Key result
Empagliflozin improves LV remodeling in nondiabetic pigs with heart failure by switching fuel to ketones.
Why the study?
Cardiac benefits of empagliflozin cannot be explained solely by antihyperglycemic effects, prompting investigation into whether they are mediated by switching myocardial fuel metabolism from glucose to ketone bodies to enhance energetics.
Does empagliflozin improve adverse left ventricular remodeling and myocardial energetics in a nondiabetic porcine model of heart failure?
Population
14 nondiabetic pigs with induced heart failure
Comparison
Empagliflozin vs placebo
Design
Randomized animal study
Follow-up
2 months
Authors
Loading...
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“Our study identifies why this drug [empagliflozin] is effective – because it improves heart function, something that has not been understood until now. Many doctors are afraid of prescribing a drug they do not understand, and our findings will help clinicians feel more comfortable giving this to patients once approved.”
“So it's not that you inhibit the progression of heart failure, but you can even regress the process. SGLT2 inhibition seems to be an alternative to the treatment of heart failure patients independently of whether there are or there are not diabetics.”
“Many cardiologists want to know mechanisms as well as clinical benefit. These remodeling data showing that these drugs reduce the size of abnormally large hearts [are] also very important for patients. There have been more than 50 publications on potential mechanisms of benefit of SGLT2 inhibitors in HFrEF, but these are the first randomized, mechanistic data.”
No immediate clinical implications; leaves open whether empagliflozin benefits nondiabetic human heart failure.
RCT (n=14)
randomized
Does empagliflozin improve adverse left ventricular remodeling and myocardial energetics in a nondiabetic porcine model of heart failure?
Empagliflozin ameliorates adverse cardiac remodeling and improves LV systolic function in a nondiabetic porcine model of heart failure by shifting myocardial metabolism from glucose to ketone bodies, free fatty acids, and branched-chain amino acids.
Santos‐Gallego et al. (2019) conducted an RCT in Heart failure (n=14). Empagliflozin vs. Placebo was evaluated on Adverse left ventricular remodeling and myocardial fuel metabolism. Empagliflozin ameliorated adverse cardiac remodeling and improved LV systolic function in nondiabetic pigs with induced heart failure by switching myocardial fuel utilization toward ketone bodies.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: