Evidence map›Paper›PMID 25239804›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2014

Computational modeling of Takotsubo cardiomyopathy: effect of spatially varying β-adrenergic stimulation in the rat left ventricle.

Sander Land, Steven A Niederer, William E Louch, Åsmund T Røe, Jan Magnus Aronsen, Daniel J Stuckey, Markus B Sikkel, Matthew H Tranter, Alexander R Lyon, Sian E Harding and 1 more

Open access · hybridAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Review
  3. Role of miR-204 in segmental cardiac effects of phenylephrine and pressure overload.Biochemical and biophysical research communications · 2023
    Article
  4. Autonomic control of ventricular function in health and disease: current state of the art.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023
    Review
  5. Molecular Mechanisms of Takotsubo Syndrome.International journal of molecular sciences · 2022
    Review
  6. Review
  7. Takotsubo Syndrome: Translational Implications and Pathomechanisms.International journal of molecular sciences · 2022
    Review
  8. Hyperthermia as a trigger for Takotsubo syndrome in a rat model.Frontiers in cardiovascular medicine · 2022
    Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
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

11 authors at 6 institutions in 3 countries.

Sander LandDepartment of Biomedical Engineering, King's College London, London, United Kingdom;
Steven A NiedererDepartment of Biomedical Engineering, King's College London, London, United Kingdom;
William E LouchInstitute for Experimental Medical Research, Oslo University Hospital Ullevål, Oslo, Norway; KG Jebsen Cardiac Research Center and Center for Heart Failure Research, University of Oslo, Oslo, Norway;
Åsmund T RøeInstitute for Experimental Medical Research, Oslo University Hospital Ullevål, Oslo, Norway; KG Jebsen Cardiac Research Center and Center for Heart Failure Research, University of Oslo, Oslo, Norway;
Jan Magnus AronsenInstitute for Experimental Medical Research, Oslo University Hospital Ullevål, Oslo, Norway; KG Jebsen Cardiac Research Center and Center for Heart Failure Research, University of Oslo, Oslo, Norway;
Daniel J StuckeyNational Heart and Lung Institute, Imperial College London, London, United Kingdom;
Markus B SikkelNational Heart and Lung Institute, Imperial College London, London, United Kingdom;
Matthew H TranterNational Heart and Lung Institute, Imperial College London, London, United Kingdom;
Alexander R LyonNational Heart and Lung Institute, Imperial College London, London, United Kingdom; National Insitute of Health Research Cardiovascular Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom; and.
Sian E HardingNational Heart and Lung Institute, Imperial College London, London, United Kingdom; National Insitute of Health Research Cardiovascular Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom; and.
Nicolas P SmithDepartment of Biomedical Engineering, King's College London, London, United Kingdom; Faculty of Engineering, University of Auckland, Auckland, New Zealand np.smith@auckland.ac.nz.
Imperial College London · GBKing's College London · GBRoyal Brompton Hospital · GBUniversity of Oslo · NOOslo University Hospital · NOUniversity of Auckland · NZ

Funding

The Virtual Physiological Rat ProjectP50GM094503 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BEARD, DANIEL A · 2011 to 2015
$11.6M
Biotechnology and Biological Sciences Research Council BB/J017272/1British Heart Foundation FS/11/67/28954British Heart Foundation RG/11/19/29264NIGMS NIH HHS 1 P50 GM094503-01Wellcome Trust WT092852
6 · The paper itself

Abstract

In Takotsubo cardiomyopathy, the left ventricle shows apical ballooning combined with basal hypercontractility. Both clinical observations in humans and recent experimental work on isolated rat ventricular myocytes suggest the dominant mechanisms of this syndrome are related to acute catecholamine overload. However, relating observed differences in single cells to the capacity of such alterations to result in the extreme changes in ventricular shape seen in Takotsubo syndrome is difficult. By using a computational model of the rat left ventricle, we investigate which mechanisms can give rise to the typical shape of the ventricle observed in this syndrome. Three potential dominant mechanisms related to effects of β-adrenergic stimulation were considered: apical-basal variation of calcium transients due to differences in L-type and sarco(endo)plasmic reticulum Ca(2+)-ATPase activation, apical-basal variation of calcium sensitivity due to differences in troponin I phosphorylation, and apical-basal variation in maximal active tension due to, e.g., the negative inotropic effects of p38 MAPK. Furthermore, we investigated the interaction of these spatial variations in the presence of a failing Frank-Starling mechanism. We conclude that a large portion of the apex needs to be affected by severe changes in calcium regulation or contractile function to result in apical ballooning, and smooth linear variation from apex to base is unlikely to result in the typical ventricular shape observed in this syndrome. A failing Frank-Starling mechanism significantly increases apical ballooning at end systole and may be an important additional factor underpinning Takotsubo syndrome.

Indexed as

Computer SimulationModels, CardiovascularAdrenergic beta-AgonistsAnimalsCalcium SignalingDisease Models, AnimalHeart VentriclesIsoproterenolLinear ModelsMagnetic Resonance Imaging, CineMyocardial ContractionMyocytes, CardiacRatsReceptors, Adrenergic, betaStroke VolumeTakotsubo CardiomyopathyAdrenergic beta-AgonistsIsoproterenolReceptors, Adrenergic, betacardiac modelingcatecholamine overloadTakotsubo cardiomyopathy

Identifiers

PMID25239804
PMCPMC4233305
OpenAlexW2134753829

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.