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Evaluation of epicardial adipose tissue in familial partial lipodystrophy

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      Abstract

      Background

      Dunnigan type Familial Partial Lipodystrophy (FPLD) is characterized by loss of subcutaneous fat from the limbs and excessive accumulation on the visceral adipose tissue (VAT). Affected individuals have insulin resistance (IR), diabetes, dyslipidemia and early cardiovascular (CV) events, due to their imbalanced distribution of total body fat (TBF). Epicardial adipose tissue (EAT) is correlated with VAT. Hence, EAT could be a new index of cardiac and visceral adiposity with great potential as a marker of CV risk in FPLD.

      Objective

      Compare EAT in FPLD patients versus healthy controls. Moreover, we aimed to verify if EFT is related to anthropometrical (ATPM) and Dual-Energy X-ray Absorptiometry (DEXA) measures, as well as laboratory blood findings. We postulated that FPLD patients have enlarged EAT.

      Methods

      This is an observational, cross-sectional study. Six patients with a confirmed mutation in the LMNA gene for FPLD were enrolled in the study. Six sex, age and BMI-matched healthy controls were also selected. EFT was measured by transthoracic echocardiography (ECHO). All participants had body fat distribution evaluated by ATPM and by DEXA measures. Fasting blood samples were obtained for biochemical profiles and also for leptin measurements.

      Results

      Median EFT was significantly higher in the FPLD group than in matched controls (6.0 ± 3.6 mm vs. 0.0 ± 2.04 mm; p = 0.0306). Additionally, FPLD patients had lower leptin values. There was no significant correlation between EAT and ATPM and DEXA measurements, nor laboratory findings.

      Conclusions

      This study demonstrates, for the first time, that EAT measured by ECHO is increased in FPLD patients, compared to healthy controls. However, it failed to prove a significant relation neither between EAT and DEXA, ATPM or laboratory variables analyzed.

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      Most cited references 33

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      Human epicardial adipose tissue: a review.

      We discuss the anatomy, physiology, and pathophysiology of epicardial adipose tissue and its relationship to coronary atherosclerosis. Epicardial fat stores triglyceride to supply free fatty acids for myocardial energy production and produces adipokines. It shares a common embryological origin with mesenteric and omental fat. Like visceral abdominal fat, epicardial fat thickness, measured by echocardiography, is increased in obesity. Epicardial fat could influence coronary atherogenesis and myocardial function because there is no fibrous fascial layer to impede diffusion of free fatty acids and adipokines between it and the underlying vessel wall as well as the myocardium. Segments of coronary arteries lacking epicardial fat or separated from it by a bridge of myocardial tissue are protected against the development of atherosclerosis in those segments. However, when epicardial fat is totally absent in congenital generalized lipodystrophy, coronary atherosclerosis can still occur. Macrophages are more numerous and densely packed in the periadventitial fat of human atherosclerotic coronary arteries with lipid cores than in that of fibrocalcific or nonatherosclerotic coronary arteries. In obese patients with multiple cardiovascular risk factors, epicardial fat around atheromatous coronaries secretes several proinflammatory cytokines and is infiltrated by macrophages, lymphocytes, and basophils. Epicardial adipokine expression in obesity without coronary atherosclerosis has not been determined. In nonobese patients, epicardial fat around atheromatous coronary arteries expresses proinflammatory cytokines but produces either less adiponectin, a vasoprotective adipokine, than fat around nonatheromatous coronaries or a similar amount compared with thoracic subcutaneous fat. Further studies should be done to test the hypothesis that adipokines produced by and released from human epicardial adipose tissue might contribute locally to the pathogenesis of coronary atherosclerosis.
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        Epicardial fat from echocardiography: a new method for visceral adipose tissue prediction.

