Tobacco Cessation and Prevention: Tobacco Cessation and Prevention Slide |

Association Between Tobacco Smoking and Pro-Inflammatory Humoral Profile in Human Epicardial Adipose Tissue: Impact of Smoking Cessation on Cytokine Levels FREE TO VIEW

Marek Orban, MD; Lukas Mach; Helena Bedanova, MD; Miroslav Soucek, MD; Tomas Konecny, MD; Petr Nemec, MD
Author and Funding Information

Center of CV Surgery and Transplantation, Brno, Czech Republic

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;150(4_S):1304A. doi:10.1016/j.chest.2016.08.1419
Text Size: A A A
Published online

SESSION TITLE: Tobacco Cessation and Prevention Slide

SESSION TYPE: Original Investigation Slide

PRESENTED ON: Sunday, October 23, 2016 at 07:30 AM - 08:30 AM

PURPOSE: Epicardial adipose tissue (EAT) is a source of a number of pro- and anti-inflammatory cytokines which could act in pathogenesis of coronary artery disease (CAD) and degenerative valve disease. A potential relationship between known cardiovascular risk factors such as smoking, and EAT humoral signalling has not been fully elucidated. Therefore, we designed and conducted a cross-sectional study to determine whether known cardiovascular risk factors are linked to levels of selected cytokines in epicardial and subcutaneous adipose tissue (SAT).

METHODS: Samples of SAT and EAT were harvested from 140 consecutive patients undergoing scheduled cardiac surgery. Tissue concentrations of tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), adipocyte fatty acid-binding protein (AFABP), leptin, and adiponectin were determined by sandwich ELISA tests, and adjusted for total protein content in the samples.

RESULTS: Information on smoking status was available in 132 patients of whom 76 (57.6%) were never smokers, 34 (25.8%) former smokers, and 22 (16.7%) current smokers. TNF-alpha concentrations in EAT and SAT were significantly higher in current smokers (CS) (SAT 42.46 ± 28.01 pg/mg; EAT 94.17 ± 85.50 pg/mg) than in never smokers (NS) (SAT 27.68 ± 27.02 pg/mg; EAT 44.60 ± 41.08 pg/mg), and former smokers (FS) (SAT 33.61 ± 44.28 pg/mg; EAT 44.63 ± 35.47 pg/mg). No difference was found between former smokers, and never smokers. P-value = 0.9486 (SAT NS vs. FS); 0.1259 (SAT FS vs. CS); 0.03880 (SAT NS vs. CS); 0.9969 (EAT NS vs. FS); 0.0179 (EAT FS vs. CS); 0.0048 (EAT NS vs. CS). Similarly, concentrations of IL-6 in EAT and SAT were significantly higher in current smokers (SAT 483.58 ± 682.16 pg/mg; EAT 677.60 ± 799.27 pg/mg) than in never smokers (SAT 206.31 ± 276.85 pg/mg; EAT 337.85 ± 423.28 pg/mg), and former smokers (SAT 201.16 ± 330.28 pg/mg; EAT 266.48 ± 315.55 pg/mg). No difference was observed between former smokers, and never smokers. P-value = 0.9689 (SAT NS vs. FS); 0.0576 (SAT FS vs. CS); 0.0455 (SAT NS vs. CS); 0.7610 (EAT NS vs. FS); 0.0075 (EAT FS vs. CS); 0.0136 (EAT NS vs. CS). Following other factors were included in a stepwise linear regression analysis: age, gender, body mass index (BMI), diabetes mellitus (DM), smoking, dyslipidaemia, and chronic use of statins, aspirin, and non-steroidal anti-inflammatory drugs. No other clinical variables were statistically significantly associated with cytokine concentrations and the effect of smoking remained unchanged. Concentrations of leptin, adiponectin and AFABP were not associated with any of the studied variables.

CONCLUSIONS: In conclusion, smoking was independently associated with higher TNF-alpha and IL-6 concentrations in EAT, and SAT.

CLINICAL IMPLICATIONS: A novel observation that pro-inflammatory cytokines are elevated in EAT in smokers could represent an important mechanism in pathogenesis of CAD and degenerative valve disease. No differences between EAT cytokine production in never and former smokers support the results of previous epidemiological studies which demonstrated the importance of smoking cessation for cardiovascular risk reduction.

DISCLOSURE: The following authors have nothing to disclose: Marek Orban, Lukas Mach, Helena Bedanova, Miroslav Soucek, Tomas Konecny, Petr Nemec

No Product/Research Disclosure Information




Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

Find Similar Articles
CHEST Journal Articles
PubMed Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543