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Assessment of Cardiac Energy Metabolism, Function, and Physiology in Patients With Heart Failure Taking
Moritz J Hundertmark1,2, Amanda Adler3, Charalambos Antoniades4
1Oxford Centre for Clinical Magnetic Resonance Research (M.J.H., H.L., S.M., F.E.M., B.R., O.R., C.T.R., L.V., M.M., S.N.), Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, John Radcliffe Hospital, UK.
Circulation
|April 18, 2023
Summary
Sodium-glucose co-transporter 2 inhibitors (SGLT2i) did not improve cardiac energy metabolism in heart failure patients. This study suggests that enhanced energy production is unlikely to be the mechanism behind SGLT2i benefits in heart failure.
Area of Science:
- Cardiology
- Metabolic Disorders
- Pharmacology
Background:
- Sodium-glucose co-transporter 2 inhibitors (SGLT2i) are effective for heart failure (HF) but their cardiac mechanism is unclear.
- Myocardial energy metabolism is impaired in all HF types, suggesting SGLT2i might improve energy production.
Purpose of the Study:
- To investigate if empagliflozin alters myocardial energetics, serum metabolomics, and cardiorespiratory fitness in HF patients.
- To explore the potential mechanism of SGLT2i in treating heart failure.
Main Methods:
- A prospective, randomized, double-blind, placebo-controlled trial (EMPA-VISION) involving 72 HF patients (HFrEF and HFpEF).
- Patients received 10 mg empagliflozin or placebo daily for 12 weeks.
- Cardiac energetics (PCr/ATP) were measured using phosphorus magnetic resonance spectroscopy during rest and dobutamine stress; serum metabolomics were also analyzed.
Main Results:
- Empagliflozin did not significantly change cardiac energetics (PCr/ATP) at rest or during stress in either HFrEF or HFpEF groups compared to placebo.
- No significant changes were observed in serum metabolomics or circulating ketone bodies.
Conclusions:
- Empagliflozin treatment for 12 weeks did not improve cardiac energetics or alter serum metabolites related to energy metabolism in HF patients.
- These findings indicate that enhanced cardiac energy metabolism is unlikely to mediate the beneficial effects of SGLT2i in heart failure.
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