Epicardial adipose tissue, inflammation, fibrosis and coronary artery diseases

Author(s):  
Francesco Fantin ◽  
Mazzali Gloria ◽  
Rizzatti Vanni ◽  
Zoico Elena ◽  
Rossi Andrea ◽  
...  

Abstract Purpose: 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, HIF1-α, number of total CD68, CD163 and CD11c were higher in CAD than in non-CAD patients, whilst serum adiponectin and CAV-1 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 and M1 pro-inflammatory CD11c (+) macrophages; HIF1-α with total, M1 pro-inflammatory CD11c (+) and M2 anti-inflammatory CD163 (+) macrophages; Caveolin-1 positively correlated with serum adiponectin.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. Level of evidence: III cross-sectional study.

Author(s):  
Tracey McLaughlin ◽  
Ingela Schnittger ◽  
Anna Nagy ◽  
Elizabeth Zanley ◽  
Yue Xu ◽  
...  

Background Inflammation in epicardial adipose tissue (EAT) may contribute to coronary atherosclerosis. Myocardial bridge is a congenital anomaly in which the left anterior descending coronary artery takes a “tunneled” course under a bridge of myocardium: while atherosclerosis develops in the proximal left anterior descending coronary artery, the bridged portion is spared, highlighting the possibility that geographic separation from inflamed EAT is protective. We tested the hypothesis that inflammation in EAT was related to atherosclerosis by comparing EAT from proximal and bridge depots in individuals with myocardial bridge and varying degrees of atherosclerotic plaque. Methods and Results Maximal plaque burden was quantified by intravascular ultrasound, and inflammation was quantified by pericoronary EAT signal attenuation (pericoronary adipose tissue attenuation) from cardiac computed tomography scans. EAT overlying the proximal left anterior descending coronary artery and myocardial bridge was harvested for measurement of mRNA and microRNA (miRNA) using custom chips by Nanostring; inflammatory cytokines were measured in tissue culture supernatants. Pericoronary adipose tissue attenuation was increased, indicating inflammation, in proximal versus bridge EAT, in proportion to atherosclerotic plaque. Individuals with moderate‐high versus low plaque burden exhibited greater expression of inflammation and hypoxia genes, and lower expression of adipogenesis genes. Comparison of gene expression in proximal versus bridge depots revealed differences only in participants with moderate‐high plaque: inflammation was higher in proximal and adipogenesis lower in bridge EAT. Secreted inflammatory cytokines tended to be higher in proximal EAT. Hypoxia‐inducible factor 1a was highly associated with inflammatory gene expression. Seven miRNAs were differentially expressed by depot: 3192‐5P, 518D‐3P, and 532‐5P were upregulated in proximal EAT, whereas miR 630, 575, 16‐5P, and 320E were upregulated in bridge EAT. miR 630 correlated directly with plaque burden and inversely with adipogenesis genes. miR 3192‐5P, 518D‐3P, and 532‐5P correlated inversely with hypoxia/oxidative stress, peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PCG1a), adipogenesis, and angiogenesis genes. Conclusions Inflammation is specifically elevated in EAT overlying atherosclerotic plaque, suggesting that EAT inflammation is caused by atherogenic molecular signals, including hypoxia‐inducible factor 1a and/or miRNAs in an “inside‐to‐out” relationship. Adipogenesis was suppressed in the bridge EAT, but only in the presence of atherosclerotic plaque, supporting cross talk between the vasculature and EAT. miR 630 in EAT, expressed differentially according to burden of atherosclerotic plaque, and 3 other miRNAs appear to inhibit key genes related to adipogenesis, angiogenesis, hypoxia/oxidative stress, and thermogenesis in EAT, highlighting a role for miRNA in mediating cross talk between the coronary vasculature and EAT.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 469-P
Author(s):  
MILOS MRAZ ◽  
ANNA CINKAJZLOVA ◽  
ZDENA LACINOVÁ ◽  
JANA KLOUCKOVA ◽  
HELENA KRATOCHVILOVA ◽  
...  

Author(s):  
Jalaledin Mirzay Razzaz ◽  
Hossein Moameri ◽  
Zahra Akbarzadeh ◽  
Mohammad Ariya ◽  
Seyed ali Hosseini ◽  
...  

