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ISSN: 2327-5146
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Ectopic Cardiac Depots, Inflammation and Cardiovascular Disease

Roever L1*, Casella-Filho A2, Dourado PMM2 and Chagas ACP2
1Laboratory of Vascular Biology, Heart Institute (InCor), HCFMUSP- University of São Paulo Medical School, São Paulo, Brazil
2Faculdade de Medicina do ABC, Santo André, Brazil
Corresponding Author : Leonardo S. Roever-Borges
Laboratory of Vascular Biology, Heart Institute (InCor)
University of São Paulo Medical School
Av. Dr. Enéas de Carvalho Aguiar, 44, 05403-900 - São Paulo, Brazil
Tel: 55-11 30695259
Fax: 55-11 30695261
E-mail: [email protected]
Received February 10, 2014; Accepted March 25, 2014; Published April 30, 2014
Citation: Roever L, Casella-Filho A, Dourado PMM, Chagas ACP (2014) Ectopic Cardiac Depots, Inflammation and Cardiovascular Disease. Gen Med (Los Angel) 2:137. doi: 10.4172/2327-5146.1000137
Copyright: © 2014 Roever L, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Ectopic fat may cause anatomic and functional abnormalities in adipocyte and adipose tissue, resulting in imbalances in the endocrine and immune system. Adiposopathy may contribute to cardiovascular disease (CVD) through pericardiac and perivascular effects on the myocardium and blood vessels. Adiposopathy may also indirectly contribute to CVD promoting or worsening major CVD risk factors such as type 2 diabetes mellitus, hypertension and dyslipidemia. CVD is the most common cause of mortality among overweight individuals, but the pathophysiologic relationship between adiposity and CVD still is poorly understood, as evidenced by “obesity paradoxes”. Underlying this uncertainty are suggestions that excessive body fat does not always increase the risk of CVD and, in some cases, may actually decrease such risks. This review aims to address the recent aspects of the relationships between ectopic fat, inflammation and CVD.

