Background: Atrial fibrillation (AF) is the most common arrhythmia. AF is highly correlated with multiple risk factors including heart failure, age, obesity, and type 2 diabetes. Among risk factors, the incidence in obesity is increasing worldwide. Recently, it was reported that SGLT2 inhibitors reduced the incidence of atrial fibrillation. However, it is unclear how the treatment with SGLT2 inhibitors has effects on vulnerability to AF. In this study, we examined the effects on the inducibility and duration of AF by treatment with SGLT2 inhibitors in diet-induced obese mice.
Methods: Mice were fed a normal chow diet (NCD) or high-fat diet (HFD). Following diet-loading, we randomly divided the animals into groups: NCD+vehicle, HFD+vehicle, and HFD+ SGLT2 treatments. Induction of AF was performed by transesophageal atrial burst pacing. Furthermore, we evaluated cardiac function, blood pressure, atrial fibrosis, and glucose tolerance at the end of the treatments.
Results: The results showed that HFD-fed mice increased the inducibility of AF compared to NCD mice. In addition, treatment with the SGLT2 inhibitor in HFD-fed mice dose-dependently reduced the inducibility and duration of AF. There were no significant differences in cardiac function, blood pressure, and fibrosis among all groups. Impairment of glucose tolerance in HFD-induced obesity was improved by treatment with the SGLT2 inhibitor.
Conclusion: Treatment with the SGLT2 inhibitor reduced the inducibility of AF and shortened the duration of AF without affecting atrial structural remodeling, suggesting that the SGLT2 inhibitor effectively prevents AF in obesity.