Evidence map›Paper›PMID 32438845›Full record

ArticleCirculation2020

Cardiac Energetics in Patients With Aortic Stenosis and Preserved Versus Reduced Ejection Fraction.

Mark A Peterzan, William T Clarke, Craig A Lygate, Hannah A Lake, Justin Y C Lau, Jack J Miller, Errin Johnson, Jennifer J Rayner, Moritz J Hundertmark, Rana Sayeed and 6 more

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Circulation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 9% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Phosphorus Magnetic Resonance Spectroscopy (Medicina (Kaunas, Lithuania) · 2023
    Pooled it
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  20. Water-suppression cycling 3-T cardiacNMR in biomedicine · 2021
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 8 institutions in 3 countries.

Mark A PeterzanOxford Centre for Clinical Magnetic Resonance Research, Division of Cardiovascular Medicine (M.A.P., J.Y.C.L., J.J.M., J.J.R., M.J.H., S.N., O.J.R.), University of Oxford, United Kingdom.
William T ClarkeWellcome Centre for Integrative Neuroimaging, FMRIB, Nuffield Department of Clinical Neurosciences (W.T.C.), University of Oxford, United Kingdom.
Craig A Lygate
Hannah A LakeDivision of Cardiovascular Medicine, Radcliffe Department of Medicine (H.A.L.), University of Oxford, United Kingdom.
Justin Y C LauOxford Centre for Clinical Magnetic Resonance Research, Division of Cardiovascular Medicine (M.A.P., J.Y.C.L., J.J.M., J.J.R., M.J.H., S.N., O.J.R.), University of Oxford, United Kingdom.
Jack J MillerOxford Centre for Clinical Magnetic Resonance Research, Division of Cardiovascular Medicine (M.A.P., J.Y.C.L., J.J.M., J.J.R., M.J.H., S.N., O.J.R.), University of Oxford, United Kingdom.
Errin JohnsonDunn School of Pathology (E.J.), University of Oxford, United Kingdom.
Jennifer J RaynerOxford Centre for Clinical Magnetic Resonance Research, Division of Cardiovascular Medicine (M.A.P., J.Y.C.L., J.J.M., J.J.R., M.J.H., S.N., O.J.R.), University of Oxford, United Kingdom.
Moritz J HundertmarkOxford Centre for Clinical Magnetic Resonance Research, Division of Cardiovascular Medicine (M.A.P., J.Y.C.L., J.J.M., J.J.R., M.J.H., S.N., O.J.R.), University of Oxford, United Kingdom.
Rana SayeedDepartment of Cardiothoracic Surgery, Oxford Heart Centre, John Radcliffe Hospital, United Kingdom (R.S., G.K., V.S.).
Mario PetrouDepartment of Cardiothoracic Surgery, Royal Brompton and Harefield National Health Service Foundation Trust, London, United Kingdom (M.P.).
George KrasopoulosDepartment of Cardiothoracic Surgery, Oxford Heart Centre, John Radcliffe Hospital, United Kingdom (R.S., G.K., V.S.).
Vivek SrivastavaDepartment of Cardiothoracic Surgery, Oxford Heart Centre, John Radcliffe Hospital, United Kingdom (R.S., G.K., V.S.).
Stefan NeubauerOxford Centre for Clinical Magnetic Resonance Research, Division of Cardiovascular Medicine (M.A.P., J.Y.C.L., J.J.M., J.J.R., M.J.H., S.N., O.J.R.), University of Oxford, United Kingdom.
Christopher T RodgersWolfson Brain Imaging Centre, University of Cambridge, United Kingdom (C.T.R.).
Oliver J RiderOxford Centre for Clinical Magnetic Resonance Research, Division of Cardiovascular Medicine (M.A.P., J.Y.C.L., J.J.M., J.J.R., M.J.H., S.N., O.J.R.), University of Oxford, United Kingdom.
Johnson & Johnson (United Kingdom) · GBJohn Radcliffe Hospital · GBCraig Technologies (United States) · USImaging Center · USJharkhand Rai University · INRoyal Brompton & Harefield NHS Foundation Trust · GBUniversity of Oxford · GBWellcome Centre for Integrative Neuroimaging · GB

Funding

Biotechnology and Biological Sciences Research Council BB/C014122/1British Heart Foundation FS/15/80/31803British Heart Foundation FS/16/70/32157British Heart Foundation FS/17/48/32907British Heart Foundation RG/18/12/34040Wellcome Trust 098436/Z/12/B
6 · The paper itself

Abstract

backgroundWhy some but not all patients with severe aortic stenosis (SevAS) develop otherwise unexplained reduced systolic function is unclear. We investigate the hypothesis that reduced creatine kinase (CK) capacity and flux is associated with this transition.

methodsWe recruited 102 participants to 5 groups: moderate aortic stenosis (ModAS) (n=13), SevAS, left ventricular (LV) ejection fraction ≥55% (SevAS-preserved ejection fraction, n=37), SevAS, LV ejection fraction <55% (SevAS-reduced ejection fraction, n=15), healthy volunteers with nonhypertrophied hearts with normal systolic function (normal healthy volunteer, n=30), and patients with nonhypertrophied, non-pressure-loaded hearts with normal systolic function undergoing cardiac surgery and donating LV biopsy (non-pressure-loaded heart biopsy, n=7). All underwent cardiac magnetic resonance imaging and

resultsIn the absence of failure, CK flux was lower in the presence of AS (by 32%,

conclusionsTotal CK capacity is reduced in SevAS, with median values lowest in those with systolic failure, consistent with reduced energy supply reserve. Despite this, in vivo magnetic resonance spectroscopy measures of resting CK flux suggest that ATP delivery is reduced earlier, at the moderate AS stage, where LV function remains preserved. These findings show that significant energetic impairment is already established in moderate AS and suggest that a fall in CK flux is not by itself a necessary cause of transition to systolic failure. However, because ATP demands increase with AS severity, this could increase susceptibility to systolic failure. As such, targeting CK capacity and flux may be a therapeutic strategy to prevent and treat systolic failure in AS.

Indexed as

Adenosine TriphosphateAdultAgedAged, 80 and overAortic Valve StenosisBiomarkersCreatine KinaseEnergy MetabolismFemaleHumansMagnetic Resonance SpectroscopyMaleMiddle AgedProspective StudiesStroke VolumeVentricular Dysfunction, LeftAdenosine TriphosphateBiomarkersCreatine Kinaseaortic valve stenosiscreatine kinaseheart failuremagnetic resonance spectroscopymetabolism

Identifiers

PMID32438845
PMCPMC7294745
OpenAlexW3026255468

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.