Obesity is an important contributing factor to the pathophysiology of atrial fibrillation (AF) and its complications by causing systemic changes, such as altered haemodynamic, increased sympathetic tone, and low-grade chronic inflammatory state. In addition, adipose tissue is a metabolically active organ that comprises various types of fat deposits with discrete composition and localization that show distinct functions. Fatty tissue differentially affects the evolution of AF, with highly secretory active visceral fat surrounding the heart generally having a more potent influence than the rather inert subcutaneous fat. A variety of proinflammatory, profibrotic, and vasoconstrictive mediators are secreted by adipose tissue, particularly originating from cardiac fat, that promote atrial remodelling and increase the susceptibility to AF. In this review, we address the role of obesity-related factors and in particular specific adipose tissue depots in driving AF risk. We discuss the distinct effects of key secreted adipokines from different adipose tissue depots and their participation in cardiac remodelling. The possible mechanistic basis and molecular determinants of adiposity-related AF are discussed, and finally, we highlight important gaps in current knowledge, areas requiring future investigation, and implications for clinical management.

中文翻译：

---

肥胖相关心房颤动：分子决定因素、机制和临床意义。

肥胖是房颤 (AF) 病理生理学及其并发症的重要影响因素，可引起全身变化，例如血流动力学改变、交感神经张力增加和低度慢性炎症状态。此外，脂肪组织是一种代谢活跃的器官，由各种类型的脂肪沉积物组成，这些脂肪沉积物具有离散的成分和定位，显示出不同的功能。脂肪组织对 AF 的进展有不同的影响，心脏周围高度分泌的活跃内脏脂肪通常比相当惰性的皮下脂肪具有更有效的影响。脂肪组织（特别是源自心脏脂肪）分泌多种促炎、促纤维化和血管收缩介质，促进心房重塑并增加房颤的易感性。在这篇综述中，我们探讨了肥胖相关因素，特别是特定脂肪组织库在驱动房颤风险中的作用。我们讨论了不同脂肪组织库中关键分泌的脂肪因子的独特作用及其在心脏重塑中的参与。讨论了肥胖相关房颤的可能机制基础和分子决定因素，最后，我们强调了当前知识中的重要差距、需要未来研究的领域以及对临床管理的影响。