Figure 3.

Postulated mechanisms by which empagliflozin might exert beneficial effects on patients with heart failure via manipulation of cardiac energy metabolism. Empagliflozin may enhance oxidative phosphorylation by inhibiting the cardiac isoform of the sodium/hydrogen‐exchanger 1 (NHE 1), promoting branched chain amino acid metabolism, and/or increasing ketone body oxidation. All of these effects would result in a measurable increase in cardiac energy production and storage, which in turn results in an increase in PCr/ATP as well as myocardial function. ATP, adenosine triphosphate; BCAA, branched chain amino acids; PCr, phosphocreatine.