The Role of Inflammation in Epicardial Adipose Tissue in Heart Diseases

2018 ◽  
Vol 24 (3) ◽  
pp. 297-309 ◽  
Author(s):  
Zdenek Matloch ◽  
Anna Cinkajzlova ◽  
Milos Mraz ◽  
Martin Haluzik
Keyword(s):  
Adipose Tissue ◽  
Epicardial Adipose Tissue ◽  
Heart Diseases ◽  
Left Ventricular ◽  
Epicardial Fat ◽  
Cellular Interactions ◽  
Endocrine Organ ◽  
Adipose Tissue Depot ◽  
Electrocardiographic Abnormalities

Epicardial adipose tissue is not only a specific adipose tissue depot but also an active endocrine organ producing numerous substances with an important role in the development of obesity-related heart diseases. It is located between myocardium and visceral pericardium and consists predominantly of adipocytes, immunocompetent cells, ganglia and interconnecting nerve branches. Several studies documented a positive correlation between pericardial and epicardial fat and left ventricular hypertrophy and septal thickening, leading to diastolic dysfunction, electrocardiographic abnormalities and facilitating cardiac failure. The cellular cross-talks between epicardial fat and myocardium may include both the vasocrine and the paracrine mechanisms. Adipokines secreted from epicardial adipose tissue, vascular and stromal cells diffuse into interstitial fluid crossing the adventitia, media and intima and modulate cardiac function and cardiomyocyte phenotype and survival. In this article, we review the significance of epicardial adipose tissue and its association with cardiovascular diseases, cellular interactions between epicardial fat and myocardium, secretions of adipokines and inflammatory mediators and a potential of epicardial fat as a therapeutic target for the prevention of obesity-related heart diseases.

scholarly journals Macrophage Accumulation and Angiogenesis in Epicardial Adipose Tissue in Cardiac Patients with or without Chronic Heart Failure

2020 ◽  
Vol 10 (17) ◽  
pp. 5871
Author(s):  
Doina Butcovan ◽  
Veronica Mocanu ◽  
Daniel V. Timofte ◽  
Victor V. Costan ◽  
Radu Danila ◽  
...  
Keyword(s):  
Heart Failure ◽  
Adipose Tissue ◽  
Coronary Artery ◽  
Chronic Heart Failure ◽  
Epicardial Adipose Tissue ◽  
Left Ventricular ◽  
Epicardial Fat ◽  
Right Atrial ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

Routinely measuring epicardial fat had become a novel tool for cardiovascular risk stratification. Structural changes in epicardial adipose tissue (EAT), including fat thickness, inflammation, and angiogenesis, have been described in coronary artery disease (CAD) patients. We proposed to measure EAT thickness and characterize inflammatory infiltrate and angiogenesis in epicardial adipose tissue in CAD patients with and without chronic heart failure (CHF), established by cardiac dysfunction on echocardiography (left ventricular ejection fraction, LVEF ≤ 50%) and symptoms of heart failure (New York Heart Association (NYHA) functional class II or III).The study included 15 patients with CAD (demonstrated by coronary angiography),, who underwent right atrial appendages (RAA) excision during coronary artery bypass graft (CABG). The study was performed by histopathological, immunohistochemical (IHC), and morphometrical analysis. EAT thickness was assessed by using morphometry applied on routine histological stains. Inflammatory cell infiltration and angiogenesis were investigated immunohistochemically by using antibodies against CD68 and CD34 markers. Diminished EAT thickness in the CAD patients with CHF was associated with increased macrophage infiltration and reduced angiogenesis of the EAT as compared to CAD patients without CHF. In conclusion, the present study on epicardial fat samples of the RAA suggested that high expression of CD68 appeared to be associated with severe deterioration of heart function in CAD patients who underwent myocardial revascularization consisting of CABG.

scholarly journals Epicardial Fat, Paracrine-mediated Inflammation and Atrial Fibrillation

2017 ◽  
Vol 2 (4) ◽  
pp. 304-307
Author(s):  
Nora Rat ◽  
Adriana Mitre ◽  
Szilamér Korodi ◽  
István Benedek ◽  
Erzsébet Lázár ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Atrial Fibrillation ◽  
Adipose Tissue ◽  
Epicardial Adipose Tissue ◽  
Coronary Plaque ◽  
Inflammatory Biomarkers ◽  
Epicardial Fat ◽  
Local Inflammation ◽  
Complex Process

