 ,2 ]
DeFillippis, Andrew P. [2 ,3 ,4 ]
McEvoy, John W. [2 ]
Hall, Michael E. [5 ]
Acien, Ana Navas [6 ,7 ]
Jones, Miranda R. [7 ]
Keith, Rachel [3 ,4 ]
Magid, Hoda S. [8 ]
Rodriguez, Carlos J. [9 ]
Barr, Graham R. [10 ]
Benjamin, Emelia J. [11 ]
Robertson, Rose Marie [12 ]
Bhatnagar, Aruni [3 ,4 ]
Blaha, Michael J. [2 ]
机构
[1] Univ Kansas, Sch Med, Dept Med, Wichita, KS 67214 USA
[2] Johns Hopkins Ciccarone Ctr Prevent Heart Dis, Baltimore, MD USA
[3] Univ Louisville, Sch Med, Diabet & Obes Ctr, Louisville, KY 40292 USA
[4] Univ Louisville, Sch Med, Div Cardiol, Louisville, KY 40292 USA
[5] Univ Mississippi, Med Ctr, Div Cardiol, Jackson, MS 39216 USA
[6] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD USA
[7] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA
[8] UC Berkeley Sch Publ Hlth, Berkeley, CA USA
[9] Wake Forest Univ, Maya Angelou Ctr Hlth Equ, Winston Salem, NC 27109 USA
[10] Columbia Univ, Med Ctr, Div Pulm Allergy & Crit Care Med, New York, NY USA
[11] Boston Univ, Sch Med, Vasc Testing & Echocardiog, Boston, MA 02118 USA
[12] Amer Heart Assoc, Chief Sci Off, Dallas, TX USA
关键词
Cigarette smoking; Smoking intensity; Tobacco regulatory science; Inflammation; Thrombosis; Vascular dysfunction; Myocardial injury; Endothelial damage; RIGHT-VENTRICULAR STRUCTURE; CORONARY-ARTERY CALCIUM; CIGARETTE-SMOKING; ENDOTHELIAL DYSFUNCTION; MYOCARDIAL-INFARCTION; PLASMA HOMOCYSTEINE; QUITTING SMOKING; RISK-FACTORS; DISEASE; INFLAMMATION;
D O I
10.1016/j.atherosclerosis.2017.01.021
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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-alpha)], thrombosis (fibrinogen, Ddimer, 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 (beta coefficients: 0.013, 0.011, 0.60 respectively), while ln-transformed cotinine was associated with the same biomarkers (b coefficients: 0.12, 0.04, 5.3 respectively) and inversely associated with aortic distensibility (b coefficient: -0.13). There was a limited association between smoking intensity and homocysteine, Ddimer, and albumin: creatinine ratio in partially adjusted models only, while there was no association with IL-2, TNF-a, 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. (C) 2017 Elsevier B.V. All rights reserved.
引用
收藏
页码:119 / 130
页数:12
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