Ectopic cardiac fat; Inflammation; Cardiac function; Atherosclerosis
Obesity is associated with significant cardiovascular morbidity and mortality [1-3]. Epicardial fat is an active organ and source of several bioactive molecules that can affect cardiac morphology and function [4-11]. Because of the close anatomical relationship to the heart, and the absence of fascia boundaries, epicardial adipose tissue may locally interact and modulate the coronary arteries and myocardium through paracrine and direct secretion of anti-inflammatory and proinflammatory adipokines [12,13]. Epicardial fat tissue surrounding the heart, called epicardial or pericardial fat, encases the coronary arteries, and is therefore a subtype of the perivascular adipose tissue that surrounds blood vessels and is clinically related to atherosclerosis and major anthropometric and metabolic predictors of increased cardiovascular risk [14-20]. A relationship between epicardial fat thickness, inflammation and cardiovascular disease has been reported [7,20] although this relationship is still under question [21]. This review will explore the current understanding of ectopic cardiac adipose tissue storage, and existing research supporting an association between ectopic cardiac fat, inflammation and cardiovascular disease.
Ectopic Cardiac Fat Depots and Local Effects
Ectopic fat depots include accumulation of adipose tissue surrounding the heart and coronary arteries, or via lipid accumulation within cardiomyocytes. Adipose tissue surrounding the heart, called epicardial or pericardial fat, encases the coronary arteries, and is therefore a subtype of the perivascular adipose tissue that surrounds blood vessels.
Previous translational work has shown that perivascular adipose tissue possesses anti contractile properties, and secreted substances such as adiponectin and the adipocyte derived relaxing factor play a role in the vasoactive properties of perivascular fat [22,23]. Interestingly, the anti contractile property of perivascular adipose tissue is abolished with the development of obesity [22]. Furthermore, obesity appears to reduce the physiological effect of perivascular fat on smooth muscle cell migration in animal models [24]. These alterations in the function of perivascular fat appear to correlate with the infiltration of the adipose tissue by macrophages and upregulation of inflammatory adipokines [25].
Consistent with this finding, epicardial fat harvested at the time of coronary artery bypass surgery was found to have higher levels of proinflammatory mediators in comparison with subcutaneous fat [26]. Inflammation in the heart may be a contributor to insulin resistance. Cytokines impair insulin signaling by activating intracellular signaling kinases such as Jun N-terminal kinase that impairs insulin signaling by increasing the serine phosphorylation of insulin resistence substrate proteins [27]. It is possible that this mechanism may potentially occur in cardiomyocytes. It has been reported that high-fat feeding increased inflammation in the obese mouse heart, as evidenced by interleukin- 6-mediated increases in macrophage and cytokine infiltration into the heart. In addition, glucose oxidation was reduced as a result of cardiac inflammation in an interleukin-6-dependent manner [28]. It remains to be demonstrated whether the local increase in myocardial inflammation directly contributes to impaired myocardial insulin action or the metabolic changes are secondary to systemic changes.
Population level research has supported the idea of a local toxic effect of pericardial fat. In the Framingham heart study, the volume of pericardial fat was associated with coronary artery calcium, but not cardio metabolic risk factors after Visceral Adipose Tissue (VAT) adjustment [29]. By contrast, VAT, which can be up to 20 times the volume of pericardial fat, was not associated with coronary artery calcium [29]. Similarly, pericardial fat was found to be associated with incident coronary heart disease in the multi-ethnic study of atherosclerosis (MESA) [30]. Additional research examining the associations of pericardial fat with measures of cardiac structure and function, and clinical cardiovascular disease, have shed further light on the idea of a local effect of pericardial fat [31,32]. First, pericardial fat volume assessed by computed tomography (CT) was found to be positively associated with (MRI) measured left atrial size in men [31]. Subsequent work supported these findings by demonstrating a positive association between pericardial adipose tissue and prevalent atrial fibrillation, which is known to be associated with left atrial size [33]. Although pericardial fat was associated with left ventricular mass, this association did not persist after additional adjustment for VAT [31]. These findings suggesthat the systemic effects of obesity appear to outweigh any local effect of pericardial fat in the case of left ventricular mass. In addition to adipose tissue surrounding the coronary arteries, intramyocardial lipid accumulation represents another manifestation of ectopic fat storage that may lead to a local adverse effect on the heart [34,35]. With the use of in vivo 1H magnetic resonance spectroscopy, higher amounts of cardiac steatosis have now been observed among individuals with impaired glucose tolerance and type-2 diabetes mellitus in comparison with lean individuals [36]. It is appropriate that the debate as to whether cardiac steatosis is merely a marker of metabolic disturbances or alternatively contributes directly to the development of cardiac dysfunction is ongoing since more studies are needed to distinguish between the two hypothesises.
In an attempt to resolve this issue, investigators used 1H magnetic resonance spectroscopy and found increases in intramyocardial lipid content after high-fat feeding in both wild-type mice and a mouse model of elevated triacylglyceride [34]. Not only did the transgenic mice demonstrate more lipid accumulation, but the increase in intramyocardial lipids was not solely triglycerides. In addition, after high-fat feeding, the transgenic, but not wild-type, mice demonstrated a reduction in systolic strain as assessed by cardiac-tagged MRI strain techniques. Overall, these findings support the possibility of a causal relationship between intramyocardial lipid accumulation and cardiac dysfunction.
Potential Mechanisms
Yudkin and colaborators [36] have hypothesized a pathogenic role of perivascular fat in local atherosclerosis via “vasocrine” pathways has been described in the vascular supply to the rat cremaster muscle [3]. This hypothesis states that fat deposits surrounding arteries that supply metabolically active tissue such as muscle, release substances that affecting vascular tone and thus limit the use of substrate to the tissues in times of excess calories. Differences in secretory products and gene expression profiles for leptin, adiponectin, IL-6, IL-8, and MCP- 1 have been demonstrated for subcutaneous fat, VAT and pericardial fat [37-43]. While animal research has demonstrated vaso-active substances expressed in aortic perivascular fat and up-regulation of pro-inflammatory gene expression in response to a high fat diet, complete expression profiles from this tissue in humans have not been described [44,45]. The composition of adipose tissue in specific deposits may also be responsible for regional differences. While pericardial fat is white adipose tissue, brown adipose tissue is known to be present in the thorax, and may not exert similar proinflammatory or vaso-active properties [46-50]. A substantial number of studies have shown that perivascular adipose tissue(PVAT) is a source of predominantly proinflammatory, cytokines and chemokines (Figure 1) [51-60].
Mazurek et al. found that epicardial PVAT from 42 patients who underwent elective coronary artery bypass graft (CABG) surgery excreted higher amounts of IL-1β, IL-6, IL- 6sR, and TNFα than subcutaneous adipose tissue from these this same patients [47,48]. In another study, IL-6 and IL-8 secretion in differentiated perivascular adipocytes was higher than in subcutaneous and peri- renal fat, as well as MCP-1 release [47-49]. Importantly, the amount of cytokines secreted by PVAT did not correlate with plasma cytokine concentrations. These findings illustrate the importance of adipose tissue location and that systemic concentrations of adipokines may not be representative of local concentrations in tissues. Also, the inflammatory properties of epicardial adipose tissue were independent of obesity. Aside from cytokines, PVAT is also a source of chemokines such as IL-8, MCP-1, and RANTES [47-50].
Although our understanding of ectopic cardiac fat depots has increased substantially in recent years, current works have uncovered areas of uncertainty. Further basic science and translational work will help clarify whether causal relations drive these associations. Many of the basic science studies -data have been limited to animal models. These will continue to be crucial to our understanding of ectopic fat depots, but additional investigations in human subjects will also be essential. Studies comparing and contrasting the different subtypes of ectopic fat have already highlighted important similarities and differences, and will continue to provide important insights. Further understanding of the effect of weight loss, drugs and exercise on specific fat depots will be equally important. Epicardial fat is an important role in inflammation and CVD [61].

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