Epicardial Fat in Nonalcoholic Fatty Liver Disease

Psychari, Stavroula N.; Rekleiti, Nectaria; Παπαϊωάννου, Νικόλαος; Varhalama, Evangelia; Drakoulis, C.; Αποστολου, Θωμασ; Iliodromitis, Efstathios K.

doi:10.1177/0003319715576672

Cited by 28 publications

(15 citation statements)

References 47 publications

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“…We also showed an independent association between EAT, NASH and significant liver fibrosis, confirming recent results [ 30 , 49 ]. Interestingly, in these patients we observed a significant independent association between EAT and atherosclerosis and between EAT and liver damage, supporting the hypothesis that the cytokines/adipocytokines secreted by epicardial adipose tissue, acting as a paracrine tissue, favor the local inflammation in vessel and liver, being responsible for the damage of these districts.…”

Section: Discussionsupporting

confidence: 92%

“…In the present study we analyzed in a large series of subjects with NAFLD whether EAT correlates with cardiovascular and liver damage and we demonstrated that EAT is associated both with subclinical atherosclerosis and NASH and significant fibrosis independently of other metabolic confounders (BMI, waist circumference, diabetes, hypertension....) and that there is a significant relationship between increased value of EAT and cardiovascular and liver damage and metabolic alterations. The relationships between EAT, and cardiovascular damage has been recently reported in selected patients series[ 16 , 27 – 30 , 49 – 52 ], however this is the first study, to our knowledge, performed in a large series of well characterized NAFLD patients in whom we demonstrated a significant correlation between EAT values and atherosclerosis as documented by the independent association with cplaques. Previous observations suggested an association between epicardial adiposity and the presence and severity of coronary artery disease[ 17 – 19 , 24 , 53 ], and more recently with vascular stiffness, another subclinical sign of carotid atherosclerosis [ 29 , 54 ].…”

Section: Discussionmentioning

confidence: 53%

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Epicardial Adipose Tissue (EAT) Thickness Is Associated with Cardiovascular and Liver Damage in Nonalcoholic Fatty Liver Disease

et al. 2016

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Background and AimsEpicardial adipose tissue (EAT) has been proposed as a cardiometabolic and hepatic fibrosis risk factor in patients with non alcoholic fatty liver disease (NAFLD). Aim of this study was to evaluate the role of EAT in NAFLD by analyzing 1) the association between EAT, the other metabolic parameters and the severity of steatosis 2) the relationship between cardiovascular (cIMT, cplaques, E/A), liver (presence of NASH and significant fibrosis) damage and metabolic risk factors including EAT 3) the relationship between EAT and genetic factors strongly influencing liver steatosis.MethodsIn a cross-sectional study, we considered 512 consecutive patients with NAFLD (confirmed by biopsy in 100). EAT, severity of steatosis, carotid intima-media thickness (cIMT) and plaques were evaluated by ultrasonography and results analysed by multiple linear and logistic regression models. Variables independently associated with EAT (mm) were female gender (p = 0.003), age (p = 0.001), BMI (p = 0.01), diastolic blood pressure (p = 0.009), steatosis grade 2 (p = 0.01) and 3 (p = 0.04), fatty liver index (p = 0.001) and statin use (p = 0.03). Variables independently associated with carotid IMT were age (p = 0.0001), hypertension (p = 0.009), diabetes (p = 0.04), smoking habits (p = 0.04) and fatty liver index (p = 0.02), with carotid plaques age (p = 0.0001), BMI (p = 0.03), EAT (p = 0.02),) and hypertension (p = 0.02), and with E/A age (p = 0.0001), diabetes (p = 0.005), hypertension (p = 0.04) and fatty liver index (p = 0.004). In the 100 patients with available liver histology non alcoholic steatohepatitis (NASH) was independently associated with EAT (p = 0.04) and diabetes (p = 0.054) while significant fibrosis with EAT (p = 0.02), diabetes (p = 0.01) and waist circumference (p = 0.05). No association between EAT and PNPLA3 and TM6SF2 polymorphisms was found.ConclusionIn patients with NAFLD, EAT is associated with the severity of liver and vascular damage besides with the known metabolic risk factors.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 53%

Epicardial Adipose Tissue (EAT) Thickness Is Associated with Cardiovascular and Liver Damage in Nonalcoholic Fatty Liver Disease

et al. 2016

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“…EAT deposition can be associated with coronary vascular disease pathogenesis mainly by the dysregulation of cardiac metabolic processes and the disruption of the epicardial and myocardial structural integrity. Other mechanisms that could be involved in the interaction between EAT and coronary vasculature are nerve damage and impaired cryoprotection of the heart[ 35 , 36 ]. Furthermore, the epicardial adipocytes exhibit and arrhythmogenic potential, a theory suggested by many clinical trials exploring the causative relationship between EAT and atrial fibrillation[ 21 ] (Figure 1 ).…”

