Associations of Cigarette Smoking With Subclinical Inflammation and Atherosclerosis:  ELSA ‐Brasil (The Brazilian Longitudinal Study of Adult Health)

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Abstract

Background

There is a need to identify sensitive biomarkers of early tobacco‐related cardiovascular disease. We examined the association of smoking status, burden, time since quitting, and intensity, with markers of inflammation and subclinical atherosclerosis.

Methods and Results

We studied 14 103 participants without clinical cardiovascular disease in ELSA‐Brasil (Brazilian Longitudinal Study of Adult Health). We evaluated baseline cross‐sectional associations between smoking parameters and inflammation (high‐sensitivity C‐reactive protein [hs CRP]) and measures of subclinical atherosclerosis (carotid intima–media thickness, ankle‐brachial index, and coronary artery calcium [ CAC]). The cohort included 1844 current smokers, 4121 former smokers, and 8138 never smokers. Mean age was 51.7±8.9 years; 44.8% were male. After multivariable adjustment, compared with never smokers, current smokers had significantly higher levels of hs CRP (β=0.24, 0.19–0.29 mg/L; P<0.001) and carotid intima–media thickness (β=0.03, 0.02–0.04 mm; P<0.001) and odds of ankle‐brachial index ≤1.0 (odds ratio: 2.52; 95% confidence interval, 2.06–3.08; P<0.001) and CAC >0 (odds ratio: 1.83; 95% confidence interval, 1.46–2.30; P<0.001). Among former and current smokers, pack‐years of smoking (burden) were significantly associated with hs CRP ( P<0.001 and P=0.006, respectively) and CAC ( P<0.001 and P=0.002, respectively). Among former smokers, hs CRP and carotid intima–media thickness levels and odds of ankle‐brachial index ≤1.0 and CAC >0 were lower with increasing time since quitting ( P<0.01). Among current smokers, number of cigarettes per day (intensity) was positively associated with hs CRP ( P<0.001) and CAC >0 ( P=0.03) after adjusting for duration of smoking.

Conclusions

Strong associations were observed between smoking status, burden, and intensity with inflammation (hs CRP) and subclinical atherosclerosis (carotid intima–media thickness, ankle‐brachial index, CAC). These markers of early cardiovascular disease injury may be used for the further study and regulation of traditional and novel tobacco products.

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Most cited references 35

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Smoke-free legislation and hospitalizations for acute coronary syndrome.

Alex McConnachie, Stuart D Pringle, Paul MacIntyre … (2008)

Previous studies have suggested a reduction in the total number of hospital admissions for acute coronary syndrome after the enactment of legislation banning smoking in public places. However, it is unknown whether the reduction in admissions involved nonsmokers, smokers, or both. Since the end of March 2006, smoking has been prohibited by law in all enclosed public places throughout Scotland. We collected information prospectively on smoking status and exposure to secondhand smoke based on questionnaires and biochemical findings from all patients admitted with acute coronary syndrome to nine Scottish hospitals during the 10-month period preceding the passage of the legislation and during the same period the next year. These hospitals accounted for 64% of admissions for acute coronary syndrome in Scotland, which has a population of 5.1 million. Overall, the number of admissions for acute coronary syndrome decreased from 3235 to 2684--a 17% reduction (95% confidence interval, 16 to 18)--as compared with a 4% reduction in England (which has no such legislation) during the same period and a mean annual decrease of 3% (maximum decrease, 9%) in Scotland during the decade preceding the study. The reduction in the number of admissions was not due to an increase in the number of deaths of patients with acute coronary syndrome who were not admitted to the hospital; this latter number decreased by 6%. There was a 14% reduction in the number of admissions for acute coronary syndrome among smokers, a 19% reduction among former smokers, and a 21% reduction among persons who had never smoked. Persons who had never smoked reported a decrease in the weekly duration of exposure to secondhand smoke (P<0.001 by the chi-square test for trend) that was confirmed by a decrease in their geometric mean concentration of serum cotinine from 0.68 to 0.56 ng per milliliter (P<0.001 by the t-test). The number of admissions for acute coronary syndrome decreased after the implementation of smoke-free legislation. A total of 67% of the decrease involved nonsmokers. However, fewer admissions among smokers also contributed to the overall reduction. 2008 Massachusetts Medical Society

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Inflammation and atherosclerosis: role of C-reactive protein in risk assessment.

Peter Libby, Paul Ridker (2004)

Inflammation participates critically in atherosclerosis. Circulating levels of several inflammatory markers rise in individuals at risk for atherosclerotic events. In particular, elevation of plasma C-reactive protein (CRP), a nonspecific acute-phase reactant that is easily and reliably measured, has strong predictive power for cardiovascular events. Indeed, measurements of high-sensitivity CRP (hs-CRP) plasma levels add to both the prognostic information gleaned from assay of plasma lipid risk factors and the risk levels estimated by means of Framingham study-based criteria. Retrospective data suggest the hypothesis that hs-CRP plasma levels may be useful for guiding use of lipid-lowering therapy in individuals who appear to be at low risk according to traditional risk assessment. A large-scale, randomized clinical trial-Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER)-will test whether rosuvastatin therapy will reduce incident cardiovascular disease in subjects with elevated plasma hs-CRP concentrations who do not meet current criteria for initiation of lipid-lowering drug therapy. Such clinical trial data may provide an evidence base for the use of plasma CRP assay as an adjuvant guide to therapy to complement the established traditional risk factors such as plasma lipid levels. Thus, medical practitioners are ushering in an era in which the biology of inflammation in atherosclerosis will find its way into clinical application.

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Associations between C-reactive protein, coronary artery calcium, and cardiovascular events: implications for the JUPITER population from MESA, a population-based cohort study.

