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.

Epicardial fat: properties, function and relationship to obesity.

Lipogenesis and the rate of fatty acid incorporation in vitro were studied in the pericardial and epicardial adipose tissue of the guinea-pig heart and in the liver and two larger adipose depots. Both lipogenesis and the rate of fatty acid incorporation were higher in the cardiac depots than in any of the other tissues studied. The rate of fatty acid incorporation were unaffected by insulin (0.1 U/ml) in the cardiac depots in contrast to all other tissues examined, and lipogenesis was increased by insulin in the cardiac depots, but not in the other adipose depots or liver. High-fat feeding increased the rate of fatty acid incorporation in vitro in all tissues examined, but the rates of lipogenesis were unchanged except in perirenal adipose tissue (decrease) and liver (increase). The data are consistent with the hypothesis that epicardial adipose tissue may act as a local energy store for cardiac muscle and have a protective role against elevated levels of free fatty acid in the coronary circulation.

Site-specific properties of pericardial and epicardial adipose tissue: the effects of insulin and high-fat feeding on lipogenesis and the incorporation of fatty acids in vitro.

The cuproenzymes lysyl oxidase, cytochrome-c oxidase, and superoxide dismutase are key factors in understanding the cardiac hypertrophy and cardiomyopathy associated with dietary copper res...

Newer Findings on a Unified Perspective of Copper Restriction and Cardiomyopathy

Although excess body fat is a significant health hazard, estimation of body fat content with the body mass index may not adequately reflect the amount of atherogenic adipose tissue (AT), i.e. visceral and ectopic fat. As opposed to subcutaneous AT that supposedly acts as a metabolic sink buffering excess dietary energy, visceral or intra-abdominal AT depots respond to several external stimuli that trigger lipolysis and secretion of free fatty acids (FFAs). Reaching the liver, FFAs accumulate in the liver and, over time, promote a chronic condition known as non-alcoholic fatty liver disease (NAFLD). The liver of the typical NAFLD patient secretes large amounts of very-low-density lipoproteins, the lipid content of which may accumulate in additional organs (skeletal muscle, heart, and pancreas). Here, we review the evidence emerging from functional and population studies that point towards an important role of ectopic fat accumulation in the pathophysiology of type 2 diabetes and cardiovascular disease. We conclude that although patients with impaired glycemic control or type 2 diabetes are at increased cardiovascular disease (CVD) risk, estimating cardiovascular risk goes wellbeyond the assessment of glycemic control and traditional CVD risk factors, and the estimation of visceral/ectopic fat deposition via readily available imaging techniquesshould be considered.

https://www.tandfonline.com/doi/pdf/10.3109/07853890.2011.605387

Mapping body fat distribution: a key step towards the identification of the vulnerable patient?

Background: To develop cardioprotection against peri-operative myocardial ischemia-reperfusion injury, we need animal models where the local metabolism and blood flow are studied concomitantly with the global circulatory consequences during regional coronary occlusion. Methods: In six anesthetized domestic pigs, the largest branch of the circumflex artery was occluded for 30 min. Microdialysate was sampled from the ischemic and non-ischemic myocardium along with continuous measurements of local coronary artery flow, global hemodynamics and registration of arrhythmias, from baseline through to 30 min of ischemia and 180 min of reperfusion. Results: During ischemia, the microdialysate glucose concentration decreased, the glycerol concentration increased and the lactate/pyruvate ratio increased significantly. For glycerol, there was a further increase at reperfusion. During ischemia, cardiac output was unchanged; however, during reperfusion there was a significant drop lasting for several minutes, longer than the period in which an increased number of arrhythmias were registered. Conclusion: The present study demonstrates deranged circulation and arrhythmias corresponding to ischemic metabolism after regional myocardial ischemia and reperfusion. Reperfusion induced more pronounced circulatory changes than the actual ischemia. A substantial increase in myocardial glycerol release seems to be a marker of ischemic metabolism and may prove to be an indicator of reperfusion injury.

Myocardial glycerol release, arrhythmias and hemodynamic instability during regional ischemia-reperfusion in an open chest pig model.

A morphological study of the sudanophilic lipids in dog and human hearts was carried out. The hearts of 5 mongrel dogs and 20 auricular appendices of human patients were utilized. The dog hearts were fixed in situ by perfusion with 2% glutaraldehyde, and the human tissue was fixed by immersion. For the ultrastructural study, some blocks of every portion of the specimen were postfixed in osmium and embedded in Epon. The topographical and quantitative study was done on frozen 20-mu sections of tissue stained with Sudan IV in propylene glycol and counterstained with hematein (Geigy). The results indicate that a significant quantity of visible triglycerides is extracellular and located in the interstitial spaces of the heart. The dimensions of these lipid droplets vary from 0.5 mu to more than 20 mu. The highest concentration was found in the epicardial region of the left ventricle, but a significant amount was found in the endocardium and in the middle portion of the myocardium. These observations indicate that a sizable portion of the heart interstitium is occupied by free droplets of triglycerides. This substrate pool is probably mobile and readily available as a source of energy.

Lipid droplets in the heart interstitium: concentration and distribution.

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Lipid droplets in the heart interstitium: concentration and distribution.