Evidence map›Paper›PMID 32246823›Full record

ReviewCardiovascular research2020

Arrhythmogenic cardiomyopathy: pathogenesis, pro-arrhythmic remodelling, and novel approaches for risk stratification and therapy.

Stephanie M van der Voorn, Anneline S J M Te Riele, Cristina Basso, Hugh Calkins, Carol Ann Remme, Toon A B van Veen

Open access · greenAbstract readReview
In one paragraph

Review in Cardiovascular research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.4field-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

44 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Disease models and AAV therapies ofMolecular therapy. Advances · 2026
    Review
  5. Article
  6. Review
  7. AAV9-mediated gene supplementation therapy prevents and rescues arrhythmogenic cardiomyopathy in Pnpla2-mutated mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Observational
  18. Article
  19. The inflammatory spectrum of cardiomyopathies.Frontiers in cardiovascular medicine · 2024
    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

6 authors at 4 institutions in 3 countries.

Stephanie M van der VoornDivision of Heart and Lungs, Department of Medical Physiology, University Medical Center Utrecht, PO Box 85060, Utrecht 3508 AB, The Netherlands.
Anneline S J M Te RieleDivision of Heart and Lungs, Department of Cardiology, University Medical Center Utrecht, PO Box 85060, Utrecht 3508 AB, The Netherlands.
Cristina BassoCardiovascular Pathology Unit, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua Medical School, Via A. Gabelli, 61 35121 Padova, Italy.
Hugh CalkinsJohns Hopkins Hospital, Sheikh Zayed Tower 7125R, Baltimore, MD 21287, USA.
Carol Ann RemmeDepartment of Clinical and Experimental Cardiology, Heart Centre, Amsterdam UMC, Location Academic Medical Center, University of Amsterdam, Amsterdam 1105AZ, The Netherlands.
Toon A B van VeenDivision of Heart and Lungs, Department of Medical Physiology, University Medical Center Utrecht, PO Box 85060, Utrecht 3508 AB, The Netherlands.
University Medical Center Utrecht · NLAmsterdam UMC Location University of Amsterdam · NLJohns Hopkins Hospital · USUniversity of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arrhythmogenic cardiomyopathy (ACM) is a life-threatening cardiac disease caused by mutations in genes predominantly encoding for desmosomal proteins that lead to alterations in the molecular composition of the intercalated disc. ACM is characterized by progressive replacement of cardiomyocytes by fibrofatty tissue, ventricular dilatation, cardiac dysfunction, and heart failure but mostly dominated by the occurrence of life-threatening arrhythmias and sudden cardiac death (SCD). As SCD appears mostly in apparently healthy young individuals, there is a demand for better risk stratification of suspected ACM mutation carriers. Moreover, disease severity, progression, and outcome are highly variable in patients with ACM. In this review, we discuss the aetiology of ACM with a focus on pro-arrhythmic disease mechanisms in the early concealed phase of the disease. We summarize potential new biomarkers which might be useful for risk stratification and prediction of disease course. Finally, we explore novel therapeutic strategies to prevent arrhythmias and SCD in the early stages of ACM.

Indexed as

Action PotentialsHeart RateVentricular RemodelingAnimalsArrhythmogenic Right Ventricular DysplasiaDeath, Sudden, CardiacGenetic Predisposition to DiseaseHumansMutationPhenotypePrevalencePrognosisRisk AssessmentRisk FactorsArrhythmiaCardiomyopathy

Identifiers

PMID32246823
PMCPMC7526754
OpenAlexW3014543651

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.