Evidence map›Paper›PMID 34685609›Full record

ReviewCells2021

Ventricular Arrhythmias in Ischemic Cardiomyopathy-New Avenues for Mechanism-Guided Treatment.

Matthew Amoni, Eef Dries, Sebastian Ingelaere, Dylan Vermoortele, H Llewelyn Roderick, Piet Claus, Rik Willems, Karin R Sipido

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 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.5field-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

30 citing papers in PubMed, 58 citations in OpenAlex.

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  15. Mitochondrial dysfunction as a central hub linking NaFrontiers in cardiovascular medicine · 2025
    Review
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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

8 authors at 2 institutions in 2 countries.

Matthew AmoniExperimental Cardiology, Department of Cardiovascular Sciences, KU Leuven, 3000 Leuven, Belgium.
Eef DriesExperimental Cardiology, Department of Cardiovascular Sciences, KU Leuven, 3000 Leuven, Belgium.
Sebastian IngelaereExperimental Cardiology, Department of Cardiovascular Sciences, KU Leuven, 3000 Leuven, Belgium.ORCID 0000-0002-6851-699X
Dylan VermoorteleImaging and Cardiovascular Dynamics, Department of Cardiovascular Sciences, KU Leuven, 3000 Leuven, Belgium.ORCID 0000-0001-8769-783X
H Llewelyn RoderickExperimental Cardiology, Department of Cardiovascular Sciences, KU Leuven, 3000 Leuven, Belgium.
Piet ClausImaging and Cardiovascular Dynamics, Department of Cardiovascular Sciences, KU Leuven, 3000 Leuven, Belgium.ORCID 0000-0002-2013-639X
Rik WillemsExperimental Cardiology, Department of Cardiovascular Sciences, KU Leuven, 3000 Leuven, Belgium.ORCID 0000-0002-5469-9609
Karin R SipidoExperimental Cardiology, Department of Cardiovascular Sciences, KU Leuven, 3000 Leuven, Belgium.
KU Leuven · BEUniversity of Cape Town · ZA

Funding

Fonds Wetenschappelijk Onderzoek G097021N
6 · The paper itself

Abstract

Ischemic heart disease is the most common cause of lethal ventricular arrhythmias and sudden cardiac death (SCD). In patients who are at high risk after myocardial infarction, implantable cardioverter defibrillators are the most effective treatment to reduce incidence of SCD and ablation therapy can be effective for ventricular arrhythmias with identifiable culprit lesions. Yet, these approaches are not always successful and come with a considerable cost, while pharmacological management is often poor and ineffective, and occasionally proarrhythmic. Advances in mechanistic insights of arrhythmias and technological innovation have led to improved interventional approaches that are being evaluated clinically, yet pharmacological advancement has remained behind. We review the mechanistic basis for current management and provide a perspective for gaining new insights that centre on the complex tissue architecture of the arrhythmogenic infarct and border zone with surviving cardiac myocytes as the source of triggers and central players in re-entry circuits. Identification of the arrhythmia critical sites and characterisation of the molecular signature unique to these sites can open avenues for targeted therapy and reduce off-target effects that have hampered systemic pharmacotherapy. Such advances are in line with precision medicine and a patient-tailored therapy.

Indexed as

AnimalsArrhythmias, CardiacCardiomyopathiesHeart VentriclesHumansMyocardial IschemiaRisk AssessmentVascular Remodelingaction potentialarrhythmiascalciumcardiac remodellingfibrosishypertrophymyocardial infarction

Identifiers

PMID34685609
PMCPMC8534043
OpenAlexW3204539549

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.