Impact of Empaglifozine on Cardiac Ectopic Fat

There is substantial evidence supporting the fact that ectopic fat accumulation is an important contributor to type 2 diabetes complications and cardiovascular risk \[1\]. Epicardial adipose tissue (EAT), located between the myocardium and the visceral layer of the pericardium has been associated with atrial fibrillation and with coronary artery disease \[2, 3\] and its abundance predicts the number of cardiac events within 8 years \[4\]. In addition, myocardial steatosis has been shown to be an independent predictor of diastolic dysfunction \[5\] \[6\]. Furthermore, in type 2 diabetic patients, bariatric surgery can reduce cardiac ectopic fat accumulation and improve cardiac function \[7\] \[8\]. When added to standard care, 10 or 25 mg/d of empagliflozin, an inhibitor of sodium-glucose cotransporter 2 (iSGLT2), significantly reduces the risk of death, cardiovascular death, and hospitalisation for heart failure among individuals with type 2 diabetes and established cardiovascular disease when compared to placebo \[9\]. The mechanisms of empagliflozin-improved cardiovascular outcomes in type 2 diabetic patients at high risk of cardiovascular events are not known. We hypotheses that empaglifozin could modulate cardiac ectopic fat and cardiac metabolism in obese type 2 diabetic patients.