Evidence map›Paper›PMID 42472352›Full record

ReviewJournal of cardiovascular electrophysiology2026

Idiopathic Ventricular Fibrillation Triggered by Purkinje-Related Extrasystoles: State-of-the-Art and Novel Therapeutic Approaches.

Giacomo Mugnai, Davide Genovese, Francesco Santoro, Luigi Di Biase, Fengwei Zou, Luca Tomasi, Carlo de Asmundis, Flavio Ribichini, Pedro Brugada, Gian-Battista Chierchia

Abstract readReview
In one paragraph

Review in Journal of cardiovascular electrophysiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

10 authors.

Giacomo MugnaiDivision of Cardiology, Cardio-Thoracic Department, University Hospital of Verona, Verona, Italy.ORCID 0000-0003-4733-9418
Davide GenoveseCardiology Unit, Cardio-Neuro-Vascular Department, Ca' Foncello Hospital, Treviso, Italy.
Francesco SantoroDepartment of Medical and Surgical Sciences, University of Foggia, Foggia, Italy.
Luigi Di BiaseCardiac Arrhythmia Center, Division of Cardiology at Montefiore-Einstein Center, Bronx, New York, USA.ORCID 0000-0001-6508-4047
Fengwei ZouCardiac Arrhythmia Center, Division of Cardiology at Montefiore-Einstein Center, Bronx, New York, USA.
Luca TomasiDivision of Cardiology, Cardio-Thoracic Department, University Hospital of Verona, Verona, Italy.
Carlo de AsmundisHeart Rhythm Management Centre, European Reference Networks Guard-Heart, Universitair Ziekenhuis Brussel Heart Rhythm Research Brussels, Postgraduate Program in Cardiac Electrophysiology and Pacing, Vrije Universiteit Brussel, Brussels, Belgium.ORCID 0000-0001-9351-0760
Flavio RibichiniDivision of Cardiology, Cardio-Thoracic Department, University Hospital of Verona, Verona, Italy.ORCID 0000-0002-6662-0304
Pedro BrugadaHeart Rhythm Management Centre, European Reference Networks Guard-Heart, Universitair Ziekenhuis Brussel Heart Rhythm Research Brussels, Postgraduate Program in Cardiac Electrophysiology and Pacing, Vrije Universiteit Brussel, Brussels, Belgium.
Gian-Battista ChierchiaHeart Rhythm Management Centre, European Reference Networks Guard-Heart, Universitair Ziekenhuis Brussel Heart Rhythm Research Brussels, Postgraduate Program in Cardiac Electrophysiology and Pacing, Vrije Universiteit Brussel, Brussels, Belgium.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ventricular fibrillation (VF) is the primary arrhythmia causing sudden cardiac death. While typically linked to structural heart disease, a significant subset of VF episodes-especially in younger individuals-is triggered by focal ectopy from the His-Purkinje system (HPS). The HPS possesses distinct electrophysiological properties that make it inherently susceptible to arrhythmogenesis. It serves a dual role, acting as both a primary source of initiating premature ventricular complexes through abnormal automaticity and triggered activity (early and delayed afterdepolarizations), and as a critical substrate maintaining VF via micro-re-entrant circuits. This narrative review comprehensively synthesizes current knowledge on Purkinje-triggered VF, from its epidemiology and clinical setting to its underlying pathophysiological and ionic mechanisms of arrhythmia initiation and perpetuation. Finally, we critically evaluate contemporary diagnostic and management strategies, contrasting conventional focal trigger-based ablation with evolving substrate-based approaches such as Purkinje "de-networking."

Indexed as

Bundle of HisCatheter AblationHeart RatePurkinje FibersVentricular FibrillationVentricular Premature ComplexesAction PotentialsAnimalsAnti-Arrhythmia AgentsDeath, Sudden, CardiacHumansRisk FactorsTreatment OutcomeAnti-Arrhythmia Agentscatheter ablationextrasystolePurkinjesudden cardiac deathventricular fibrillation

Identifiers

PMID42472352
PMCPMC13576609

What OpenQuestion holds

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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.