Atrial fibrillation (AF) is a continually growing health-care burden that often presents together with metabolic disorders, including diabetes mellitus and obesity. Current treatments often fall short of preventing AF and its adverse outcomes. Accumulating evidence suggests that metabolic disturbances can promote the development of AF through structural and electrophysiological remodelling, but the underlying mechanisms that predispose an individual to AF are aetiology-dependent, thus emphasizing the need for tailored therapeutic strategies to treat AF that target an individual’s metabolic profile. AF itself can induce changes in glucose, lipid and ketone metabolism, mitochondrial function and myofibrillar energetics (as part of a process referred to as ‘metabolic remodelling’), which can all contribute to atrial dysfunction. In this Review, we discuss our current understanding of AF in the setting of metabolic disorders, as well as changes in atrial metabolism that are relevant to the development of AF. We also describe the potential of available and emerging treatment strategies to target metabolic remodelling in the setting of AF and highlight key questions and challenges that need to be addressed to improve outcomes in these patients.

心房颤动 (AF) 是一种不断加重的医疗负担，通常与糖尿病和肥胖等代谢性疾病同时出现。目前的治疗方法往往不足以预防房颤及其不良后果。越来越多的证据表明，代谢紊乱可以通过结构和电生理重塑促进房颤的发展，但个体易患房颤的潜在机制是病因依赖性的，因此强调需要针对个体的代谢特征制定量身定制的治疗策略来治疗房颤。房颤本身可以引起葡萄糖、脂质和酮代谢、线粒体功能和肌原纤维能量学的变化（作为“代谢重塑”过程的一部分），这些都可能导致心房功能障碍。在这篇综述中，我们讨论了我们目前对代谢紊乱背景下房颤的理解，以及与房颤发生相关的心房代谢的变化。我们还描述了现有的和新兴的治疗策略在 AF 情况下针对代谢重塑的潜力，并强调了为改善这些患者的预后而需要解决的关键问题和挑战。