Abstract
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.
Highlights
Atrial fibrillation (AF) is the most frequent type of arrhythmia occurring, especially among patients with more advanced age
This review summarizes the knowledge about the role of mitochondrial dysfunction in the pathogenesis of AF and gives an overview of the current treatment options to ameliorate the condition of mitochondria to prevent the arrhythmia or improve prognosis
In another animal study using the model of alloxan-induced diabetes mellitus, treatment with alogliptin resulted in improved ∆Ψm and mitochondrial biogenesis via activation of the PGC-1α/NRF1/Tfam signaling pathway that was paralleled by preservation of the left atrial diameter, lowering of hs-CRP levels, upregulation of superoxide dismutase and improved atrial electrical function [67]
Summary
Atrial fibrillation (AF) is the most frequent type of arrhythmia occurring, especially among patients with more advanced age. In younger patients without structural heart defects, the pulmonary vein arrhythmogenesis frequently acts as the initiating trigger for AF, mostly paroxysmal, and recurrences can be successfully prevented by pulmonary vein ablation [7]. In elderly patients, the key initiating factors are atrial tissue degeneration and comorbidities affecting the atrial metabolism and atrial structure, more frequently leading to persistent or permanent AF [8,9]. They are responsible for synthesis of adenosine 50 triphosphate (ATP), which provides energy for almost all intracellular processes, including mechanical work and active ion transport. This review summarizes the knowledge about the role of mitochondrial dysfunction in the pathogenesis of AF and gives an overview of the current treatment options to ameliorate the condition of mitochondria to prevent the arrhythmia or improve prognosis
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