Evidence map›Paper›PMID 17530396›Full record

ReviewHeart failure reviews2007

Reperfusion injury as a therapeutic challenge in patients with acute myocardial infarction.

Antonio Rodríguez-Sinovas, Yaser Abdallah, Hans Michael Piper, David Garcia-Dorado

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 91 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Postconditioning with Nitrates Protects Against Myocardial Reperfusion Injury: A New Use for an Old Pharmacological Agent.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Review
  14. Review
  15. Article
  16. Article
  17. Classification of contraction bands using immunohistochemistry.The American journal of forensic medicine and pathology · 2015
    Article
  18. Chromogranin A: a paradoxical player in angiogenesis and vascular biology.Cellular and molecular life sciences : CMLS · 2015
    Review
  19. Autophagy, a process within reperfusion injury: an update.International journal of clinical and experimental pathology · 2014
    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

4 authors at 2 institutions in 2 countries.

Antonio Rodríguez-SinovasLaboratorio de Cardiología Experimental, Servicio de Cardiología, Hospital Universitario Vall d'Hebron, Passeig Vall d'Hebron 119, Barcelona 08035, Spain.
Yaser Abdallah
Hans Michael Piper
David Garcia-Dorado
University of Giessen · DEVall d'Hebron Hospital Universitari · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiomyocyte death secondary to transient ischemia occurs mainly during the first minutes of reperfusion, in the form of contraction band necrosis involving sarcolemmal rupture. Cardiomyocyte hypercontracture caused by re-energisation and pH recovery in the presence of impaired cytosolic Ca(2+) control as well as calpain-mediated cytoskeletal fragility play prominent roles in this type of cell death. Hypercontracture can propagate to adjacent cells through gap junctions. More recently, opening of the mitochondrial permeability transition pore has been shown to participate in reperfusion-induced necrosis, although its precise relation with hypercontracture has not been established. Experimental studies have convincingly demonstrated that infarct size can be markedly reduced by therapeutic interventions applied at the time of reperfusion, including contractile blockers, inhibitors of Na(+)/Ca(2+) exchange, gap junction blockers, or particulate guanylyl cyclase agonists. However, in most cases drugs for use in humans have not been developed and tested for these targets, while the effect of existing drugs with potential cardioprotective effect is not well established or understood. Research effort should be addressed to elucidate the unsolved issues of the molecular mechanisms of reperfusion-induced cell death, to identify and validate new targets and to develop appropriate drugs. The potential benefits of limiting infarct size in patients with acute myocardial infarction receiving reperfusion therapy are enormous.

Indexed as

Ischemic Preconditioning, MyocardialMyocardial ReperfusionAcute DiseaseApoptosisHumansMitochondriaMyocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacNecrosisSarcoplasmic Reticulum

Identifiers

PMID17530396
OpenAlexW2035917039

What OpenQuestion holds

Textmetadata
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.