AbstractAtrial fibrillation is the most frequent arrhythmia in adults, becoming more frequent with age. Recent clinical studies demonstrated that epicardial fat is linked with atrial fibrillation induction and recurrence. The arrhythmogenic mechanism consists in the fact that the epicardial adipose tissue is metabolically active, inducing local inflammation and enhancing the oxidative stress, which lead to atrial fibrillation as well as atherosclerosis. Having metabolic activity and secreting various anti- and pro-inflammatory biomarkers, the fat surrounding the heart has been linked to the complex process of coronary plaque vulnerabilization. This clinical update aims to summarize the role of epicardial adipose tissue in the pathogenesis, persistence, and severity of atrial fibrillation.

scholarly journals Epicardial adipose tissue: pathophysiology and role in the development of cardiovascular diseases

2018 ◽  
Vol 17 (4) ◽  
pp. 254-263 ◽  
Author(s):  
E. G. Uchasova ◽  
O. V. Gruzdeva ◽  
Yu. A. Dyleva ◽  
O. E. Akbasheva
Keyword(s):  
Adipose Tissue ◽  
Cardiovascular Diseases ◽  
Molecular Mechanisms ◽  
Epicardial Adipose Tissue ◽  
Important Predictor ◽  
Epicardial Fat ◽  
Paracrine Signaling ◽  
Total Fat ◽  
Visceral Adipose

Visceral adipose tissue is an important predictor of cardiovascular diseases, which carry more risk than total fat accumulation. Epicardial fat, a special form of visceral fat deposited around the heart, is considered an important predictor of the risk of cardiovascular disease, taking into account the production and release of adipocytokines. Recently, the number of experimental and clinical data proving the physiological and metabolic significance of epicardial fat is increasing. The thickness and volume of epicardial adipose tissue (EAT) have a strong correlation with obesity, impaired fasting glucose, insulin resistance, metabolic syndrome and atherosclerosis. Moreover, it is now clear that the connection between EAT and the heart is regulated by complex two directional pathways, since not only adipokines regulate cardiac function, but the heart affects EAT via paracrine signaling. Further study of the molecular mechanisms regulating the interaction between the heart and EAT will improve our understanding of the role of the latter in cardiac physiology and the development of disease mechanisms.

scholarly journals Impact of epicardial adipose tissue increase after ST elevation Myocardial Infarction (STEMI) on IL-13 and left ventricular remodelling

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
V Parisi ◽  
S Cabaro ◽  
V D'Esposito ◽  
L Petraglia ◽  
M Conte ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Epicardial Adipose Tissue ◽  
Protective Role ◽  
Left Ventricular ◽  
Funding Source ◽  
National Budget ◽  
Group 2 ◽  
Public Grant ◽  
Group 1

Abstract Background The role of epicardial adipose tissue (EAT) in myocardial diseases is well established, and several evidence suggest that EAT may negatively affect left ventricular (LV) remodelling through an imbalanced production and secretion of pro and anti-inflammatory cytokines. Of these, the IL-13 it is known to play a positive activity on cardiac remodelling. Nowadays, the crosstalk between EAT and the myocardium is still poorly understood and the effects of myocardial ischemia on morphological and functional properties of EAT are almost unknown. Purpose In the present study we explored whether an increase of EAT thickness after STEMI might be associated with unfavourable LV remodelling at 3 months (T1). We also evaluated the relationship between changes (Δ) of EAT thickness and systemic levels of Interleukin (IL)-13 which is known to play a favourable activity on LV remodelling after STEMI. Methods We enrolled 66 patients with first STEMI, undergoing primary percutaneous angioplasty. At baseline and at 3 months we performed a complete echocardiogram, including EAT maximal thickness assessment, and determined circulating levels of IL-13. Results At 3 months after STEMI, the population was stratified into two groups according to different EAT remodelling after cardiac event: Group 1, patients with an increased EAT thickness (Δ EAT>1; 30 patients) and Group 2, patients with unchanged or decreased EAT thickness (Δ EAT<1). The two groups did not differ for age, gender and atherosclerotic risk factors. Group 1 had a worse LV remodelling at 3 months with higher LV diastolic and systolic volumes, lower LV ejection fraction (p=0.003; p=0.013; p=0.013 respectively) and worse diastolic function (E/e'; p=0.011). Of interest, EAT thickness increase was paralleled by circulating IL-13 reduction (p=0.022). Conclusion Myocardial injury can result in EAT increase which is associated to worse LV remodelling probably through the loss of the protective role of IL-13. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): This research has been funded by the University of Naples “Federico II” and “Compagnia di San Paolo e l'Istituto Banco di Napoli” within the competitive grant STAR 2018; Valentina Parisi is the principal investigator

