Evidence map›Paper›PMID 15852034›Full record

ReviewBritish journal of pharmacology2005

Phase 2 ventricular arrhythmias in acute myocardial infarction: a neglected target for therapeutic antiarrhythmic drug development and for safety pharmacology evaluation.

Hugh Clements-Jewery, David J Hearse, Michael J Curtis

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 61 citations in OpenAlex.

  1. Trial
  2. Review
  3. Temporal variability of T-wave morphology and risk of sudden cardiac death in patients with coronary artery disease.Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc · 2021
    Article
  4. Article
  5. Electrophysiologic Effects of Growth Hormone Post-Myocardial Infarction.International journal of molecular sciences · 2020
    Review
  6. Review
  7. Review
  8. Review
  9. KATP Channels in the Cardiovascular System.Physiological reviews · 2016
    Review
  10. Optogenetic determination of the myocardial requirements for extrasystoles by cell type-specific targeting of ChannelRhodopsin-2.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Do endothelin receptor antagonists have an antiarrhythmic potential during acute myocardial infarction? Evidence from experimental studies.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2010
    Review
  17. Article
  18. Article
  19. miRNAs at the heart of the matter.Journal of molecular medicine (Berlin, Germany) · 2008
    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

3 authors at 1 institution in 1 country.

Hugh Clements-JeweryCardiovascular Division, King's College London, London, UK.
David J Hearse
Michael J Curtis
King's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ventricular fibrillation (VF), a cause of sudden cardiac death (SCD) in the setting of acute myocardial infarction (MI), remains a major therapeutic challenge. In humans, VF may occur within minutes or hours after the onset of chest pain, so its precise timing in relation to the onset of ischaemia is variable. Moreover, because VF usually occurs unobserved, out of hospital, and is usually lethal in the absence of intervention, its precise timing of onset is actually unknown in most patients. In animal models, the timing of susceptibility to VF is much better characterised. It occurs in two distinct phases. Early VF (defined as phase 1 VF, with possible subphases 1a and 1b in some animal species) occurs during the first 30 min of ischaemia when most myocardial injury is still reversible. Late VF, defined as phase 2 VF, occurs when myocardial necrosis is becoming established (after more than 90 min of ischaemia). Although much is known about the mechanisms and pharmacology of phase 1 VF, little is known about phase 2 VF. By reviewing a range of different types of data we have outlined the likely mechanisms and clinical relevance of phase 2 VF, and have evaluated possible future directions to help evolve a strategy for its suppression by drugs. The possibility that a proarrhythmic effect on phase 2 VF contributes to the adverse cardiac effects of certain cardiac and noncardiac drugs is also discussed in relation to the emerging field of safety pharmacology. It is concluded that suppression of phase 2 as well as phase 1 VF will almost certainly be necessary if drugs of the future are to achieve what drugs of the past and present have failed to achieve: full protection against SCD. Likewise, safety will require avoidance of exacerbation of phase 2 as well as phase 1 VF.

Indexed as

AnimalsAnti-Arrhythmia AgentsArrhythmias, CardiacHumansMyocardial InfarctionAnti-Arrhythmia Agents

Identifiers

PMID15852034
PMCPMC1576179
OpenAlexW2055441411

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.