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Review article
Epicardial adipose tissue: A cardiovascular risk marker to evaluate in chronic kidney disease
Tejido adiposo epicárdico: un marcador de riesgo cardiovascular a evaluar en la enfermedad renal crónica
Luis D’Marcoa,
Corresponding author
luisgerardodg@hotmail.com

Corresponding author.
, Marie Cortezb, María Salazarb, Marcos Lima-Martínezb, Valmore Bermúdezc
a Hospital Clínico Universitario, INCLIVA, Nephrology Department, Valencia, Spain
b Unidad Avanzada de Investigación y Diagnóstico Ecográfico y Renal, Clínica Puerto Ordaz, Venezuela
c Universidad Simón Bolívar, Facultad de Ciencias de la Salud, Barranquilla, Colombia
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Chronic kidney disease &#40;CKD&#41; is a true inflammatory condition and it is associated with multiple cardiovascular &#40;CV&#41; risk factors&#46;<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">1</span></a> In fact&#44; patients with CKD are at significantly higher risk of suffering a CV event than individuals in the general population with normal kidney function&#46;<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">2</span></a> The main causes of CV complication in these patients are left ventricular hypertrophy and coronary arterial disease&#46;<a class="elsevierStyleCrossRefs" href="#bib0270"><span class="elsevierStyleSup">3&#44;4</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Clinical evidence has shown that visceral adipose tissue &#40;VAT&#41; is an important CV risk marker&#46;<a class="elsevierStyleCrossRefs" href="#bib0280"><span class="elsevierStyleSup">5&#44;6</span></a> For example&#44; there seems to be a connection between VAT and CV disease in diseases which are as common as metabolic syndrome&#44; diabetes and arterial hypertension&#46;<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">7</span></a> Recognition that adipocytes are a type of cell with complex functioning and endocrine&#44; paracrine and autocrine capacity has aroused interest in researching them in disciplines such as molecular biology&#44; endocrinology&#44; nephrology&#44; cardiology and immunology&#46; This makes it a fertile ground for scientific debate&#44; given their broad heterogeneity in terms of location&#44; functions&#44; proteomics and metabolomics&#46; In fact&#44; these characteristics are of particular importance in VAT&#44; where changes in function and volume are associated with greater cardiometabolic risk&#46;<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">8</span></a></p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Epicardial adipose tissue</span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Anatomy and function</span><p id="par0015" class="elsevierStylePara elsevierViewall">Different regions of extra-abdominal adipose tissue have been studied in recent years&#46; Thus epicardial adipose tissue &#40;EAT&#41; has been said to be a specific risk marker in coronary disease&#46;<a class="elsevierStyleCrossRefs" href="#bib0300"><span class="elsevierStyleSup">9&#44;10</span></a> More specifically&#44; EAT represents the fat that is confined within the pericardial sac and located on the surface of the heart&#44; covering the epicardial portion of the coronary arteries&#46;<a class="elsevierStyleCrossRef" href="#bib0310"><span class="elsevierStyleSup">11</span></a> It varies in volume within a range from 68<span class="elsevierStyleHsp" style=""></span>cm<span class="elsevierStyleSup">3</span> to 124<span class="elsevierStyleHsp" style=""></span>cm<span class="elsevierStyleSup">3</span>&#44; representing approximately from 15&#37; to 20&#37; of total cardiac volume and covering approximately 80&#37; of the cardiac surface&#46;<a class="elsevierStyleCrossRef" href="#bib0305"><span class="elsevierStyleSup">10</span></a> In physiological terms it has mechanical&#44; biochemical and heat-regulating functions&#46;<a class="elsevierStyleCrossRef" href="#bib0315"><span class="elsevierStyleSup">12</span></a> Nevertheless&#44; under pathological conditions EAT affects the heart and coronary arteries locally by means of paracrine and vasocrine activity&#44; with the secretion of proinflammatory cytokines&#46;<a class="elsevierStyleCrossRefs" href="#bib0320"><span class="elsevierStyleSup">13&#8211;15</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">The EAT may be detected by means of different imaging techniques&#46; Ultrasound scan was one of the first techniques used for this purpose&#44; and it is both economical and rapid to use&#46; Nevertheless&#44; magnetic resonance imaging and computed axial tomography &#40;CAT&#41; are able to give a better and more suitable visualisation and measurement of the tissue&#44; due to their high spatial resolution&#46;<a