Arthur Agatston, Khurram Nasir, Ron Blankstein … (2011)

The JUPITER trial showed that some patients with LDL-cholesterol concentrations less than 3·37 mmol/L ( 100). We calculated 5-year number needed to treat (NNT) by applying the benefit recorded in JUPITER to the event rates within each CAC strata. Median follow-up was 5·8 years (IQR 5·7-5·9). 444 (47%) patients in the MESA JUPITER population had CAC scores of 0 and, in this group, rates of coronary heart disease events were 0·8 per 1000 person-years. 74% of all coronary events were in the 239 (25%) of participants with CAC scores of more than 100 (20·2 per 1000 person-years). For coronary heart disease, the predicted 5-year NNT was 549 for CAC score 0, 94 for scores 1-100, and 24 for scores greater than 100. For cardiovascular disease, the NNT was 124, 54, and 19. In the total study population, presence of CAC was associated with a hazard ratio of 4·29 (95% CI 1·99-9·25) for coronary heart disease, and of 2·57 (1·48-4·48) for cardiovascular disease. hsCRP was not associated with either disease after multivariable adjustment. CAC seems to further stratify risk in patients eligible for JUPITER, and could be used to target subgroups of patients who are expected to derive the most, and the least, absolute benefit from statin treatment. Focusing of treatment on the subset of individuals with measurable atherosclerosis could allow for more appropriate allocation of resources. National Institutes of Health-National Heart, Lung, and Blood Institute. Copyright © 2011 Elsevier Ltd. All rights reserved.

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Author and article information

Contributors

Paulo A. Lotufo: palotufo@usp.br

Michael J. Blaha: mblaha1@jhmi.edu

Journal

Journal ID (nlm-ta): J Am Heart Assoc

Journal ID (iso-abbrev): J Am Heart Assoc

Journal ID (doi): 10.1002/(ISSN)2047-9980

Journal ID (publisher-id): JAH3

Journal ID (hwp): ahaoa

Title: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

Publisher: John Wiley and Sons Inc. (Hoboken )

ISSN (Electronic): 2047-9980

Publication date (Electronic): 24 June 2017

Publication date Collection: June 2017

Volume: 6

Issue: 6 ( doiID: 10.1002/jah3.2017.6.issue-6 )

Electronic Location Identifier: e005088

Affiliations

[ ¹ ] Johns Hopkins Ciccarone Center for the Prevention of Heart Disease Baltimore MD

[ ² ] Department of Medicine University of Kansas School of Medicine Wichita KS

[ ³ ] School of Medicine University of Louisville KY

[ ⁴ ] Center for Clinical and Epidemiologic Research University of São Paulo Brazil

[ ⁵ ] School of Medicine University of São Paulo Brazil

[ ⁶ ] Postgraduate Studies Program and Hospital de Clínicas de Porto Alegre Universidade Federal do Rio Grande do Sul Porto Alegre Brazil

Author notes

[*] [* ] Correspondence to: Michael J. Blaha, MD, MPH, Blalock 524 D1, 600 N. Wolfe St, Baltimore, MD 21287. E‐mail: mblaha1@ 123456jhmi.edu

Paulo A. Lotufo, MD, DrPH, Center for Clinical and Epidemiological Research, University of São Paulo, Av Lineu Prestes, 2565 São Paulo, Brazil. E‐mail: palotufo@ 123456usp.br

[†]

Dr Kianoush and Dr Yakoob are co‐first authors.

Article

Publisher ID: JAH32318

DOI: 10.1161/JAHA.116.005088

PMC ID: 5669156

PubMed ID: 28647689

SO-VID: 3c5e28fe-1335-4eb6-9266-a88b85c1b282

License:

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

History

Date received : 23 November 2016

Date accepted : 05 May 2017

Page count

Figures: 2, Tables: 6, Pages: 15, Words: 10375

Funding

Funded by: American Heart Association Tobacco Regulation and Addiction Center (A‐TRAC)

Funded by: NIH

Award ID: 1 P50 HL120163‐01

Funded by: Brazilian Ministry of Health

Funded by: Brazilian Ministry of Science and Technology

Funded by: National Counsel of Technological and Scientific Development (CNPq) ‐ National Research Council

Award ID: 01 06 0010.00 RS

Award ID: 01 06 0212.00 BA

Award ID: 01 06 0300.00 ES

Award ID: 01 06 0278.00 MG

Award ID: 01 06 0115.00 SP

Award ID: 01 06 0071.00 RJ

Custom metadata

source-schema-version-number 2.0

component-id jah32318

cover-date June 2017

details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.2.1 mode:remove_FC converted:27.10.2017

ScienceOpen disciplines: Cardiovascular Medicine

Keywords: atherosclerosis,inflammation,smoking,subclinical atherosclerosis risk factor,tobacco products,imaging,ultrasound

Data availability:

ScienceOpen disciplines: Cardiovascular Medicine

Keywords: atherosclerosis, inflammation, smoking, subclinical atherosclerosis risk factor, tobacco products, imaging, ultrasound

Associations of Cigarette Smoking With Subclinical Inflammation and Atherosclerosis: ELSA‐Brasil (The Brazilian Longitudinal Study of Adult Health)

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Abstract

Background

Methods and Results

Conclusions

Related collections

Karger: Cardiovascular System

Most cited references 35

Smoke-free legislation and hospitalizations for acute coronary syndrome.

Inflammation and atherosclerosis: role of C-reactive protein in risk assessment.

Associations between C-reactive protein, coronary artery calcium, and cardiovascular events: implications for the JUPITER population from MESA, a population-based cohort study.

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