Dynamics of epicardiac fat and heart function in type 2 diabetic patients initiated with SGLT-2 inhibitors

Abstract

Purpose: The aim of this study was to assess the dynamics of epicardiac adipose tissue (EAT) thickness and total volume as well as that of systolic and diastolic dysfunction in a group of patients with type 2 diabetes (T2D) after initiation of sodium glucose cotransporter 2 (SGLT 2) inhibitors therapy. Patients and methods: This prospective, observational study included 53 patients with T2D who received SGLT-2 inhibitors for 24 weeks. In all patients, echocardiographic screening for EAT, systolic and diastolic dysfunction and non-contrast computed tomography scans were performed, both before and after 24 weeks of SGLT-2 inhibition. Imagistic evaluation was followed by the association’s analysis between the dynamics of EAT and heart function, as well as the patient’s clinical and biological parameters. We considered a decrease or increase of more than 10% in EAT as being clinically significant. Results: The mean volume of EAT decreased significantly after SGLT 2 inhibition (37.8±17.2 vs. 20.7±7 cm3; p<0.001). Median values of EAT thickness also decreased significantly (5.95 vs. 3.01 mm; p<0.001). Most patients, 75.4% (40/53), presented more than 10% decrease in EAT volume, 9.5% (5/53) had stable EAT volume values, while in 15.1% (8/53) the means of EAT volume increased. 73.5% of the patients had diastolic dysfunction type 1 (DD 1) at baseline. No significant change was observed in the left ventricular ejection fraction or diastolic dysfunction after 24 weeks of treatment. Although not statistically significant, an improvement in cardiac function has been noticed throughout the duration of 1 year of treatment with SGLT 2 inhibitors. Conclusion: This study showed the beneficial effect of SGLT 2 inhibitors on EAT after a short period of treatment, but there were no significant changes in the systolic function during the 1st year of study. However, reducing epicardial fat has led to remission of diastolic dysfunction.