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Atherosclerosis. 2017 Mar;258:119-130. doi: 10.1016/j.atherosclerosis.2017.01.021. Epub 2017 Jan 19.

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

Author information

1
Department of Medicine, University of Kansas School of Medicine, Wichita, KS, USA; Johns Hopkins Ciccarone Center for Prevention of Heart Disease, Baltimore, MD, USA.
2
Johns Hopkins Ciccarone Center for Prevention of Heart Disease, Baltimore, MD, USA; Diabetes and Obesity Center, University of Louisville School of Medicine, Louisville, KY, USA; Division of Cardiology, University of Louisville School of Medicine, Louisville, KY, USA.
3
Johns Hopkins Ciccarone Center for Prevention of Heart Disease, Baltimore, MD, USA.
4
University of Mississippi Medical Center, Division of Cardiology, Jackson, MS, USA.
5
Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
6
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
7
Diabetes and Obesity Center, University of Louisville School of Medicine, Louisville, KY, USA; Division of Cardiology, University of Louisville School of Medicine, Louisville, KY, USA.
8
UC Berkeley School of Public Health, Berkley, CA, USA.
9
Maya Angelou Center for Health Equity, Wake Forest University, Winston-Salem, NC, USA.
10
Columbia University Medical Center, Division of Pulmonary, Allergy and Critical Care Medicine, New York, NY, USA.
11
Boston University, School of Medicine, Vascular Testing and Echocardiography, Boston, MA, USA.
12
American Heart Association, Chief Science Office, Dallas, TX, USA.
13
Johns Hopkins Ciccarone Center for Prevention of Heart Disease, Baltimore, MD, USA. Electronic address: mblaha1@jhmi.edu.

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.

KEYWORDS:

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

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