Epicardial fat and liver disease; the contribution of cardio autonomic nervous system function

Ulucan, Şeref; Katlandur, Hüseyin; Kaya, Zeynettin

doi:10.1016/j.jhep.2015.01.008

Cited by 6 publications

(5 citation statements)

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“…In this line, cross-sectional and prospective studies showed that both liver and visceral fat are independent risk factors for presence and occurrence of cardiovascular events [8,9]. So, we included both visceral and epicardial fat in the model for fibrosis to demonstrate that the effect of epicardial fat is independent of that of visceral fat.Finally, in response to Ulucan and colleagues [11] we agree with the authors that the interference of epicardial fat with the autonomic nervous system could be one of the mechanisms linking this ectopic fat to liver damage. Accordingly, further clinical and experimental studies are needed in this topic.…”

supporting

confidence: 67%

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Epicardial fat in patients with non-alcoholic fatty liver disease

Petta

Craxı̀

2015

Journal of Hepatology

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We recently reported that epicardial fat thickness is significantly associated with the severity of liver fibrosis in patients with nonalcoholic fatty liver disease (NAFLD), and that in this clinical setting, morphological and functional cardiac alterations by echocardiography are inversely related with the severity of liver damage [1]. Of note, these associations were maintained after correction for both cardiometabolic and hepatic confounders including visceral adiposity.In their letter [10], Corrao and colleagues suggest that some cytokines/adipocytokines as well as adiponectin, transforming growth factor b1, e-selectin, endothelin, and fibroblast growth factor 21 could explain the link we observed between the severity of liver disease and the presence of cardiac alterations. In this line in our paper we already suggested that ''the inflammatory state that characterize NAFLD/NASH might be able to act systemically, affecting the homeostasis of different organs, including the heart, as already demonstrated for systemic atherosclerosis [2] and kidney damage [3]''. Therefore we are planning to study the relationship between cytokines/adipocytokines levels, liver damage and cardiac alterations in NAFLD, as well as the role of genetic variants associated with NAFLD and its severity on the presence of cardiac alterations. We recently reported that gene variants in the PNPLA3 and TMS6F2 genes, can modulate the risk of atherosclerosis as well as the occurrence of cardiovascular events in patients with NAFLD or at high NAFLD risk [4,5].Corrao and colleagues also question the approach we used for the multivariate model, assessing variables independently associated with severe liver fibrosis. Specifically, they raised concerns about the inclusion in the model of both visceral obesity and epicardial fat, because considered as a phenomenon of collinearity. We thank the authors to correctly explain this phenomenon and the implication that it can produce on data interpretation. However, we respectfully think that our analysis is not biased by collinearity. Epicardial fat [6], as well as other ectopic fat depots like liver or dorsocervical fat [7], are obviously strongly related to visceral obesity. However, they do not depend on visceral obesity only, because they can have an independent role in affecting liver and systemic damage. In this line, cross-sectional and prospective studies showed that both liver and visceral fat are independent risk factors for presence and occurrence of cardiovascular events [8,9]. So, we included both visceral and epicardial fat in the model for fibrosis to demonstrate that the effect of epicardial fat is independent of that of visceral fat.Finally, in response to Ulucan and colleagues [11] we agree with the authors that the interference of epicardial fat with the autonomic nervous system could be one of the mechanisms linking this ectopic fat to liver damage. Accordingly, further clinical and experimental studies are needed in this topic.

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supporting

confidence: 67%

“…Finally, in response to Ulucan and colleagues [11] we agree with the authors that the interference of epicardial fat with the autonomic nervous system could be one of the mechanisms linking this ectopic fat to liver damage. Accordingly, further clinical and experimental studies are needed in this topic.…”

supporting

confidence: 67%

Epicardial fat in patients with non-alcoholic fatty liver disease

Petta

Craxı̀

2015

Journal of Hepatology

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“…EAT is abundant with ganglionated plexi, cholinergic and adrenergic nerves. While adrenergic stimulation causes increased calcium entry, cholinergic stimulation leads to shortening of action potential duration resulting in triggered activity and early after depolarization 62 Finally studies have demonstrated an association between alterations in the autonomic nervous system and the development of AF 63 . It has been shown that EAT plays a role in cardio autonomic function.…”

Section: Possible Mechanismsmentioning

confidence: 99%

Role of adipose tissue in the pathogenesis of cardiac arrhythmias

et al. 2016

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Epicardial adipose tissue is present in normal healthy individuals. It is a unique fat depot that, under physiologic conditions, plays a cardioprotective role. However, excess epicardial adipose tissue has been shown to be associated with prevalence and severity of atrial fibrillation. In arrhythmogenic right ventricular cardiomyopathy and myotonic dystrophy, fibrofatty infiltration of the myocardium is associated with ventricular arrhythmias. In the ovine model of ischemic cardiomyopathy, the presence of intramyocardial adipose or lipomatous metaplasia has been associated with increased propensity to ventricular tachycardia. These observations suggest a role of adipose tissue in the pathogenesis of cardiac arrhythmias. In this article, we review the role of cardiac adipose tissue in various cardiac arrhythmias and discuss the possible pathophysiologic mechanisms.

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“…148 Conversely, up to a quarter of patients with NAFLD are lean and not all patients with obesity have NAFLD. 149 Up to one quarter of obese individuals do not have MetS features 150 and are dubbed metabolically healthy obese, though it is still unclear if those individuals are also protected from CVD.…”

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confidence: 99%

Epidemiological modifiers of non-alcoholic fatty liver disease: Focus on high-risk groups

Lonardo

Bellentani

Argo

et al. 2015

Digestive and Liver Disease

403

318

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We aimed to illustrate the epidemiology of nonalcoholic fatty liver disease in high-risk groups, which were identified based on existing literature. To this end, PubMed was searched to retrieve original articles published through May 2015 using relevant and pertinent keywords "nonalcoholic fatty liver disease" and "diabetes", "obesity", "hyperlipidemia", "familial heterozygous hypobelipoproteinemia", "hypertension", "metabolic syndrome", "ethnicity", "family history" or "genetic polymorphisms".We found that age, sex and ethnicity are major physiologic modifiers of the risk of nonalcoholic fatty liver disease, along with belonging to "nonalcoholic fatty liver disease families" and carrying risk alleles for selected genetic polymorphisms. Metabolic syndrome, diabetes, obesity, mixed hyperlipidaemia and hypocholesterolemia due to familial hypobetalipoproteinaemia are the major metabolic modifiers of nonalcoholic fatty liver disease risk. Compared to these metabolic conditions, however, arterial hypertension appears to carry a relatively more modest risk of nonalcoholic fatty liver disease.A better understanding of the epidemiology of nonalcoholic fatty liver disease may result in a more liberal policy of case finding among high-risk groups.

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Epicardial fat and liver disease; the contribution of cardio autonomic nervous system function

Cited by 6 publications

References 6 publications

Epicardial fat in patients with non-alcoholic fatty liver disease

Epicardial fat in patients with non-alcoholic fatty liver disease

Role of adipose tissue in the pathogenesis of cardiac arrhythmias

Epidemiological modifiers of non-alcoholic fatty liver disease: Focus on high-risk groups

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