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In an HFrEF experimental model, our working group demonstrated an increase in myocardial consumption of ketone bodies related to empagliflozin treatment.28 The higher presence of plasma ketone bodies associated with SGLT2 inhibitors provides the heart with a more efficient energy substrate than glucose or fatty acids.29 Better energy efficiency would be especially useful in situations of energy decline, such as HF or myocardial ischemia, where it could help mitigate inflammation and fibrosis.30 Specifically in HF patients, an increase in ketone bodies has resulted in better ventricular contractility.31 In our experimental model, optimization of metabolic status was the basis for explaining the regression in adverse remodeling, reductions in volumes and hypertrophy, and improvements in both systolic28 and diastolic32 function
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