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ISSN: 2638-5910

Archives of Diabetes & Obesity

Research Article(ISSN: 2638-5910)

Epicardial Adipose Tissue Inflammation and Fibrosis: Relationships with Coronary Artery Diseases Volume 3 - Issue 4

Rizzatti Vanni1, Fantin Francesco2, Mazzali Gloria1, Zoico Elena2, Rossi Andrea1, Faggian Giuseppe1, Onorati Francesco1, Santini Francesco3 and Zamboni Mauro1*

  • 1Department of Surgery, Dentistry, Maternity and Infant, Section of Geriatrics, University of Verona, Italy;
  • 2Department of Medicine, Section of Geriatrics, University of Verona, Italy
  • 3Department of Surgery, Dentistry, Maternity and Infant Section of Cardiac Surgery, University of Verona, Italy
  • 4Division of Cardiac Surgery, University of Genova, Italy

Received:May 28, 2021;   Published: June 4, 2021

Corresponding author: Mauro Zamboni, Department of Surgery, Clinica Geriatrica, Ospedale Maggiore, Healthy Aging Center, University of Verona, Verona, Italy

DOI: 10.32474/ADO.2021.03.000166

Abstract PDF

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Aims: Accumulation of epicardial adipose tissue (EAT) is associated with severity and progression of coronary artery disease (CAD). The aim of this study was to compare EAT fibrosis, inflammation, Hypoxia-inducible factor 1-alpha (HIF1-α) and caveolin-1 (CAV-1) between subjects with and without CAD.

Methods and Results: Body mass index (BMI), waist circumference (WC), glucose, insulin, homeostasis model assessment index, serum leptin and adiponectin were evaluated in EAT of patients with and without CAD undergoing elective surgery. Biopsies were collected from EAT. Immunohistochemistry for macrophages CD68, CD11c, CD163, HIF1-α and CAV-1 was performed and Masson Trichrome staining to define the degree of fibrosis. A total of 22 male patients (age range from 51-80 years), were studied: 12 CAD and 10 non-CAD undergoing elective surgery.

Fibrosis (1.29 ± 0.71 vs 0.54 ± 0.40, p<0.01), HIF1-α (2.39 ± 1.64 vs 1.01 ± 0.94, p<0.05), number of total CD68 (74.25 ± 49.39 vs 37.33 ± 18.28, p<0.05), CD163 (57.75 ± 38.23 vs 31.11 ± 18.54, p<0.05) and CD11c (6.67 ± 4.73 vs 2.05 ± 1.13, p<0.01) were higher in CAD than in non-CAD patients, whilst serum adiponectin (8.25 ± 7.52 vs 15.06 ± 11.11, p<0.05), and CAV-1 (0.0790 ± 0.0268 vs 0.0987 ± 0.0164, p<0.05) significantly lower. In 4 patients with CAD, but in none in those without, macrophages aggregated in crown like structure were found. Fibrosis correlated with HIF1-α (r= 0.644, p < 0.01) and M1 pro-inflammatory CD11c (+) macrophages (r=0.601, p<0.01); HIF1-α with total, M1 pro-inflammatory CD11c (+) and M2 anti-inflammatory CD163 (+) macrophages (r=0.5313, p<0.05; r=0.6385, p<0.01; r=0.6730, p<0.001, respectively); Caveolin-1 positively correlated with serum adiponectin (r=0.4347, p<0.05).

Conclusions: CAD patients displays a dysfunctional EAT characterized by greater inflammation, fibrosis, HIF1-α and lower CAV. Our results seem to suggest that adiponectin may decline CAD risk even by determining an increase of CAV-1.

Keywords: Epicardial Adipose Tissue; HIF‐1α; Fibrosis; Inflammation; Coronary Artery Disease

Abbreviations: BMI, Body Mass Index; WC, Waist Circumference; HOMA, Homeostasis Model Assessment; CAV-1, caveolin 1; ADIP DIAMETER, diameter of adipocytes; HIF1-α, number of adipocytes nuclei positive for Hypoxia-inducible factor 1-alpha M CD68, Total Macrophages; M2 CD163, Anti-inflammatory Macrophages; M1 CD11c, Proinflammatory Macrophages *p<0.05, **p<0.01, ***p<0.01.

Abstract| Introduction| Material and Methods| Statistical Analysis| Results| Discussion| Conflict of Interest:| Acknowledgements| References|