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.