Epicardial adipose tissue as a mediator of cardiac arrhythmias

Obesity is associated with higher risks of cardiac arrhythmias. Although this may be partly explained by concurrent cardiometabolic ill-health, growing evidence suggests that increasing adiposity independently confers risk for arrhythmias. Among fat depots, epicardial adipose tissue (EAT) exhibits a...

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Published inAmerican journal of physiology. Heart and circulatory physiology Vol. 322; no. 2; pp. H129 - H144
Main Authors Patel, Kiran Haresh Kumar, Hwang, Taesoon, Se Liebers, Curtis, Ng, Fu Siong
Format Journal Article
LanguageEnglish
Published United States American Physiological Society 01.02.2022
SeriesIntegrative Cardiovascular Physiology and Pathophysiology
Subjects
Adipose tissue
Adipose Tissue - metabolism
Adipose Tissue - pathology
Animals
Arrhythmia
Arrhythmias, Cardiac - metabolism
Arrhythmias, Cardiac - pathology
Body fat
Cardiac arrhythmia
Cytokines
Cytokines - metabolism
Fatty acids
Fibrosis
Heart
Humans
Inflammation
Ion Channels - metabolism
Myocardium
Pericardium - metabolism
Pericardium - pathology
Review
Secretome
Weight reduction
epicardial adipose tissue
inflammation
arrhythmia
obesity
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Summary:Obesity is associated with higher risks of cardiac arrhythmias. Although this may be partly explained by concurrent cardiometabolic ill-health, growing evidence suggests that increasing adiposity independently confers risk for arrhythmias. Among fat depots, epicardial adipose tissue (EAT) exhibits a proinflammatory secretome and, given the lack of fascial separation, has been implicated as a transducer of inflammation to the underlying myocardium. The present review explores the mechanisms underpinning adverse electrophysiological remodeling as a consequence of EAT accumulation and the consequent inflammation. We first describe the physiological and pathophysiological function of EAT and its unique secretome and subsequently discuss the evidence for ionic channel and connexin expression modulation as well as fibrotic remodeling induced by cytokines and free fatty acids that are secreted by EAT. Finally, we highlight how weight reduction and regression of EAT volume may cause reverse remodeling to ameliorate arrhythmic risk.
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ISSN:0363-6135
1522-1539
1522-1539
DOI:10.1152/ajpheart.00565.2021