The Role of Epicardial Adipose Tissue Lymphocytes in Low-Grade Inflammation and Coronary Artery Disease

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 469-P
Author(s):  
MILOS MRAZ ◽  
ANNA CINKAJZLOVA ◽  
ZDENA LACINOVÁ ◽  
JANA KLOUCKOVA ◽  
HELENA KRATOCHVILOVA ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Adipose Tissue ◽  
Coronary Artery ◽  
Epicardial Adipose Tissue ◽  
Low Grade ◽  
Artery Disease ◽  
Low Grade Inflammation

Epicardial adipose tissue: the genetics behind an emerging cardiovascular marker

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J.A Sousa ◽  
M.G Serrao ◽  
M Temtem ◽  
A Pereira ◽  
M Santos ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Cardiovascular Risk ◽  
Genetic Risk ◽  
Epicardial Adipose Tissue ◽  
Genetic Risk Score ◽  
Renin Angiotensin System ◽  
Epicardial Fat ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Genetic Burden

Abstract Background Increasing evidence points epicardial adipose tissue (EAT) as an emerging cardiovascular risk marker. Whether genetic polymorphisms are associated with a higher EAT burden is still unknow. Genetic risk score (GRS) is an emerging method that attempts to establish correlation between single nucleotide polymorphisms (SNPs) and clinical phenotypes. Aim Evaluate the role of genetic burden and its association to EAT. Methods 996 patients (mean age 59±8, 78% male) were prospectively enrolled in a single center. EAT was measured on cardiac CT using a modified simplified method. Patients were divided into 2 groups (above vs. below the median EAT volume). We studied different polymorphisms across the following gene-regulated pathways: oxidation, renin-angiotensin system, cellular, diabetes/obesity and dyslipidemia pathways. Genotyping was performed by TaqMan allelic discrimination assay. A multiplicative genetic risk score (mGRS) was constructed and represents the genetic burden of the different polymorphisms studied. To evaluate the relation between genetics and EAT volume, we compared both groups by: global mGRS, gene cluster/axis mGRS and individual SNPs. Results Patients with above-median EAT volume were older, had higher body mass index (BMI) and higher prevalence of hypertension, diabetes and dyslipidemia (p<0.05). Patients with higher EAT volumes presented a higher global mean GRS (p<0.001), with the latter remaining an independent predictor for higher EAT volumes (OR 1.3, 95% CI 1.2–1.5), alongside age and BMI. In the analysis by gene clusters, patients with more epicardial fat consistently presented a higher polymorphism burden (translated by a higher mGRS level) across numerous pathways: oxidation, renin-angiotensin system, cellular, diabetes/obesity and dyslipidemia. After adjusting for confounders and other univariate predictors of higher fat volume, the following have emerged as independently related to higher EAT volumes: mGRS comprising the genes of different clusters, age and BMI. Amongst the 33 genes analyzed, only MTHFR677 polymorphisms (a gene with a critical role in regulating plasma homocysteine levels) emerged as significantly related to higher EAT volumes in our population (OR 1.4, 95% CI: 1.100–1.684, p=0.005). Conclusion Patients with a higher polymorphism burden in genes involved in the oxidation, renin-angiotensin, cellular, diabetes/obesity and dyslipidemia pathways present higher levels of epicardial fat. This potential association seems to be independent from the expected association between epicardial fat and cardiovascular risk factors. To our knowledge, this is the first time such genetic profiling has been done, casting further insight into this complex matter. Funding Acknowledgement Type of funding source: None

scholarly journals Quantification of Epicardial and Thoracic Adipose Tissue using WOA Optimized CNN