class="elsevierStyleCrossRefs" href="#bib0335"><span class="elsevierStyleSup">16&#44;17</span></a> Additionally&#44; CAT makes it possible to simultaneously evaluate coronary arterial calcium &#40;CAC&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0345"><span class="elsevierStyleSup">18&#44;19</span></a><a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a> describes a cardiac CAT study&#44; showing the EAT coloured&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Other cardiac fat deposits</span><p id="par0025" class="elsevierStylePara elsevierViewall">EAT must not be confused with another type of localised cardiac fat deposit&#58; pericardial adipose tissue &#40;PAT&#41; which&#44; unlike EAT&#44; is located outside the visceral pericardium over the external surface of the parietal pericardium&#46;<a class="elsevierStyleCrossRef" href="#bib0355"><span class="elsevierStyleSup">20</span></a> Both tissues have different origins&#58; EAT originates in the splacno pleural layer of the mesoderm&#44; as does VAT&#44; while PAT originates in the primitive thoracic mesenchyme&#59; this is why local circulation too differs in both tissues&#59; thus epicardial fat is irrigated by the coronary arteries &#40;sharing the same microcirculation as the myocardium&#41;&#44; while pericardial fat is irrigated by the pericardiophrenic branches of the internal mammary artery&#46;<a class="elsevierStyleCrossRef" href="#bib0315"><span class="elsevierStyleSup">12</span></a> Due to this close relationship between EAT&#44; the myocardium and the coronary arteries&#44; the volume and function of EAT has been linked to the genesis and progression of coronary atherosclerosis&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Epicardial adipose tissue and metabolism</span><p id="par0030" class="elsevierStylePara elsevierViewall">Current evidence indicates that it is possible that adipose tissue next to coronary vessel walls permits the diffusion or transport through the <span class="elsevierStyleItalic">vasa vasorum</span> of proinflammatory cytokines or adipocytokines produced by the adipocytes&#44; such as tumour necrosis factor alpha&#44; interleukin 6 &#40;IL-6&#41;&#44; leptin&#44; resistin and visfatin&#44; among others&#46;<a class="elsevierStyleCrossRef" href="#bib0325"><span class="elsevierStyleSup">14</span></a> As a whole these elements cause local endothelial dysfunction&#44; with an increase in the lipotoxicity-mediated expression of adhesion and oxidative stress molecules towards the endoplasmatic reticule via overload of free fatty acids in the surrounding tissues&#44; where hypertrigliceridemia and insulin resistance associated with obesity and metabolic syndrome degrade the conditions of this microenvironment&#46;<a class="elsevierStyleCrossRefs" href="#bib0325"><span class="elsevierStyleSup">14&#44;21</span></a> Finally&#44; this process favours the binding and increased dwell time in the subendothelium of low-density lipoproteins and other proatherogenic ApoB lipoproteins&#44; such as intermediate density lipoprotein and &#40;a&#41; lipoprotein&#46; The oxidative and non-oxidative modifications of these proteins make the subendothelium a niche for immunocompetent cells such as macrophages&#44; T cells&#44; monocytes and modified smooth muscle cells&#46; When these cells interact within this medium they give rise to the functional and morphological alterations that typify the atherosclerotic plaque&#46;<a class="elsevierStyleCrossRefs" href="#bib0365"><span class="elsevierStyleSup">22&#44;23</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">The possibility that EAT may activate myocardiocyte pathways that alter its proteomic pattern and in turn its endocrine secretor capacity is far more interesting&#46; The discovery of natriuretic peptides therefore altered the view of the heart as a simple mechanical pump&#44; showing it to be an organ that is able to modify its performance by interacting with the rest of the organism by producing these hormonal messengers&#46; Three natriuretic peptides have been studied to date&#44; including atrial natriuretic peptide &#40;ANP&#44; produced in the atria&#41;&#44; type B natriuretic peptide B &#40;BNP&#44; produced in the ventricles&#41; and type C natriuretic peptide &#40;CNP&#44; produced in the endothelial cells&#41;&#46; In general&#44; ANP and BNP are secreted in very small amounts&#44; although some conditions &#40;such as CKD&#41;&#44; which involve an increase in the mechanical loading and stress of the wall due to ventricular hypertrophy&#44; hypertension&#44; inflammation&#44; fibrosis and hypoxia&#44; may stimulate the production and secretion of these mediators&#46; High levels of both markers are therefore well-known cardiovascular risk markers&#46;<a