Mauriello Alfredo, Correra Adriana, Molinari Riccardo, Del Vecchio Gerardo Elia, Tessitore Viviana, D'Andrea Antonello, Russo Vincenzo
Cardiology Unit, Department of Medical and Translational Sciences, University of Campania "Luigi Vanvitelli", Monaldi Hospital, 80131 Naples, Italy.
Cardiology and Intensive Care Unit, Department of Cardiology, Umberto I Hospital, 84014 Nocera Inferiore, Italy.
Biomedicines. 2024 Nov 27;12(12):2720. doi: 10.3390/biomedicines12122720.
Despite great progress in treating atrial fibrillation (AF), especially with the development of increasingly effective invasive techniques for AF ablation, many unanswered questions remain regarding the pathogenic mechanism of the arrhythmia and its prevention methods. The development of AF is based on anatomical and functional alterations in the cardiomyocyte resulting from altered ionic fluxes and cardiomyocyte electrophysiology. Electric instability and electrical remodeling underlying the arrhythmia may result from oxidative stress, also caused by possible mitochondrial dysfunction. The role of mitochondrial dysfunction in the pathogenesis of AF is not yet fully elucidated; however, the reduction in AF burden after therapeutic interventions that improve mitochondrial fitness tends to support this concept. This selected review aims to summarize the mechanisms of mitochondrial dysfunction related to AF and the current pharmacological treatment options that target mitochondria to prevent or improve the outcome of AF.
尽管在心房颤动（AF）的治疗方面取得了巨大进展，尤其是随着AF消融的侵入性技术越来越有效，但关于这种心律失常的发病机制及其预防方法仍有许多未解决的问题。AF的发生基于离子通量和心肌细胞电生理学改变导致的心肌细胞解剖学和功能改变。心律失常背后的电不稳定性和电重构可能由氧化应激引起，而氧化应激也可能由线粒体功能障碍导致。线粒体功能障碍在AF发病机制中的作用尚未完全阐明；然而，改善线粒体健康的治疗干预后AF负担的减轻倾向于支持这一概念。这篇精选综述旨在总结与AF相关的线粒体功能障碍机制以及目前针对线粒体预防或改善AF结局的药物治疗选择。
