Epicardial Adipose Tissue in Cardiovascular Disease

Author(s):  
Gabriela Berg ◽  
Verónica Miksztowicz ◽  
Celina Morales ◽  
Magalí Barchuk
2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Regitse H. Christensen ◽  
Bernt Johan von Scholten ◽  
Christian S. Hansen ◽  
Magnus T. Jensen ◽  
Tina Vilsbøll ◽  
...  

Author(s):  
Yun Hwan Kim ◽  
Min Ki Jeong ◽  
Hyuntae Park ◽  
Sang Kab Park

Regular exercise has been proven to prevent hypertension and to help in the management of hypertension. There is a lack of studies examining changes in these issues as a result of Taekwondo training intervention. The aim of the current trial is to identify the effects of a regular Taekwondo (TKD) training program on health-related physical fitness (HRPF), cardiovascular disease (CVD) risk factors, inflammatory factors, and epicardial adipose tissue (EAT) in elderly women with hypertension. To accomplish this, 20 participants, who were older women with hypertension, were divided into a TKD group (n = 10) and a control group (n = 10). The TKD program was conducted in program for 90 min, three times a week, for 12 weeks. Outcomes, including body composition, blood pressure (BP), HRPF, cardiovascular risk factor and EAT, were measured before and after the Taekwondo program. The 12-week TKD program improved body composition, BP, HRPF, CVD risk factor, and EAT in elderly women with hypertension relative to controls. Meanwhile, EAT and interukin-1β (r = 0.530, p < 0.05), monocyte chemotactic protein-1 (r = 0.524, p < 0.05), triglyceride (r = 0.493, p < 0.05) and sedentary behavior (r = 0.459, p < 0.05) presented a positive correlation, while EAT and lean body mass (r = −0.453, p < 0.05) showed a negative correlation. The 12-week regular TKD training intervention was found to be effective in reducing the thickness of EAT measured by multi-detector computed tomography and can also enhance health-related physical fitness and risk factors of CVD in older individuals with hypertension.


2017 ◽  
Vol 114 (2) ◽  
pp. 336-346 ◽  
Author(s):  
Esther Díaz-Rodríguez ◽  
Rosa M Agra ◽  
Ángel L Fernández ◽  
Belén Adrio ◽  
Tomás García-Caballero ◽  
...  

AbstractAimsIn patients with cardiovascular disease, epicardial adipose tissue (EAT) is characterized by insulin resistance, high pro-inflammatory chemokines, and low differentiation ability. As dapagliflozin reduces body fat and cardiovascular events in diabetic patients, we would like to know its effect on EAT and subcutaneous adipose tissue (SAT).Methods and resultsAdipose samples were obtained from 52 patients undergoing heart surgery. Sodium-glucose cotransporter 2 (SGLT2) expression was determined by real-time polymerase chain reaction (n = 20), western blot, and immunohistochemistry. Fat explants (n = 21) were treated with dapagliflozin and/or insulin and glucose transporters expression measured. Glucose, free fatty acid, and adipokine levels (by array) were measured in the EAT secretomes, which were then tested on human coronary endothelial cells using wound healing assays. Glucose uptake was also measured using the fluorescent glucose analogue (6NBDG) in differentiated stromal vascular cells (SVCs) from the fat pads (n = 11). Finally, dapagliflozin-induced adipocyte differentiation was assessed from the levels of fat droplets (AdipoRed staining) and of perilipin. SGLT2 was expressed in EAT. Dapagliflozin increased glucose uptake (20.95 ± 4.4 mg/dL vs. 12.97 ± 4.1 mg/dL; P < 0.001) and glucose transporter type 4 (2.09 ± 0.3 fold change; P < 0.01) in EAT. Moreover, dapagliflozin reduced the secretion levels of chemokines and benefited wound healing in endothelial cells (0.21 ± 0.05 vs. 0.38 ± 0.08 open wound; P < 0.05). Finally, chronic treatment with dapagliflozin improved the differentiation of SVC, confirmed by AdipoRed staining [539 ± 142 arbitrary units (a.u.) vs. 473 ± 136 a.u.; P < 0.01] and perilipin expression levels (121 ± 10 vs. 84 ± 11 a.u.).ConclusionsDapagliflozin increased glucose uptake, reduced the secretion of pro-inflammatory chemokines (with a beneficial effect on the healing of human coronary artery endothelial cells), and improved the differentiation of EAT cells. These results suggest a new protective pathway for this drug on EAT from patients with cardiovascular disease.