Abstract Objectives Insulin resistance is the most common metabolic change associated with obesity. The present study aimed to investigate the relationship between insulin resistance and body composition especially adipose tissue in a randomized Tehrani population. Methods This study used data of 2,160 individuals registered in a cross-sectional study on were randomly selected from among subjects who were referred to nutrition counseling clinic in Tehran, from April 2016 to September 2017. Insulin resistance was calculated by homeostasis model assessment formula. The odds ratio (95% CI) was calculated using logistic regression models. Results The mean age of the men was 39 (±10) and women were 41 (±11) (the age ranged from 20 to 50 years). The risk of increased HOMA-IR was 1.03 (95% CI: 1.01–1.04) for an increase in one percent of Body fat, and 1.03 (95% CI: 1.00–1.05) for an increase in one percent of Trunk fat. Moreover, the odds ratio of FBS for an increase in one unit of Body fat percent and Trunk fat percent increased by 1.05 (adjusted odds ratio [95% CI: 1.03, 1.06]) and 1.05 (95% CI: 1.02, 1.08). Also, the risk of increased Fasting Insulin was 1.05 (95% CI: 1.03–1.07) for an increase in one unit of Body fat percent, and 1.05 (95% CI: 1.02–1.08) for an increase in one unit of Trunk fat percent. Conclusions The findings of the present study showed that there was a significant relationship between HOMA-IR, Fasting blood sugar, Fasting Insulin, and 2 h Insulin with percent of Body fat, percent of Trunk fat.


2010 ◽  
Vol 55 (10) ◽  
pp. A70.E660
Author(s):  
Nikolaos Alexopoulos ◽  
Dalton S. McLean ◽  
Matthew Janik ◽  
Chesnal Arepalli ◽  
Arthur E. Stillman ◽  
...  

2014 ◽  
Vol 55 (3) ◽  
pp. 197-203 ◽  
Author(s):  
Se-Hong Kim ◽  
Ju-Hye Chung ◽  
Beom-June Kwon ◽  
Sang-Wook Song ◽  
Whan-Seok Choi

2020 ◽  
Author(s):  
Emmanuel Cosson ◽  
Minh Tuan Nguyen ◽  
Imen Rezgani ◽  
Sopio Tatulashvili ◽  
Meriem Sal ◽  
...  

Abstract Background Epicardial adipose tissue (EAT) has anatomic and functional proximity to the heart and is considered a novel diagnostic marker and therapeutic target in cardiometabolic diseases. The aim of this study was to evaluate whether EAT volume was associated with coronary artery calcification (CAC) in people living with diabetes, independently of confounding factors.Methods We included all consecutive patients with diabetes whose EAT volume and CAC score were measured using computed tomography between January 1, 2019 and September 30, 2020 in the Department of Diabetology-Endocrinology-Nutrition at Avicenne Hospital, France. Determinants of EAT volume and a CAC score ≥ 100 Agatston units (AU) were evaluated.Results The study population comprised 409 patients (218 men). Mean (± standard deviation) age was 57 ± 12 years, and 318, 56 and 35, had type 2 (T2D), type 1 (T1D), or another type of diabetes, respectively. Mean body mass index (BMI) was 29 ± 6 kg/m², mean AET volume 93 ± 38 cm3. EAT volume was positively correlated with age, BMI, pack-year smoking history and triglyceridaemia, but negatively correlated with HDL-cholesterol level. Furthermore, it was lower in people with retinopathy, but higher in men, in Caucasian people, in patients on antihypertensive and lipid-lowering medication, in people with nephropathy, and finally in individuals with a CAC ≥ 100 AU (CAC < 100 vs CAC ≥ 100: 89 ± 35 vs 109 ± 41 cm3, respectively, p < 0.05). In addition to EAT volume, other determinants of CAC ≥ 100 AU (n = 89, 22%) were age, T2D, ethnicity, antihypertensive and lipid-lowering medication, cumulative tobacco consumption, retinopathy, macular edema and macrovascular disease. Multivariable analysis considering all these determinants as well as gender and BMI, showed that EAT volume was independently associated with CAC ≥ 100 AU (per 10 cm3 increase: OR 1.11 [1.02–1.20]).Conclusions EAT volume was independently associated with CAC. As it may play a role in coronary atherosclerosis in patients with diabetes, reducing EAT volume through physical exercise, improved diet and pharmaceutical interventions may improve future cardiovascular risk outcomes in this population.


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