class="elsevierStyleCrossRefs" href="#bib0375"><span class="elsevierStyleSup">24&#8211;26</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Classically&#44; research in this area has concentrated on exploring the haemodynamic effects of these hormones on the heart-kidney axis&#46; Nevertheless&#44; in the last decade the discovery of receptors in the adipose tissue for natriuretic peptides has opened a productive area of study of hormonal signalling between these tissues and its metabolic effects&#46; These effects go beyond the initial concept that adipose tissue solely intervenes in the removal of natriuretic peptides from the circulation&#46; However&#44; it was then found that adipose tissue expresses natriuretic peptide receptor-1 and 2 &#40;NPR-1 and NPR-2&#41; protein&#44; which is able to interact with ANP as well as with BNP with a high degree of affinity&#44; activating c-protein kinase G signalling via guanilate cyclase-GMP translocation&#44; activating the hormone-sensitive lipase within the adipocyte and then lipolysis&#46; On the other hand&#44; the activation of the MAP kinase&#47;p38 cascade causes an increase in the oxidisation of fatty acids and the activation of thermogenesis by induction of UCP1 synthesis&#46;<a class="elsevierStyleCrossRef" href="#bib0390"><span class="elsevierStyleSup">27</span></a> Thus the overload of fatty acids within adipose tissue may affect many tissues&#44; such as hepatic tissue &#40;stimulating the production of hepatic glucose&#41;&#44; beta cells &#40;apoptosis and alterations in the insulin secretion pattern&#41;&#44; nerve tissue &#40;altering the production and clearance of Tau proteins&#41;&#44; striated muscle tissue &#40;insulin resistance&#41; and cardiomyocyte tissue &#40;changing the energy consumption pattern&#44; with higher O2 consumption&#44; cardiotoxicity and increased arrythmogenesis&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0395"><span class="elsevierStyleSup">28</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">On the contrary&#44; signalling by receptor NPR-3&#8212;the expression of which increases in type 2 diabetes and obesity&#8212;leads to internalisation and degradation of the natriuretic peptides&#44; cancelling out any systemic beneficial effect of these hormones&#46; In fact&#44; a low concentration of ANP&#44; BNP and CNP is associated with the presence of insulin resistance and diabetes&#46;<a class="elsevierStyleCrossRef" href="#bib0400"><span class="elsevierStyleSup">29</span></a></p></span></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Epicardial adipose tissue and chronic kidney disease</span><p id="par0050" class="elsevierStylePara elsevierViewall">Although the literature which evaluates EAT in CKD is always developing&#44; some studies have detected a connection between EAT and the presence of CAC in small groups of patients with kidney involvement&#46; One of the first studies was undertaken in 80 patients with CKD under dialysis and 27 controls&#46;<a class="elsevierStyleCrossRef" href="#bib0405"><span class="elsevierStyleSup">30</span></a> They were tested to detect atherosclerosis-inflammation-malnutrition syndrome &#40;AIM&#41; by measuring serum levels of albumin and reactive C protein&#44; while CAT and EAT were quantified by CAT&#46; EAT was significantly associated with the components of AIM syndrome&#44; and there was a proportional relationship between the increase in the volume of EAT and the presence of CAC&#46; Kerr et al&#46; studied 94 patients with grade 3&#8211;5 CKD who were not in dialysis&#44; reporting a lineal correlation with increased EAT and CAC and including other cytokines&#44; such as IL-6 and fibroblastic growth factor 23&#44; among others&#46;<a class="elsevierStyleCrossRef" href="#bib0410"><span class="elsevierStyleSup">31</span></a> Another study in a cohort of 411 patients with grade 4&#8211;5 CKD in dialysis who were being evaluated for kidney transplant found that EAT is a risk factor for alterations in myocardial perfusion&#44; as is the presence of CAC&#46;<a class="elsevierStyleCrossRef" href="#bib0350"><span class="elsevierStyleSup">19</span></a> EAT was found to be independently associated with CAC when predicting myocardial perfusion defects&#46; Karatas et al&#46; recently proved that the thickness of the EAT measured by echocardiograph is significantly greater in patients undergoing haemodialysis in comparison with those in pre-dialysis stages or healthy subjects&#46;<a class="elsevierStyleCrossRef" href="#bib0415"><span class="elsevierStyleSup">32</span></a> Likewise&#44; using a sub-analysis of the RIND study &#40;Renagel in new dialysis trial&#41;&#44; which firstly studied the presence of CAC and calcium and phosphorus alterations in patients who were commencing treatment with dialysis&#44; it was found