Section: Epicardial Fat Type 2 Diabetes Mellitus and Coronary Arterymentioning

confidence: 99%

Effects of antidiabetic drugs on epicardial fat

Xourgia¹,

Papazafiropoulou²,

Μelidonis³

2018

WJD

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Epicardial adipose tissue is defined as a deposit of adipocytes with pathophysiological properties similar to those of visceral fat, located in the space between the myocardial muscle and the pericardial sac. When compared with subcutaneous adipose tissue, visceral adipocytes show higher metabolic activity, lipolysis rates, increased insulin resistance along with more steroid hormone receptors. The epicardial adipose tissue interacts with numerous cardiovascular pathways via vasocrine and paracrine signalling comprised of pro- and anti-inflammatory cytokines excretion. Both the physiological differences between the two tissue types, as well as the fact that fat distribution and phenotype, rather than quantity, affect cardiovascular function and metabolic processes, establish epicardial fat as a biomarker for cardiovascular and metabolic syndrome. Numerous studies have underlined an association of altered epicardial fat morphology, type 2 diabetes mellitus (T2DM) and adverse cardiovascular events. In this review, we explore the prospect of using the epicardial adipose tissue as a therapeutic target in T2DM and describe the underlying mechanisms by which the antidiabetic drugs affect the pathophysiological processes induced from adipose tissue accumulation and possibly allow for more favourable cardiovascular outcomes though epicardial fat manipulation.

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“… 7 – 9 Adiponectin is an adipokine secreted from EAT that has anti-inflammatory, antiatherogenic, and antihypertrophic via multiple cell-signaling mechanisms. 10 Adiponectin levels are reduced in different pathologic conditions, including metabolic syndrome, nonalcoholic fatty liver disease, diabetes, obesity, and ischemic heart disease 11 , 12 and have been also suggested as an independent prognostic biomarker in AF. 13 …”

Section: Introductionmentioning

confidence: 99%

Opposite relations of epicardial adipose tissue to left atrial size in paroxysmal and permanent atrial fibrillation

et al. 2018

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Objectives:Atrial fibrillation has been associated with obesity in epidemiological studies. Epicardial adipose tissue is an ectopic fat depot in the proximity of atria, with endocrine and inflammatory properties that is implicated in the pathophysiology of atrial fibrillation. Inflammation also has a role in atrial arrhythmogenesis. The aim of this study was to investigate the potential relations of epicardial adipose tissue to left atrial size and to adiponectin and the pro-inflammatory mediators, high-sensitivity C-reactive protein, and interleukin-6 in paroxysmal and permanent atrial fibrillation.Methods:This was a cross-sectional study of 103 atrial fibrillation patients, divided into two subgroups of paroxysmal and permanent atrial fibrillation, and 81 controls, in sinus rhythm. Echocardiography was used for estimation of epicardial adipose tissue and left atrial size and high-sensitivity C-reactive protein, interleukin-6 and adiponectin were measured in all subjects.Results:Atrial fibrillation patients had significantly larger epicardial adipose tissue compared with controls (0.43 ± 0.17 vs 0.34 ± 0.17 cm, p = 0.002). Atrial fibrillation presence was independently related to epicardial adipose tissue thickness (b = 0.09, p = 0.002). Opposite associations of epicardial adipose tissue with left atrial volume existed in atrial fibrillation subgroups; in the paroxysmal subgroup, epicardial adipose tissue was directly related to left atrial volume (R = 0.3, p = 0.03), but in the permanent one the relation was inverse (R = −0.7, p < 0.0001). Adiponectin, high-sensitivity C-reactive protein and interleukin-6 were elevated in both atrial fibrillation groups. Only interleukin-6 was related to epicardial adipose tissue size.Conclusion:Opposite associations of epicardial adipose tissue with left atrial size in paroxysmal and permanent Atrial fibrillation and elevated inflammatory markers, suggest a role of epicardial adipose tissue and inflammation in the fibrotic and remodeling process.

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Epicardial Fat in Nonalcoholic Fatty Liver Disease

Cited by 28 publications

References 47 publications

Epicardial Adipose Tissue (EAT) Thickness Is Associated with Cardiovascular and Liver Damage in Nonalcoholic Fatty Liver Disease

Epicardial Adipose Tissue (EAT) Thickness Is Associated with Cardiovascular and Liver Damage in Nonalcoholic Fatty Liver Disease

Effects of antidiabetic drugs on epicardial fat

Opposite relations of epicardial adipose tissue to left atrial size in paroxysmal and permanent atrial fibrillation

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