Key result
SGLT2 inhibitors mitigate atrial remodeling and may lower AF risk via reduced inflammation and fibrosis.
Why the study?
Despite clinical trial data indicating SGLT2 inhibitors may significantly influence atrial remodeling, their overall effectiveness in this setting remains under debate.
SGLT2 inhibitors demonstrate potential in mitigating atrial remodeling and reducing the risk of atrial fibrillation through complex molecular mechanisms, though their specific clinical role in AF management remains under debate.
Supports mechanistic rationale for SGLT2 inhibitors in AF; leaves open clinical efficacy pending dedicated RCTs.
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.
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Minciună et al. (2024) conducted a review in Atrial remodeling, atrial fibrillation, and heart failure. SGLT2 inhibitors was evaluated. SGLT2 inhibitors mitigate atrial remodeling and potentially reduce atrial fibrillation risk by modulating inflammation, oxidative stress, mitochondrial function, and fibrosis.
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