Conte Maddalena, Petraglia Laura, Cabaro Serena, Valerio Vincenza, Poggio Paolo, Pilato Emanuele, Attena Emilio, Russo Vincenzo, Ferro Adele, Formisano Pietro, Leosco Dario, Parisi Valentina
Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy.
Casa di Cura San Michele, Maddaloni, Italy.
Front Cardiovasc Med. 2022 Jun 30;9:932262. doi: 10.3389/fcvm.2022.932262. eCollection 2022.
Atrial Fibrillation (AF) is the most frequent cardiac arrhythmia and its prevalence increases with age. AF is strongly associated with an increased risk of stroke, heart failure and cardiovascular mortality. Among the risk factors associated with AF onset and severity, obesity and inflammation play a prominent role. Numerous recent evidence suggested a role of epicardial adipose tissue (EAT), the visceral fat depot of the heart, in the development of AF. Several potential arrhythmogenic mechanisms have been attributed to EAT, including myocardial inflammation, fibrosis, oxidative stress, and fat infiltration. EAT is a local source of inflammatory mediators which potentially contribute to atrial collagen deposition and fibrosis, the anatomical substrate for AF. Moreover, the close proximity between EAT and myocardium allows the EAT to penetrate and generate atrial myocardium fat infiltrates that can alter atrial electrophysiological properties. These observations support the hypothesis of a strong implication of EAT in structural and electrical atrial remodeling, which underlies AF onset and burden. The measure of EAT, through different imaging methods, such as echocardiography, computed tomography and cardiac magnetic resonance, has been proposed as a useful prognostic tool to predict the presence, severity and recurrence of AF. Furthermore, EAT is increasingly emerging as a promising potential therapeutic target. This review aims to summarize the recent evidence exploring the potential role of EAT in the pathogenesis of AF, the main mechanisms by which EAT can promote structural and electrical atrial remodeling and the potential therapeutic strategies targeting the cardiac visceral fat.
心房颤动（AF）是最常见的心律失常，其患病率随年龄增长而增加。AF与中风、心力衰竭和心血管死亡率风险增加密切相关。在与AF发作和严重程度相关的危险因素中，肥胖和炎症起着重要作用。最近的大量证据表明，心外膜脂肪组织（EAT），即心脏的内脏脂肪库，在AF的发生发展中起作用。几种潜在的致心律失常机制已归因于EAT，包括心肌炎症、纤维化、氧化应激和脂肪浸润。EAT是炎症介质的局部来源，可能导致心房胶原沉积和纤维化，这是AF的解剖学基础。此外，EAT与心肌的紧密相邻使得EAT能够穿透并产生心房心肌脂肪浸润，从而改变心房电生理特性。这些观察结果支持EAT在心房结构和电重构中起重要作用的假说，而心房结构和电重构是AF发作和负担的基础。通过不同的成像方法，如超声心动图、计算机断层扫描和心脏磁共振成像来测量EAT，已被提议作为预测AF的存在、严重程度和复发的有用预后工具。此外，EAT越来越成为一个有前景的潜在治疗靶点。本综述旨在总结最近探索EAT在AF发病机制中的潜在作用、EAT促进心房结构和电重构的主要机制以及针对心脏内脏脂肪的潜在治疗策略的证据。
