Sodium-glucose cotransporter 2 inhibitors potentially prevent atrial fibrillation by balancing sodium and calcium handling disorders and mitigating mitochondrial dysfunction in atrial myocytes.
Do SGLT2 inhibitors prevent atrial fibrillation in patients with type 2 diabetes and heart failure?
This review highlights the potential mechanisms by which SGLT2 inhibitors prevent atrial fibrillation, specifically through improving ion handling and mitochondrial function in atrial myocytes.
Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are a novel class of glucose-lowering agents that significantly improve the prognosis of patients with type 2 diabetes (T2D) and heart failure. SGLT2i has recently been implicated in the treatment of atrial fibrillation (AF) with clinical data demonstrating that these agents decrease the incidence of AF events in patients with T2D. Fundamental findings have suggested that SGLT2i may alleviate atrial electrical and structural remodeling. The underlying mechanisms of SGLT2i are likely associated with balancing the sodium and calcium handling disorders and mitigating the mitochondrial dysfunction in atrial myocytes. This review illustrates the advances in understanding the underlying mechanisms of SGLT2i as an evolving treatment modality for AF.
Peng et al. (Tue,) conducted a review in Atrial Fibrillation. Sodium-Glucose Cotransporter 2 Inhibitors (SGLT2i) was evaluated. Sodium-glucose cotransporter 2 inhibitors potentially prevent atrial fibrillation by balancing sodium and calcium handling disorders and mitigating mitochondrial dysfunction in atrial myocytes.