that each 10<span class="elsevierStyleHsp" style=""></span>cc increase in the volume of EAT increased mortality by 6&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0420"><span class="elsevierStyleSup">33</span></a> Factors such as CAC and age were also associated with increased mortality&#46; Other publications have reported similar findings&#46;<a class="elsevierStyleCrossRefs" href="#bib0425"><span class="elsevierStyleSup">34&#8211;36</span></a> However&#44; other researchers found that EAT is not an isolated risk predictor&#44; but rather that it is a cofactor associated with the body mass index &#40;BMI&#41; and other obesity scales&#46;<a class="elsevierStyleCrossRefs" href="#bib0440"><span class="elsevierStyleSup">37&#44;38</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">In populations at risk and in patients with CKD&#44; EAT is not only associated with CAC&#46; Recent studies have shown that there is an association between EAT and extracoronary vascular calcifications in the aorta&#44; heart valves and carotid arteries&#46;<a class="elsevierStyleCrossRef" href="#bib0430"><span class="elsevierStyleSup">35</span></a> A lineal correlation has also been reported between an increase in EAT volume&#44; carotid intima-media thickness and left ventricular hypertrophy&#46;<a class="elsevierStyleCrossRefs" href="#bib0450"><span class="elsevierStyleSup">39&#44;40</span></a></p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Obesity&#44; nutrition and the kidneys</span><p id="par0060" class="elsevierStylePara elsevierViewall">Nutritional alterations are often found in patients with kidney disease&#46; The impact of kidney disease on body composition is in itself a morbimortality factor in this population&#46;<a class="elsevierStyleCrossRef" href="#bib0460"><span class="elsevierStyleSup">41</span></a> The most outstanding factors which lead to morbimortality include the presence of diabetes&#44; hypertension&#44; dyslipidemia&#44; chronic inflammatory states&#44; a lack of protein and calories in the diet&#44; immune dysfunction&#44; the depletion of lean mass&#44; micronutrient deficiency and a negative nitrogen balance&#44; among others&#46;<a class="elsevierStyleCrossRefs" href="#bib0465"><span class="elsevierStyleSup">42&#44;43</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">Although obesity is known to be a CV risk factor and obese patients are at higher risk of suffering CKD and even progressing more swiftly to advanced CKD once they are under dialysis&#44; paradoxically survival is longer the higher their BMI &#40;inverse epidemiology&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0470"><span class="elsevierStyleSup">43&#8211;45</span></a> Although this phenomenon is contrary to what is observed in the general population&#44; it has been observed in some risk groups &#40;the elderly and patients with congestive heart failure&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0485"><span class="elsevierStyleSup">46&#44;47</span></a> Possible explanations for these findings include protein-calorie deficiency&#44; a reduction in nutritional reserves&#44; metabolic acidosis and inflammation&#46;<a class="elsevierStyleCrossRef" href="#bib0495"><span class="elsevierStyleSup">48</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">More specifically&#44; this paradox observed in patients with CKD is associated with PEW &#40;protein-energy wasting&#41; and inflammation&#46;<a class="elsevierStyleCrossRef" href="#bib0500"><span class="elsevierStyleSup">49</span></a> Thus patients who have a lower BMI or bodyweight may have a higher degree of PEW&#44; and this would be the cause of increased morbimortality&#46; On the contrary&#44; overweight patients would have less deficiency in their ingestion of protein or energy and lower probability of developing PEW&#46;<a class="elsevierStyleCrossRefs" href="#bib0505"><span class="elsevierStyleSup">50&#44;51</span></a> Moreover&#44; it is known that undernourished patients are more susceptible to the harmful effects of the inflammatory process&#46;<a class="elsevierStyleCrossRef" href="#bib0500"><span class="elsevierStyleSup">49</span></a></p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Conclusions</span><p id="par0075" class="elsevierStylePara elsevierViewall">Finally&#44; EAT is associated with cardiovascular risk in the general population as well as in kidney patients&#46; It has yet to be determined whether&#44; once CKD progresses to advanced stages or treatment with dialysis begins&#44; changes are caused at EAT level which influence the prognosis of patients&#46; Future studies will have to be designed to cover this interesting question&#46;<elsevierMultimedia ident="tb0005"></elsevierMultimedia></p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Conflict