Evidence map›Paper›PMID 30310998›Full record

ArticleBasic research in cardiology2018

The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection-evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology.

Sean M Davidson, Sapna Arjun, Maryna V Basalay, Robert M Bell, Daniel I Bromage, Hans Erik Bøtker, Richard D Carr, John Cunningham, Arjun K Ghosh, Gerd Heusch and 8 more

Open access · hybridAbstract readConference Proceedings
In one paragraph

Article in Basic research in cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
11.8field-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

36 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Evidence for the Benefits of Melatonin in Cardiovascular Disease.Frontiers in cardiovascular medicine · 2022
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

18 authors at 10 institutions in 6 countries.

Sean M DavidsonThe Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, 67 Chenies Mews, London, WC1E 6HX, UK.
Sapna ArjunThe Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, 67 Chenies Mews, London, WC1E 6HX, UK.
Maryna V BasalayThe Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, 67 Chenies Mews, London, WC1E 6HX, UK.
Robert M BellThe Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, 67 Chenies Mews, London, WC1E 6HX, UK.
Daniel I BromageSchool of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, UK.
Hans Erik BøtkerDepartment of Cardiology, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.
Richard D CarrThe Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, 67 Chenies Mews, London, WC1E 6HX, UK.
John CunninghamCentre for Nephrology, UCL Medical School, Royal Free Campus, Rowland Hill Street, London, NW3 2PF, UK.
Arjun K GhoshThe Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, 67 Chenies Mews, London, WC1E 6HX, UK.
Gerd HeuschWest German Heart and Vascular Center, Institute for Pathophysiology, University of Essen Medical School, Essen, Germany.
Borja IbanezCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Petra KleinbongardWest German Heart and Vascular Center, Institute for Pathophysiology, University of Essen Medical School, Essen, Germany.
Sandrine LecourCardioprotection Group, Hatter Institute for Cardiovascular Research in Africa, University of Cape Town, Cape Town, South Africa.
Helen MaddockCentre for Sport, Exercise and Life Sciences, Faculty of Health and Life Sciences, Coventry University, Priory Street, Coventry, CV1 5FB, UK.
Michel OvizeINSERM U1060, CarMeN Laboratory, Université de Lyon and Service d'explorations Fonctionnelles Cardiovasculaires Groupement Hospitalier Est, 59 Boulevard Pinel, 69500, Bron, France.
Malcolm WalkerThe Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, 67 Chenies Mews, London, WC1E 6HX, UK.
Marlene WiartINSERM U1060, CarMeN Laboratory, Université de Lyon and Service d'explorations Fonctionnelles Cardiovasculaires Groupement Hospitalier Est, 59 Boulevard Pinel, 69500, Bron, France.
Derek M YellonThe Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, 67 Chenies Mews, London, WC1E 6HX, UK. D.Yellon@ucl.ac.uk.
University College London · GBWest German Heart and Vascular Center Essen · DEAarhus University Hospital · DKBritish Heart Foundation · GBCoventry University · GBHospices Civils de Lyon · FRHospital Universitario Fundación Jiménez Díaz · ESInserm · FRThe Royal Free Hospital · GBUniversity of Cape Town · ZA

Funding

British Heart Foundation PG/16/85/32471British Heart Foundation PG/18/44/33790Department of HealthMedical Research Council MR/L002043/1
6 · The paper itself

Abstract

Due to its poor capacity for regeneration, the heart is particularly sensitive to the loss of contractile cardiomyocytes. The onslaught of damage caused by ischaemia and reperfusion, occurring during an acute myocardial infarction and the subsequent reperfusion therapy, can wipe out upwards of a billion cardiomyocytes. A similar program of cell death can cause the irreversible loss of neurons in ischaemic stroke. Similar pathways of lethal cell injury can contribute to other pathologies such as left ventricular dysfunction and heart failure caused by cancer therapy. Consequently, strategies designed to protect the heart from lethal cell injury have the potential to be applicable across all three pathologies. The investigators meeting at the 10th Hatter Cardiovascular Institute workshop examined the parallels between ST-segment elevation myocardial infarction (STEMI), ischaemic stroke, and other pathologies that cause the loss of cardiomyocytes including cancer therapeutic cardiotoxicity. They examined the prospects for protection by remote ischaemic conditioning (RIC) in each scenario, and evaluated impasses and novel opportunities for cellular protection, with the future landscape for RIC in the clinical setting to be determined by the outcome of the large ERIC-PPCI/CONDI2 study. It was agreed that the way forward must include measures to improve experimental methodologies, such that they better reflect the clinical scenario and to judiciously select combinations of therapies targeting specific pathways of cellular death and injury.

Indexed as

CardiologyMedical OncologyMyocardial InfarctionStrokeAnimalsAntineoplastic AgentsCytoprotectionHumansIschemic Preconditioning, MyocardialMyocardial Reperfusion InjuryAntineoplastic AgentsAnthracycline cardiotoxicityCardioprotectionIschaemic strokeMyocardial ischaemiaNeuroprotectionReperfusion

Identifiers

PMID30310998
PMCPMC6182684
OpenAlexW2896014870

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.