2019 ◽  
Vol 8 (9S2) ◽  
pp. 720-724
Keyword(s):  
Adipose Tissue ◽  
Optimization Algorithm ◽  
Selection Process ◽  
Heart Diseases ◽  
Epicardial Fat ◽  
Fat Depots ◽  
Krill Herd ◽  
Whale Optimization ◽  
Fully Automatic ◽  
Paracardial Fat

Cardiac fat depots are associated with the heart diseases. Epicardial fat and thoracic fat plays the major role in the development of cardiovascular disease. The increased thickness of the epicardial and thoracic fat leads to several diseases such as metabolic syndrome, coronary atherosclerosis, etc. It is necessary to quantify the epicardial adipose tissue and thoracic adipose tissue. There are different imaging and assessing techniques for epicardial and thoracic adipose tissue quantification. These tissues can be quantified automatically or manually from the CT and MRI cardiac scans. The quantification of the epicardial fat and thoracic fat requires segmentation of these fats by various segmentation methods and then they are quantified. This project proposes the fully automatic segmentation and quantification of the epicardial and thoracic adipose tissues from the cardiac CT scan images using the krill herd optimization algorithm and fuzzy c-means segmentation algorithm. The whale optimization algorithm performs the feature selection process. The fuzzy cmeans algorithm is used for the segmentation process by means of clustering which segments the epicardial fat and paracardial adipose tissue(EAT &PAT) from the input image. The segmented epicardial and paracardial fat region are then used for the quantification process which provides the epicardial and thoracic fat volume. The thoracic fat is the combination of the epicardial and paracardial fat. This proposed system is implemented by using the MATLAB code. The proposed system is simple, fully automatic and produces accurate results.

scholarly journals Epicardial Adipose Tissue Role as a Marker of Higher Vulnerability in Patients with Coronary Artery Disease

2018 ◽  
Vol 3 (2) ◽  
pp. 77-83 ◽  
Author(s):  
Tiberiu Nyulas ◽  
Mirabela Morariu ◽  
Nora Rat ◽  
Emese Marton ◽  
Victoria Ancuta Rus ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Left Ventricular Ejection Fraction ◽  
Left Ventricle ◽  
Epicardial Adipose Tissue ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
The Mean ◽  
Group 2 ◽  
Group 1

Abstract Background: Epicardial adipose tissue (EAT) has been recently identified as a major player in the development of the atherosclerotic process. This study aimed to investigate the role of EAT as a marker associated with a higher vulnerability of atheromatous coronary plaques in patients with acute myocardial infarction (AMI) as compared to patients with stable angina. Material and methods: This analysis enrolled a total of 89 patients, 47 with stable angina (SA) and 42 with AMI, who underwent echocardiographic investigations and epicardial fat measurement in 2D-parasternal long axis view. The study lot was divided as follows: Group 1 included patients with prior AMI, and Group 2 included patients with SA. Results: There were no significant differences between the two groups regarding cardiovascular risk factors, excepting smoking status, which was recorded more frequently in Group 1 as compared to Group 2 (36.17% vs. 11.63%, p = 0.02). The mean epicardial fat diameter was 9.12 ± 2.28 mm (95% CI: 8.45–9.79 mm) in Group 1 and 6.30 ± 2.03 mm (95% CI: 5.675–6.93 mm) in Group 2, the difference being highly significant statistically (p <0.0001). The mean value of left ventricular ejection fraction was significantly lower in patients with AMI (Group 1 – 47.60% ± 7.96 vs. Group 2 – 51.23% ± 9.05, p = 0.04). EAT thickness values showed a weak but significant positive correlation with the level of total cholesterol (r = −0.22, p = 0.03) and with the value of end-systolic left ventricle diameter (r = 0.33, = 0.001). Conclusions: The increased thickness of EAT was associated with other serum- or image-based biomarkers of disease severity, such as the left ventricular ejection fraction, end-systolic diameter of the left ventricle, and total cholesterol. Our results indicate that EAT is significantly higher in patients with acute coronary syndrome, proving that EAT could serve as a marker of vulnerability in cardiovascular diseases.

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