Key result
SGLT2 inhibitors may reduce AF incidence via decreased epicardial fat and improved LV diastolic function.
Why the study?
SGLT2 inhibitors have been observed to decrease the incidence of atrial fibrillation, but the physiological mechanisms underlying this protective effect require further clarification.
Do SGLT2 inhibitors prevent atrial fibrillation in patients with diabetes mellitus or heart failure?
Do SGLT2 inhibitors prevent atrial fibrillation in patients with diabetes mellitus or heart failure?
This review outlines the potential mechanisms by which SGLT2 inhibitors reduce the incidence of atrial fibrillation, highlighting risk factor modulation and off-target effects as key drivers.
Does not yet support routine AF prevention; extends mechanistic rationale for dedicated RCTs.
Atrial fibrillation, the most common cardiac arrhythmia, results in substantial morbidity and mortality related to its increased risks of stroke, heart failure, and impaired cognitive function. The incidence and prevalence of atrial fibrillation in the general population is rising, making atrial fibrillation treatment and management of its risk factors highly relevant clinical targets. One well-studied risk factor for the development of atrial fibrillation is diabetes mellitus. Inhibitors of sodium-glucose cotransporter 2 (SGLT2), common medications used to treat diabetes mellitus, have been observed to decrease the incidence of atrial fibrillation. This review discusses the SGLT2 and its role in glucose homeostasis, molecules inhibiting the transporter, possible physiological mechanisms responsible for the decreased incident atrial fibrillation in patients treated with SGLT2 inhibitors and proposes mechanistic studies to further our understanding of the biological processes involved.
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Shetty et al. (2022) conducted a review in Atrial fibrillation and Type 2 Diabetes Mellitus. SGLT2 inhibitors was evaluated. SGLT2 inhibitors may reduce the incidence of atrial fibrillation through mechanisms such as epicardial fat reduction, improved left ventricular diastolic function, and off-target cardiomyocyte effects.
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