Muszyński Paweł, Bonda Tomasz A
Department of General and Experimental Pathology, Medical University of Bialystok, Mickiewicza 2c, 15-222 Bialystok, Poland.
J Clin Med. 2021 May 28;10(11):2385. doi: 10.3390/jcm10112385.
Despite the enormous progress in the treatment of atrial fibrillation, mainly with the use of invasive techniques, many questions remain unanswered regarding the pathomechanism of the arrhythmia and its prevention methods. The development of atrial fibrillation requires functional changes in the myocardium that result from disturbed ionic fluxes and altered electrophysiology of the cardiomyocyte. Electrical instability and electrical remodeling underlying the arrhythmia may result from a cellular energy deficit and oxidative stress, which are caused by mitochondrial dysfunction. The significance of mitochondrial dysfunction in the pathogenesis of atrial fibrillation remains not fully elucidated; however, it is emphasized by the reduction of atrial fibrillation burden after therapeutic interventions improving the mitochondrial welfare. This review summarizes the mechanisms of mitochondrial dysfunction related to atrial fibrillation and current pharmacological treatment options targeting mitochondria to prevent or improve the outcome of atrial fibrillation.
尽管在心房颤动的治疗方面取得了巨大进展，主要是通过侵入性技术的应用，但关于心律失常的发病机制及其预防方法仍有许多问题未得到解答。心房颤动的发生需要心肌发生功能变化，这是由离子通量紊乱和心肌细胞电生理改变引起的。心律失常背后的电不稳定和电重构可能源于细胞能量不足和氧化应激，而这是由线粒体功能障碍所致。线粒体功能障碍在心房颤动发病机制中的意义尚未完全阐明；然而，改善线粒体功能的治疗干预后心房颤动负荷的降低凸显了其重要性。本综述总结了与心房颤动相关的线粒体功能障碍机制以及目前针对线粒体以预防或改善心房颤动结局的药物治疗选择。
