The failing heart--an engine out of fuel.

  title={The failing heart--an engine out of fuel.},
  author={Stefan Neubauer},
  journal={The New England journal of medicine},
  volume={356 11},
  • S. Neubauer
  • Published 15 March 2007
  • Medicine
  • The New England journal of medicine
and it can severely reduce a patient’s quality of life. It consumes approximately 2% of the National Health Service budget in the United Kingdom, and in the United States, the total annual cost of treatment for heart failure is approximately $28 billion. Moreover, the financial burden of heart failure will increase in coming decades because of the aging population and the improved treatments of its causes. Over the past 20 years, there has been considerable progress in the treatment of chronic… 

Figures and Tables from this paper


With the exception of heart failure caused by reversible conditions, the condition usually worsens with time and is associated with significantly reduced physical and mental health, resulting in a markedly decreased quality of life.

Metabolic modulation in heart failure: high time for a definitive clinical trial

The putative role for myocardial energetic deficiency in the pathogenesis of HF and the consequent rationale for treating this energy deficiency clinically by metabolic modulation using 3-ketoacyl coenzyme A thiolase inhibition, late sodium current inhibition and carnitine palmitoyl transferase inhibition is increasingly recognised.

A sugar for congestive heart failure patients

There is no cure for CHF and current therapies try to achieve relief of symptoms, improving a patient’s quality of life, and possibly lessening the progression of disease.

Heart failure: a metabolic issue?

A unique combination of cardiac and peripheral effects result in a marked improvement in exercise tolerance and New York Heart Association class and support a larger use of trimetazidine and other metabolic modulators in the management of heart failure.

Heart Failure and Drug Therapies: A Metabolic Review

This review will highlight cardiac metabolism in both the healthy and failing heart and then discuss the metabolic effects of heart failure drugs.

Arrhythmogenic and metabolic remodelling of failing human heart

Recent developments in human HF investigations of electrophysiology remodelling, metabolic remodelling and β‐adrenergic remodelling are summarized and promising new technologies for HF research are discussed.

Enhancing the metabolic substrate: PPAR-alpha agonists in heart failure

PPARα agonists may improve outcomes in patients suffering from systolic heart failure by augmenting myocardial ATP production in addition to targeting maladaptive hypertrophic pathways.

How high-density lipoprotein fuels the failing heart.

Nakajima et al3 now provide novel insights in the regulatory changes of cellular substrate use in the pathogenesis of heart failure, indicating a relative metabolic shift away from fatty acids to glucose oxidation in advanced heart failure.

Sweet as sugar: excessive glucose metabolism in the failing heart.

  • J. Ussher
  • Biology, Medicine
    Future cardiology
  • 2014
P Pereira and colleagues have elucidated the role of the cardiac myocyte glucose transporter 1 (GLUT1) in the failing heart, and its contribution to the alterations in cardiac energy metabolism that accompany HF progression, and demonstrated that GLUT1 expression is increased in the heart 4 weeks following transverse aortic constriction.

Modern view on chronic heart failure therapy: guidelines‑2020 key messages and adjuvant therapy

A rational approach in the management of patients with CHF is to add adjuvant phosphocreatine therapy to the standard treatment strategy according to the current clinical guidelines, which provides an additional improvement in prognosis and a decrease in mortality rates in patients.



Heart failure: diagnosis and healthcare burden.

Despite improvements in management, mortality in the first year after diagnosis remains high, although thereafter it falls to 10% per annum, and hospital admissions for heart failure are predicted to rise by 50% over the next 25 years.

Cardiac metabolism as a target for the treatment of heart failure.

The authors show that recombinant glucagon-like peptide 1 (rGLP-1) dramatically improves left ventricular, systemic, and coronary flow hemodynamics in dogs with advanced dilated cardiomyopathy, and the basis for this functional improvement appears to be related to the restoration of insulin sensitivity in the failing heart.

Heart Failure

  • S. Silver
  • Medicine
    The New England journal of medicine
  • 2003
The June 13, 2007, issue of JAMA includes an article about the role of a new type of treatment for heart failure using biventricular pacemakers.

Modulation of Myocardial Energetics: Emerging Evidence for a Therapeutic Target in Cardiovascular Disease

The report by Lee and colleagues points toward the promise of an alternative approach based on favorably influencing the efficiency of myocardial energetics, thereby increasing cardiac performance without depending on changes in oxygen consumption or improvement in hemodynamics.

A randomized trial of the angiotensin-receptor blocker valsartan in chronic heart failure.

Valsartan significantly reduces the combined end point of mortality and morbidity and improves clinical signs and symptoms in patients with heart failure, when added to prescribed therapy, and raises concern about the potential safety of this specific combination.

The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. U.S. Carvedilol Heart Failure Study Group.

Carvedilol reduces the risk or death as well as the risk of hospitalization for cardiovascular causes in patients with heart failure who are receiving treatment with digoxin, diuretics, and an angiotensin-converting-enzyme inhibitor.

Metabolic therapy for heart failure.

First clinical trial with etomoxir in patients with chronic congestive heart failure.

Etomoxir, which has no acute inotropic or vasodilatory properties and is thought to increase gene expression of the sarcoplasmic reticulum Ca(2+)-ATPase and the alpha-myosin heavy chain, improved clinical status, central haemodynamics at rest and during exercise, and left ventricular ejection fraction in patients with chronic heart failure.

The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators.

Blockade of aldosterone receptors by spironolactone, in addition to standard therapy, substantially reduces the risk of both morbidity and death among patients with severe heart failure.