Title:Epicardial Adipocyte-derived TNF-α Modulates Local Inflammation in Patients with Advanced Coronary Artery Disease
Volume: 20
Issue: 1
Author(s): Nikoleta Karampetsou , Aspasia Tzani*, Ilias P. Doulamis, Evanthia Bletsa, Aggeliki Minia, Vaia Pliaka , Nikos Tsolakos, Evangelos Oikonomou , Dimitris Tousoulis , Konstantinos Kontzoglou , Leonidas G. Alexopoulos, Despoina N. Perrea , Paulos Patapis and Ioannis A. Chloroyiannis
Affiliation:
- Laboratory for Experimental Surgery and Surgical Research “N.S Christeas”, National and Kapodistrian University
of Athens, School of Medicine, Athens, Greece
Keywords:
Epicardial adipose tissue, coronary artery disease, coronary artery bypass graft surgery, inflammation, TNF-α, IL-1α.
Abstract:
Background: Epicardial Adipose Tissue (EAT) surrounds the epicardium and can mediate
harmful effects related to Coronary Artery Disease (CAD).
Objective: We explored the regional differences between adipose stores surrounding diseased and
non-diseased segments of coronary arteries in patients with advanced CAD.
Methods: We enrolled 32 patients with known CAD who underwent coronary artery bypass graft
(CABG) surgery. Inflammatory mediators were measured in EAT biopsies collected from a region
of the Left Anterior Descending Artery (LAD) with severe stenosis (diseased segment) and without
stenosis (non-diseased segment).
Results: Mean age was 64.3±11.1 years, and mean EAT thickness was 7.4±1.9 mm. Dyslipidemia
was the most prevalent comorbidity (81% of the patients). Out of a total of 11 cytokines, resistin
(p=0.039), matrix metallopeptidase 9 (MMP-9) (p=0.020), C-C motif chemokine ligand 5 (CCL-5)
(p=0.021), and follistatin (p=0.038) were significantly increased in the diseased compared with the
non-diseased EAT segments. Indexed tumor necrosis factor-alpha (TNF-α), defined as the diseased
to non-diseased cytokine levels ratio, was significantly correlated with increased EAT thickness
both in the whole cohort (p=0.043) and in a subpopulation of patients with dyslipidemia (p=0.009).
Treatment with lipid-lowering agents significantly decreased indexed TNF-α levels (p=0.015). No
significant alterations were observed in the circulating levels of these cytokines with respect to
CAD-associated comorbidities.
Conclusion: Perivascular EAT is a source of cytokine secretion in distinct areas surrounding the
coronary arteries in patients with advanced CAD. Adipocyte-derived TNF-α is a prominent mediator
of local inflammation.
