Related Experiment Video
Updated: May 25, 2026

Testing the Efficacy of Pharmacological Agents in a Pericardial Target Delivery Model in the Swine
Published on: July 7, 2016
Targeting myocardial substrate metabolism in heart failure: potential for new therapies
Hossein Ardehali1, Hani N Sabbah, Michael A Burke
1Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. h-ardehali@northwestern.edu
Insights
Heart failure patients have altered cardiac metabolism, with a shift from fatty acids to glucose and reduced ATP. Targeting these metabolic changes offers a promising therapeutic strategy for heart failure.
Area of Science:
- Cardiology
- Biochemistry
- Molecular Biology
Background:
- Heart failure incidence and prevalence are rising globally.
- Patients with heart failure often have viable but dysfunctional heart muscle.
- Cardiac metabolism in heart failure is understudied despite its potential therapeutic relevance.
Purpose of the Study:
- To review metabolic alterations in heart failure, focusing on fatty acid and glucose metabolism, and AMP-activated kinase.
- To highlight the potential of targeting cardiac energetics for heart failure treatment.
- To advocate for increased research into cardiac metabolic pathways for novel therapeutic development.
Main Methods:
- Review of existing literature on cardiac metabolism in heart failure.
- Analysis of metabolic shifts, including substrate utilization (fatty acid vs. glucose) and ATP levels.
- Examination of the role of AMP-activated kinase in heart failure pathophysiology.
Main Results:
- Heart failure is associated with altered cardiomyocyte energetics.
- A shift from fatty acid to glucose as the preferred metabolic substrate occurs in heart failure.
- Reduced adenosine triphosphate (ATP) levels are observed in failing hearts.
Conclusions:
- Current heart failure therapies do not target metabolic pathways.
- Understanding cardiac metabolic regulation is crucial for developing new treatments.
- Targeting myocardial energetics in viable heart tissue presents a promising therapeutic avenue for heart failure.
Abstract:
The incidence and prevalence of heart failure have increased significantly over the past few decades. Available data suggest that patients with heart failure independent of the aetiology have viable but dysfunctional myocardium that is potentially salvageable. Although a great deal of research effort has focused on characterizing the molecular basis of heart failure, cardiac metabolism in this disorder remains an understudied discipline. It is known that many aspects of cardiomyocyte energetics are altered in heart failure. These include a shift from fatty acid to glucose as a preferred substrate and a decline in the levels of ATP. Despite these demonstrated changes, there are currently no approved drugs that target metabolic enzymes or proteins in heart failure. This is partly due to our limited knowledge of the mechanisms and pathways that regulate cardiac metabolism. Better characterization of these pathways may potentially lead to new therapies for heart failure. Targeting myocardial energetics in the viable and potentially salvageable tissue may be particularly effective in the treatment of heart failure. Here, we will review metabolic changes that occur in fatty acid and glucose metabolism and AMP-activated kinase in heart failure. We propose that cardiac energetics should be considered as a potential target for therapy in heart failure and more research should be done in this area.
Related Concept Videos
Heart Failure V: Medical Management
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Cardiomyopathy V: Interprofessional Care
Heart Failure VI: Adjunct Therapies
Heart Failure Drugs: Inotropic Agents
Heart Failure Drugs: β-Blockers