Evidence map›Paper›PMID 34831426›Full record

ReviewCells2021

Arrhythmogenic Remodeling in the Failing Heart.

Zoltán Husti, András Varró, István Baczkó

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Molecular mechanisms and intervention approaches of heart failure (Review).International journal of molecular medicine · 2025
    Review
  7. Review
  8. Article
  9. Tumour necrosis factor alpha-induced protein 3-interacting protein 3 overexpression protects against arrhythmogenic remodelling in the heart failure mice.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2024
    Article
  10. Article
  11. Disease severity, arrhythmogenesis, and fibrosis are related to longer action potentials in tetralogy of Fallot.Clinical research in cardiology : official journal of the German Cardiac Society · 2024
    Article
  12. Article
  13. Ion channel trafficking implications in heart failure.Frontiers in cardiovascular medicine · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Contemporary management of ventricular arrhythmias in heart failure.American journal of cardiovascular disease · 2023
    Review
  19. Article
  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.

Zoltán HustiDepartment of Pharmacology and Pharmacotherapy, University of Szeged, 6720 Szeged, Hungary.
András VarróDepartment of Pharmacology and Pharmacotherapy, University of Szeged, 6720 Szeged, Hungary.
István BaczkóDepartment of Pharmacology and Pharmacotherapy, University of Szeged, 6720 Szeged, Hungary.ORCID 0000-0002-9588-0797
University of Szeged · HU

Funding

Hungarian Academy of Sciences 20004Ministry of Human Capacities 20391-3/2018/FEKUSTRATMinistry of Human Capacities EFOP-3.6.2-16-2017-00006National Research, Development and Innovation Office GINOP-2.3.2-15-2016-00006National Research, Development and Innovation Office NKFIH K128851National Research, Development and Innovation Office NKFIH K135464
6 · The paper itself

Abstract

Chronic heart failure is a clinical syndrome with multiple etiologies, associated with significant morbidity and mortality. Cardiac arrhythmias, including ventricular tachyarrhythmias and atrial fibrillation, are common in heart failure. A number of cardiac diseases including heart failure alter the expression and regulation of ion channels and transporters leading to arrhythmogenic electrical remodeling. Myocardial hypertrophy, fibrosis and scar formation are key elements of arrhythmogenic structural remodeling in heart failure. In this article, the mechanisms responsible for increased arrhythmia susceptibility as well as the underlying changes in ion channel, transporter expression and function as well as alterations in calcium handling in heart failure are discussed. Understanding the mechanisms of arrhythmogenic remodeling is key to improving arrhythmia management and the prevention of sudden cardiac death in patients with heart failure.

Indexed as

Action PotentialsAnimalsArrhythmias, CardiacCalcium SignalingHeart FailureHumansRisk AssessmentVentricular Remodelingarrhythmiasatrial fibrillationcalcium handlingheart failurepotassium currentsremodelingsudden cardiac deathventricular fibrillation

Identifiers

PMID34831426
PMCPMC8623396
OpenAlexW3211880388

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.