Evidence map›Paper›PMID 33509397›Full record

ArticleJournal of the American College of Cardiology2021

Etiology-Dependent Impairment of Diastolic Cardiomyocyte Calcium Homeostasis in Heart Failure With Preserved Ejection Fraction.

Michael Frisk, Christopher Le, Xin Shen, Åsmund T Røe, Yufeng Hou, Ornella Manfra, Gustavo J J Silva, Isabelle van Hout, Einar S Norden, J Magnus Aronsen and 14 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of the American College of Cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
13.7field-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.

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

75 citing papers in PubMed, 117 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Assessment of Exercise Intolerance and Evaluation for HFpEF: A Literature Review of Pathophysiology, Diagnosis, and Management.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  9. Unifying and unique roles of non-coding RNA biomarkers in liver and heart fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026
    Review
  10. Restoration of mitochondrial CaJournal of molecular and cellular cardiology · 2026
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026
    Review
  18. Review
  19. The pathophysiological role of MiRNAs in heart failure.Frontiers in cardiovascular medicine · 2026
    Review
  20. Article

15 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

24 authors at 5 institutions in 3 countries.

Michael FriskInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway. Electronic address: https://twitter.com/IEMRLouch.
Christopher LeInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.
Xin ShenInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.
Åsmund T RøeInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.
Yufeng HouInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.
Ornella ManfraInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.
Gustavo J J SilvaInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.
Isabelle van HoutDepartment of Physiology, HeartOtago, University of Otago, Otago, New Zealand.
Einar S NordenInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway; Bjørknes College, Oslo, Norway.
J Magnus AronsenInstitute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Martin LaasmaaInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.
Emil K S EspeInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.
Fouad A ZoueinDepartment of Pharmacology and Toxicology, American University of Beirut Medical Center, Faculty of Medicine, Riad El-Solh, Beirut, Lebanon.
Regis R LambertDepartment of Physiology, HeartOtago, University of Otago, Otago, New Zealand.
Christen P DahlDepartment of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Research Institute for Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Ivar SjaastadInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway; Department of Cardiology, Oslo University Hospital, Ullevål, Oslo, Norway.
Ida G LundeInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.
Sean CoffeyDepartment of Medicine and HeartOtago, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Alessandro CataliottiInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.
Lars GullestadDepartment of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Research Institute for Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Theis TønnessenInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway; Department of Cardiothoracic Surgery, Oslo University Hospital Ullevål, Oslo, Norway.
Peter P JonesDepartment of Physiology, HeartOtago, University of Otago, Otago, New Zealand.
Raffaele AltaraInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway. Electronic address: https://twitter.com/IEMRLouch.
William E LouchInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.
Oslo University Hospital · NOInstitutt for Eksperimentell Medisinsk Forskning · NOUniversity of Otago · NZUniversity of Oslo · NOAmerican University of Beirut Medical Center · LB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWhereas heart failure with reduced ejection fraction (HFrEF) is associated with ventricular dilation and markedly reduced systolic function, heart failure with preserved ejection fraction (HFpEF) patients exhibit concentric hypertrophy and diastolic dysfunction. Impaired cardiomyocyte Ca

objectivesThis study examined whether distinct cardiomyocyte phenotypes underlie the heart failure entities of HFrEF and HFpEF.

methodsT-tubule structure was investigated in left ventricular biopsies obtained from HFrEF and HFpEF patients, whereas cardiomyocyte Ca

resultsHFpEF patients exhibited increased t-tubule density in comparison with control subjects. Super-resolution imaging revealed that higher t-tubule density resulted from both tubule dilation and proliferation. In contrast, t-tubule density was reduced in patients with HFrEF. Augmented collagen deposition within t-tubules was observed in HFrEF but not HFpEF hearts. A causative link between mechanical stress and t-tubule disruption was supported by markedly elevated ventricular wall stress in HFrEF patients. In HFrEF rats, t-tubule loss was linked to impaired systolic Ca

conclusionsAlthough t-tubule disruption and impaired cardiomyocyte Ca

Indexed as

AgedAged, 80 and overCalciumEchocardiographyFemaleHeart Failure, DiastolicHomeostasisHumansMaleMiddle AgedMyocytes, CardiacCalciumcalcium cycling/excitation-contraction couplingheart failure with preserved ejection fractionpathophysiologyremodelingtransverse tubuleswall stress

Identifiers

PMID33509397
PMCPMC7840890
OpenAlexW3123807922

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.