Mitochondrial Dysfunction in Atrial Fibrillation: Needs Strong Pharmacological Approach

Despite great progress in the treatment of atrial fibrillation (AF), especially with the development of increasingly effective invasive techniques, many questions remain unanswered regarding the pathogenic mechanism of the arrhythmia and its prevention methods. The development of AF is based on anatomical and functional changes in the myocardium that result from disturbed ion flows and altered electrophysiology of the cardiomyocyte. Electrical instability and electrical remodeling underlying arrhythmia may result from oxidative stress, caused by mitochondrial dysfunction. The role of mitochondrial dysfunction in the pathogenesis of AF is not yet completely clarified; however, it is emphasized by the reduction of AF burden after therapeutic interventions that improve mitochondrial well-being. This selected review aims to summarize the mechanisms of mitochondrial dysfunction related to AF and current pharmacological treatment options tar-geting mitochondria to prevent or improve the outcome of AF.