Evidence map›Paper›PMID 37199155›Full record

ArticleCirculation2023

Retained Metabolic Flexibility of the Failing Human Heart.

William D Watson, Peregrine G Green, Andrew J M Lewis, Per Arvidsson, Giovanni Luigi De Maria, Håkan Arheden, Einar Heiberg, William T Clarke, Christopher T Rodgers, Ladislav Valkovič and 3 more

Registry-linked trialOpen access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06747429 (Cardiac Metabolic Reprogramming by a Nutritional Intervention), which is not on this map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
16.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT06747429 narecruitingnot on this mapstarted 2026, after this paper: background citation

Cardiac Metabolic Reprogramming by a Nutritional Intervention: the High Fat Diet for Heart Failure (HF4HF) Study, a proof-of Concept Randomized Controlled Trial

TypeinterventionalSponsorFundación Centro Nacional de Investigaciones Cardiovasculares Carlos IIIRan2026 to 2026Enrolled80ConditionsNon-ischemic Dilated Cardiomyopathy, Heart Failure With Reduced Ejection FractionArmsHigh fat diet, Standard diet
3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
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  10. Article
  11. CK2α Deficiency Drives Myocardial Fibrosis via Desmin-Induced Mitochondrial Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
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  18. Article
  19. Biomarkers of Cardiac Metabolic Flexibility in Health, HFrEF and HFpEF.International journal of molecular sciences · 2026
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 8 institutions in 4 countries.

William D Watson *Oxford Centre for Magnetic Resonance Research (W.D.W., P.G.G., A.J.M.L., P.A., L.V., S.N., O.J.R.), University of Oxford, UK.ORCID 0000-0002-2279-6594
Peregrine G Green *Oxford Centre for Magnetic Resonance Research (W.D.W., P.G.G., A.J.M.L., P.A., L.V., S.N., O.J.R.), University of Oxford, UK.
Andrew J M LewisOxford Centre for Magnetic Resonance Research (W.D.W., P.G.G., A.J.M.L., P.A., L.V., S.N., O.J.R.), University of Oxford, UK.ORCID 0000-0002-3714-6711
Per ArvidssonOxford Centre for Magnetic Resonance Research (W.D.W., P.G.G., A.J.M.L., P.A., L.V., S.N., O.J.R.), University of Oxford, UK.ORCID 0000-0002-2262-3562
Giovanni Luigi De MariaDepartment of Cardiology, Oxford University Hospitals NHS Foundation Trust, UK (G.L.D.M.).
Håkan ArhedenClinical Physiology, Department of Clinical Sciences Lund, Lund University, Skåne University Hospital, Lund, Sweden (P.A., H.A., E.H.).ORCID 0000-0002-6124-3159
Einar HeibergClinical Physiology, Department of Clinical Sciences Lund, Lund University, Skåne University Hospital, Lund, Sweden (P.A., H.A., E.H.).
William T ClarkeWellcome Centre for Integrative Neuroimaging, FMRIB, Nuffield Department of Clinical Neurosciences (W.T.C.), University of Oxford, UK.ORCID 0000-0001-7159-7025
Christopher T RodgersWolfson Brain Imaging Centre (C.T.R.), University of Cambridge, UK.ORCID 0000-0003-1275-1197
Ladislav ValkovičOxford Centre for Magnetic Resonance Research (W.D.W., P.G.G., A.J.M.L., P.A., L.V., S.N., O.J.R.), University of Oxford, UK.ORCID 0000-0003-2567-3642
Stefan NeubauerOxford Centre for Magnetic Resonance Research (W.D.W., P.G.G., A.J.M.L., P.A., L.V., S.N., O.J.R.), University of Oxford, UK.ORCID 0000-0001-9017-5645
Neil Herring *Department for Physiology, Anatomy and Genetics (P.G.G., N.H.), University of Oxford, UK.ORCID 0000-0001-8453-6133
Oliver J Rider *Oxford Centre for Magnetic Resonance Research (W.D.W., P.G.G., A.J.M.L., P.A., L.V., S.N., O.J.R.), University of Oxford, UK.ORCID 0000-0003-1295-7769
University of Oxford · GBLund University · SEInstitute of Measurement Science of the Slovak Academy of Sciences · SKJohn Radcliffe Hospital · GBOxford University Hospitals NHS Trust · GBTwitter (United States) · USUniversity of Cambridge · GBWellcome Centre for Integrative Neuroimaging · GB

Funding

British Heart Foundation FS/18/50/33807British Heart Foundation FS/SCRF/20/32005British Heart Foundation PG/2019/34842
6 · The paper itself

Abstract

backgroundThe failing heart is traditionally described as metabolically inflexible and oxygen starved, causing energetic deficit and contractile dysfunction. Current metabolic modulator therapies aim to increase glucose oxidation to increase oxygen efficiency of adenosine triphosphate production, with mixed results.

methodsTo investigate metabolic flexibility and oxygen delivery in the failing heart, 20 patients with nonischemic heart failure with reduced ejection fraction (left ventricular ejection fraction 34.9±9.1) underwent separate infusions of insulin+glucose infusion (I+G) or Intralipid infusion. We used cardiovascular magnetic resonance to assess cardiac function and measured energetics using phosphorus-31 magnetic resonance spectroscopy. To investigate the effects of these infusions on cardiac substrate use, function, and myocardial oxygen uptake (MVo

resultsAt rest, we found that the heart had considerable metabolic flexibility. During I+G, cardiac glucose uptake and oxidation were predominant (70±14% total energy substrate for adenosine triphosphate production versus 17±16% for Intralipid;

conclusionsOur findings show that even in nonischemic heart failure with reduced ejection fraction with severely impaired systolic function, significant cardiac metabolic flexibility is retained, including the ability to alter substrate use to match both arterial supply and changes in workload. Increasing LCFA uptake and oxidation is associated with improved myocardial energetics and contractility. Together, these findings challenge aspects of the rationale underlying existing metabolic therapies for heart failure and suggest that strategies promoting fatty acid oxidation may form the basis for future therapies.

Indexed as

Heart FailureVentricular Dysfunction, LeftAdenosine TriphosphateEnergy MetabolismFatty AcidsGlucoseHumansMyocardiumOxygenStroke VolumeVentricular Function, LeftAdenosine TriphosphateFatty AcidsGlucoseOxygenadenosine triphosphateheart failuremagnetic resonance spectroscopymetabolism

Identifiers

PMID37199155
PMCPMC10417210
OpenAlexW4377010453

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.