        To validate transthoracic echocardiography as an easy and reliable imaging method for visceral adipose tissue (VAT) prediction. VAT is recognized as an important indicator of high cardiovascular and metabolic risk. Several methods are applied to estimate VAT, with different results. We selected 60 healthy subjects (29 women, 31 men, 49.5 +/- 16.2 years) with a wide range of body mass indexes. Each subject underwent transthoracic echocardiogram and magnetic resonance imaging (MRI) to measure epicardial fat thickness on the right ventricle. Measurements of epicardial adipose tissue thickness were obtained from the same echocardiographic and MRI views and points. MRI was also used to measure VAT cross-sectional areas at the level of L4 to L5. Anthropometric indexes were also measured. Subjects with predominant visceral fat accumulation showed higher epicardial adipose tissue thickness than subjects with predominant peripheral fat distribution: 9.97 +/- 2.88 vs. 4.34 +/- 1.98 (p = 0.005) and 7.19 +/- 2.74 vs. 3.43 +/- 1.64 (p = 0.004) in men and women, respectively. Simple linear regression analysis showed an excellent correlation between epicardial adipose tissue and waist circumference (r = 0.895, p = 0.01) and MRI abdominal VAT (r = 0.864, p = 0.01). Multiple regression analysis showed that epicardial adipose tissue thickness (r(2) = 0.442, p = 0.02) was the strongest independent variable correlated to MRI VAT. Bland test confirmed the good agreement between the two methods. Epicardial adipose tissue showed a strong correlation with anthropometric and imaging measurements of VAT. Hence, transthoracic echocardiography could be an easy and reliable imaging method for VAT prediction.
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          Epicardial fat: properties, function and relationship to obesity.

           C Rabkin (2007)
          Epicardial fat is a relatively neglected component of the heart. The purpose of this review was to examine the anatomic and biochemical data on epicardial fat; to examine the relationship of epicardial fat to obesity and to explore the potential role of epicardial fat in the relationship of obesity to coronary atherothrombotic disease. Epicardial fat covers 80% of the heart's surface and constitutes 20% of total heart weight. It is present along the distribution of the coronary arteries, over the right ventricle especially along the right border, anterior surface and at the apex. There is three- to fourfold more epicardial fat associated with the right than the left ventricle. Putative physiologic functions of epicardial fat are based on observational data and include: buffering coronary arteries against the torsion induced by the arterial pulse wave and cardiac contraction, facilitating coronary artery remodelling, regulating fatty acid homeostasis in the coronary microcirculation and providing fatty acids to cardiac muscle as a local energy source in times of high demand. A considerable amount of the data on epicardial fat originates from autopsy series that have the inherent problem that conditions leading to death may have altered body composition and adiposity. With this caveat, data indicate that epicardial fat mass increases age until age 20-40 years but thereafter the amount of epicardial fat is not dependent on age. The amount of epicardial fat correlates with heart weight but the presence of myocardial ischemia and hypertrophy does not alter the ratio of epicardial fat to cardiac muscle mass. A number of properties differentiate epicardial fat from other fat depots specifically its smaller adipocytes size; different fatty acid composition, high protein content; high rates of fatty acid incorporation, fatty acid synthesis, insulin-induced lipogenesis or fatty acid breakdown; low rates of glucose utilization, low expression (mRNA) of lipoprotein lipase, stearoyl-CoA desaturase and acetyl-CoA carboxylase-alpha, and slow regression during weight loss. There is a significant direct relationship between the amount of epicardial fat and general body adiposity. Clinical imaging studies have demonstrated a strong direct correlation between epicardial fat and abdominal visceral adiposity. Several lines of evidence support a role for epicardial fat in the pathogenesis of coronary artery disease, namely the close anatomic relationship between epicardial fat and coronary arteries; the positive correlation between the amount of epicardial fat and the presence of coronary atherosclerosis and the ability of adipose tissue to secrete hormones and cytokines that modulate coronary artery atherothrombosis. Thus, epicardial fat maybe an important factor responsible for cardiovascular disease in obesity.
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            Author and article information

            Affiliations
            [ ]Metabolism Unit, State Institute of Diabetes and Endocrinology, IEDE, Rio de Janeiro, Brazil
            [ ]National Cardiology Institute of Laranjeiras, Rio de Janeiro, Brazil
            Contributors
            godoymatos@openlink.com.br
            dracynthiavalerio@gmail.com
            julibbraganca@gmail.com
            rico_de_oliveira@yahoo.com.br
            rlzagury@globo.com
            rodolfolustosa@yahoo.com.br
            gabccamargo@gmail.com
            cesar_nascimento@terra.com.br
            rom_br@yahoo.com
            Journal
            Diabetol Metab Syndr
            Diabetol Metab Syndr
            Diabetology & Metabolic Syndrome
            BioMed Central (London )
            1758-5996
            1 April 2015
            1 April 2015
            2015
            : 7
            4391299 24 10.1186/s13098-015-0024-5
            © Godoy-Matos et al.; licensee BioMed Central. 2015

            This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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            © The Author(s) 2015

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