of interests</span><p id="par0105" class="elsevierStylePara elsevierViewall">The authors have no conflict of interests to declare&#46;</p></span></span>"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Chronic kidney disease represents a true inflammatory state&#44; and is related to multiple cardiovascular risk factors&#46; Coronary artery disease is the major complication&#44; and has usually been associated with non-classical or uraemic related factors that include the disturbance of calcium and phosphorus metabolism&#44; among others&#46; Recent clinical evidence shows that specific body fat deposition like epicardial adipose tissue is an additional factor to consider when evaluating cardiovascular risk in the general population and kidney patients&#46; Direct interaction of this tissue and coronary vessels with consequent mediation of pro-atherogenic substances have a local process ending in endothelial damage&#46; Although the population of renal patients has been poorly evaluated&#44; future studies should determine precisely whether an increase in epicardial fat is truly associated with cardiovascular morbidity and mortality in this risk group&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">La enfermedad renal cr&#243;nica representa un verdadero estado inflamatorio y est&#225; relacionada con m&#250;ltiples factores de riesgo cardiovascular&#46; La enfermedad arterial coronaria es una de sus principales complicaciones y usualmente ha sido asociada con factores de riesgo cardiovascular no cl&#225;sicos o propios de pacientes ur&#233;micos como las alteraciones del metabolismo del calcio y el f&#243;sforo&#44; entre otros&#46; Evidencia cl&#237;nica reciente muestra que el dep&#243;sito de grasa &#243;rgano espec&#237;fico&#44; como el tejido adiposo epic&#225;rdico&#44; es un factor de riesgo adicional a tener en cuenta en el momento de la evaluaci&#243;n de riesgo cardiovascular en la poblaci&#243;n general y en los pacientes renales&#46; La interacci&#243;n directa de este tejido con los vasos coronarios y la consecuente mediaci&#243;n de sustancias proaterog&#233;nicas generan un proceso local que termina en la producci&#243;n de da&#241;o endotelial&#46; Aunque la poblaci&#243;n de enfermos renales ha sido evaluada escasamente&#44; estudios futuros determinar&#225;n con precisi&#243;n si un incremento en la adiposidad epic&#225;rdica est&#225; verdaderamente asociado a la morbimortalidad cardiovascular en este grupo de riesgo&#46;</p></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; D&#8217;Marco L&#44; Cortez M&#44; Salazar M&#44; Lima-Mart&#237;nez M&#44; Berm&#250;dez V&#46; Tejido adiposo epic&#225;rdico&#58; un marcador de riesgo cardiovascular a evaluar en la enfermedad renal cr&#243;nica&#46; Clin Investig Arterioscler&#46; 2020&#59;32&#58;129&#8211;134&#46;</p>"
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          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Computed axial tomography&#46; The magenta colour shows the epicardial adipose tissue&#46; Personal archive image&#46;</p>"
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          "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Key concepts</span><p id="par0080" class="elsevierStylePara elsevierViewall"><ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">&#8226;</span><p id="par0085" class="elsevierStylePara elsevierViewall">The risk of suffering a cardiovascular event is 10 times higher in chronic kidney patients than it is in the general population&#46;</p></li><li class="elsevierStyleListItem" id="lsit0010"><span class="elsevierStyleLabel">&#8226;</span><p id="par0090" class="elsevierStylePara elsevierViewall">Vascular calcifications consist of calcium deposits in the vascular intima and media&#59; calcifications of the heart valves are also included within this denomination&#46; Patients with CKD exhibit all of their forms&#46;</p></li><li class="elsevierStyleListItem" id="lsit0015"><span class="elsevierStyleLabel">&#8226;</span><p id="par0095" class="elsevierStylePara elsevierViewall">Epicardial adipose tissue is fat that is confined within the pericardial sac located on the surface of the heart&#59; it covers the epicardial portion of the coronary arteries&#46;</p></li><li class="elsevierStyleListItem" id="lsit0020"><span class="elsevierStyleLabel">&#8226;</span><p id="par0100" class="elsevierStylePara elsevierViewall">Nutritional alterations are common in kidney patients&#46; They run from severe protein-calorie deficiencies to chronic inflammatory conditions&#46;</p></li></ul></p></span></span>"
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es en pt

¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?

Você é um profissional de saúde habilitado a prescrever ou dispensar medicamentos