Sodium-glucose cotransporter 2 inhibitors (SGLT2is) may influence atrial remodeling through various molecular mechanisms, potentially preventing atrial fibrillation and heart failure.
Do SGLT2 inhibitors improve atrial remodeling and prevent the progression of atrial fibrillation and heart failure?
This review highlights the potential molecular mechanisms by which SGLT2 inhibitors may mitigate atrial remodeling, offering insights into their role in preventing atrial fibrillation and heart failure progression.
Atrial cardiomyopathy and remodeling play pivotal roles in the development of atrial fibrillation (AF) and heart failure (HF), involving complex changes in atrial structure and function. These changes facilitate the progression of AF and HF by creating a dynamic interplay between mechanical stress and electrical disturbances in the heart. Sodium-glucose cotransporter 2 inhibitors (SGLT2is), initially developed for the management of type 2 diabetes, have demonstrated promising cardiovascular benefits, being currently one of the cornerstone treatments in HF management. Despite recent data from randomized clinical trials indicating that SGLT2is may significantly influence atrial remodeling, their overall effectiveness in this context is still under debate. Given the emerging evidence, this review examines the molecular mechanisms through which SGLT2is exert their effects on atrial remodeling, aiming to clarify their potential benefits and limitations. By exploring these mechanisms, this review aims to provide insights into how SGLT2is can be integrated into strategies for preventing the progression of atrial remodeling and HF, as well as the development of AF.
Minciună et al. (Sat,) conducted a review in Atrial remodeling, atrial fibrillation, and heart failure. Sodium-glucose cotransporter 2 inhibitors (SGLT2is) was evaluated. Sodium-glucose cotransporter 2 inhibitors (SGLT2is) may influence atrial remodeling through various molecular mechanisms, potentially preventing atrial fibrillation and heart failure.