Pericardial Fat Is Associated With the Risk of Ventricular Arrhythmia in Asian Patients

Tam, Weng Chio; Lin, Yung Kuo; Chan, Wing P.; Huang, Jen Hung; Hsieh, Ming Hsiung; Chen, Shih Ann; Chen, Yi Jen

doi:10.1253/circj.cj-16-0047

Cited by 26 publications

(23 citation statements)

References 38 publications

(26 reference statements)

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“…MS could significantly increase the volume of pericardial fat and visceral fat [ 4 ]. An increased pericardial fat volume is associated with an increased incidence of cardiac arrhythmias [ 5 , 6 ]. Increased adiposis and fibrosis area in atrial and ventricular tissues have been found in individuals with MS [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have demonstrated that the amount of pericardial fat is associated with the occurrence of atrial fibrillation (AF) and that catheter ablation of the pericardial fat pad can decrease the occurrence of AF [5]. Another study also showed that a high-fat diet could increase the risk of ventricular arrhythmias [6]. Adipose tissues were not only considered a deposit of energy but also as an endocrine organ responsible for the secretion of bioactive molecules termed "adipocytokines" [7].…”

Section: Introductionmentioning

confidence: 99%

“…Adipose tissues were not only considered a deposit of energy but also as an endocrine organ responsible for the secretion of bioactive molecules termed "adipocytokines" [7]. Previous studies have shown that adipocytokines, either from peripheral or pericardial fat, may comprise several cytokines and proinflammatory mediators that could modulate the genesis of atrial and ventricular arrhythmias [5,6]. Mazurek et al investigated human epicardial adipose tissue and found that epicardial adipose tissue was a source of several cytokines, including monocyte chemotactic protein 1, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, all of which may promote the genesis of atherosclerosis [7].…”

Section: Introductionmentioning

confidence: 99%

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Effects of Secretome from Fat Tissues on Ion Currents of Cardiomyocyte Modulated by Sodium-Glucose Transporter 2 Inhibitor

et al. 2020

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Sodium-glucose transporter 2 (SGLT2) inhibitors were shown to decrease mortality from cardiovascular diseases in the EMPA-REG trial. However, the effects of empagliflozin (EMPA) for cardiac arrhythmia are not yet clarified. A total of 20 C57BL/6J mice were divided into four groups: (1) The control group were fed standard chow, (2) the metabolic syndrome (MS) group were fed a high-fat diet, (3) the empagliflozin (EMPA) group were fed a high-fat diet and empagliflozin 10 mg/kg daily, and (4) the glibenclamide (GLI) group were fed a high-fat diet and glibenclamide 0.6 mg/kg daily. All mice were sacrificed after 16 weeks of feeding. H9c2 cells were treated with adipocytokines from the pericardial and peripheral fat from the study groups. The delayed-rectifier potassium current (IK) and L-type calcium channel current (ICa,L) were measured by the whole-cell patch clamp techniques. Adipocytokines from the peripheral and pericardial fat tissues of mice with MS could decrease the IK and increase the ICa,L of cardiomyocytes. After treating adipocytokines from pericardial fat, the IK in the EMPA and GLI groups were significantly higher than that in the MS group. The IK of the EMPA group was also significantly higher than the GLI group. The ICa,L of the EMPA and GLI groups were significantly decreased overload compared with that of the MS group. However, there was no significant difference of IK and ICa,L among study groups after treating adipocytokines from peripheral fat. Adipocytokines from pericardial fat but not peripheral fat tissues after EMPA therapy attenuated the effects of IK decreasing and ICa,L increasing in the MS cardiomyocytes, which may contribute to anti-arrhythmic mechanisms of sodium-glucose transporter 2 (SGLT2) inhibitors.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of Secretome from Fat Tissues on Ion Currents of Cardiomyocyte Modulated by Sodium-Glucose Transporter 2 Inhibitor

et al. 2020

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“…Fat around the heart can be divided into pericardial adipose tissue and visceral EAT. Pericardial fat is defined by fat surrounding the parietal pericardium while visceral EAT is defined by fat between the myocardium and visceral pericardium (Tam et al, 2016). EAT covers 80% of the heart and is present mostly along the coronary arteries, in the atrioventricular/intraventricular grooves, over the right ventricle (three or four times more than the left ventricle) especially along the right border, anterior surface and at the apex.…”

Section: Types Of Fat and Arrhythmia Developmentmentioning

confidence: 99%

“…EAT and pericardial fat quantified by magnetic resonance imaging (MRI) is associated with the development of ventricular tachycardia (VT), ventricular fibrillation (VF) and long-term overall mortality in patients with systolic heart failure (HF; Wu et al, 2015). In an Asian population, pericardial fat thickness was also associated with increased frequency of premature ventricular contractions (Tam et al, 2016).…”

Section: Types Of Fat and Arrhythmia Developmentmentioning

confidence: 99%

Linking Arrhythmias and Adipocytes: Insights, Mechanisms, and Future Directions

et al. 2018

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Obesity and atrial fibrillation have risen to epidemic levels worldwide and may continue to grow over the next decades. Emerging evidence suggests that obesity promotes atrial and ventricular arrhythmias. This has led to trials employing various strategies with the ultimate goal of decreasing the atrial arrhythmic burden in obese patients. The effectiveness of these interventions remains to be determined. Obesity is defined by the expansion of adipose mass, making adipocytes a prime candidate to mediate the pro-arrhythmogenic effects of obesity. The molecular mechanisms linking obesity and adipocytes to increased arrhythmogenicity in both the atria and ventricles remain poorly understood. In this focused review, we highlight areas of potential molecular interplay between adipocytes and cardiomyocytes. The effects of adipocytes may be direct, local or remote. Direct effect refers to adipocyte or fatty infiltration of the atrial and ventricular myocardium itself, possibly causing increased dispersion of normal myocardial electrical signals and fibrotic substrate of adipocytes that promote reentry or adipocytes serving as a direct source of aberrant signals. Local effects may originate from nearby adipose depots, specifically epicardial adipose tissue (EAT) and pericardial adipose tissue, which may play a role in the secretion of adipokines and chemokines that can incite inflammation given the direct contact and disrupt the conduction system. Adipocytes can also have a remote effect on the myocardium arising from their systemic secretion of adipokines, cytokines and metabolites. These factors may lead to mitochondrial dysfunction, oxidative stress, autophagy, mitophagy, autonomic dysfunction, and cardiomyocyte death to ultimately produce a pro-arrhythmogenic state. By better understanding the molecular mechanisms connecting dysfunctional adipocytes and arrhythmias, novel therapies may be developed to sever the link between obesity and arrhythmias.

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Cardiac Arrhythmia Due to Epicardial Fat: Is It a Modifiable Risk?

Okumura

2017

Curr Cardiovasc Risk Rep

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Pericardial Fat Is Associated With the Risk of Ventricular Arrhythmia in Asian Patients

Cited by 26 publications

References 38 publications

Effects of Secretome from Fat Tissues on Ion Currents of Cardiomyocyte Modulated by Sodium-Glucose Transporter 2 Inhibitor

Effects of Secretome from Fat Tissues on Ion Currents of Cardiomyocyte Modulated by Sodium-Glucose Transporter 2 Inhibitor

Linking Arrhythmias and Adipocytes: Insights, Mechanisms, and Future Directions

Cardiac Arrhythmia Due to Epicardial Fat: Is It a Modifiable Risk?

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