Key result
Metformin, SGLT2 inhibitors, and statins show promise in AF by targeting mitochondrial dysfunction.
Why the study?
Many unanswered questions remain regarding the pathogenic mechanisms of AF and its prevention methods, with the role of mitochondrial dysfunction not yet fully elucidated.
Targeting mitochondrial dysfunction and oxidative stress with agents like SGLT2 inhibitors and metformin represents a promising pharmacological approach to preventing atrial fibrillation, though dedicated randomized trials are required.
Hypothesis-generating for mitochondrial-targeted AF therapies; leaves open confirmation in dedicated RCTs.
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.
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Mauriello et al. (2024) conducted a review in Atrial Fibrillation. Mitochondria-targeting pharmacological agents was evaluated. Pharmacological agents such as metformin, SGLT2 inhibitors, and statins appear promising for treating atrial fibrillation by targeting underlying mitochondrial dysfunction and oxidative stress.
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