2015 ◽  
Vol 416 ◽  
pp. 77-87 ◽  
Author(s):  
Ricardo Lage ◽  
Isabel Moscoso ◽  
Ángel Fernández-Trasancos ◽  
María Cebro ◽  
Marinela Couselo ◽  
...  

2021 ◽  
Author(s):  
Xinyu Zou ◽  
Yingrui Li ◽  
Qiang She ◽  
Bin Liu

Abstract Background and aims: Increased epicardial adipose tissue (EAT) has been proposed as a risk factor for essential hypertension (EH). The aim of this study was to investigate the association of EAT with EH.Methods and results: PubMed, EMBASE, and Cochrane databases were systematically reviewed to identify relevant studies assessing the association of EAT thickness (EAT-t) and volume (EAT-v) with EH. There were 39 observational studies and 8,983 subjects included in the meta-analysis. The analysis indicated that hypertensive patients had a higher mean of EAT-t (SMD=0.64, 95% CI: 0.44-0.83, p<0.001) and EAT-v (SMD: 0.69, 95% CI:0.34-0.1.05, p<0.001) than normotensive individuals. Accordingly, we calculated pooled odds ratio (OR) and 95% confidence intervals (CI) for the association of EAT with EH, and the results showed that EAT-t (OR: 1.59, 95% CI: 1.09–2.33, P<0.001) and EAT-v (OR: 1.82, 95% CI: 1.33–2.19, P<0.001) were associated with essential hypertension. Additionally, higher mean of EAT-t (SMD=0.85, 95% CI=0.49-0.1.21, p<0.001) and EAT-v (SMD=0.83, 95% CI=0.31-1.34, p=0.002) were found in non-dipper hypertensive patients than those in dipper patients, but we didn’t find significant difference in EAT-t among patients with different grades of hypertension. We also investigated the association of EAT with complications in hypertensive patients, and the results showed that EAT was increased in patients with arteriosclerotic cardiovascular disease (ASCVD) or cardiac hypertrophy and dysfunction than those without. Conclusions: The increase in EAT was associated with the occurrence and complications of EH. The findings provide new information regarding the occurrence and complications of EH.


2020 ◽  
Vol 11 ◽  
pp. 204201882092882 ◽  
Author(s):  
Regitse Højgaard Christensen ◽  
Bernt Johan von Scholten ◽  
Louise Lang Lehrskov ◽  
Peter Rossing ◽  
Peter Godsk Jørgensen

Type 2 diabetes (T2D) is associated with an increased risk of cardiovascular disease and heart failure, which highlights the need for improved understanding of factors contributing to the pathophysiology of these complications as they are the leading cause of mortality in T2D. Patients with T2D have high levels of epicardial adipose tissue (EAT). EAT is known to secrete inflammatory factors, lipid metabolites, and has been proposed to apply mechanical stress on the cardiac muscle that may accelerate atherosclerosis, cardiac remodeling, and heart failure. High levels of EAT in patients with T2D have been associated with atherosclerosis, diastolic dysfunction, and incident cardiovascular events, and this fat depot has been suggested as an important link coupling diabetes, obesity, and cardiovascular disease. Despite this, the predictive potential of EAT in general, and in patients with diabetes, is yet to be established, and, up until now, the clinical relevance of EAT is therefore limited. Should this link be established, importantly, studies show that this fat depot can be modified both by pharmacological and lifestyle interventions. In this review, we first introduce the role of adipose tissue in T2D and present mechanisms involved in the pathophysiology of EAT and pericardial adipose tissue (PAT) in general, and in patients with T2D. Next, we summarize the evidence that these fat depots are elevated in patients with T2D, and discuss whether they might drive the high cardiometabolic risk in patients with T2D. Finally, we discuss the clinical potential of cardiac adipose tissues, address means to target this depot, and briefly touch upon underlying mechanisms and future research questions.


2013 ◽  
Vol 226 (1) ◽  
pp. 129-133 ◽  
Author(s):  
Mehmet Nuri Turan ◽  
Ozkan Gungor ◽  
Gulay Asci ◽  
Fatih Kircelli ◽  
Turker Acar ◽  
...  

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