Evidence map›Paper›PMID 40004861›Full record

ReviewJournal of clinical medicine2025

Substrates of Sudden Cardiac Death in Hypertrophic Cardiomyopathy.

Matteo Sclafani, Giulio Falasconi, Giacomo Tini, Beatrice Musumeci, Diego Penela, Andrea Saglietto, Luca Arcari, Chiara Bucciarelli-Ducci, Emanuele Barbato, Antonio Berruezo and 1 more

Abstract readReview
In one paragraph

Review in Journal of clinical medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Atrial electrophysiology in hypertrophic cardiomyopathy: current insights and knowledge gaps.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2026
    Review
  2. Article
  3. A New Era in the Management of Hypertrophic Cardiomyopathy.Reviews in cardiovascular medicine · 2025
    Review
  4. Article
  5. 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

11 authors.

Matteo SclafaniRoyal Brompton and Harefield Hospitals, Guy's and St Thomas' NHS Foundation Trust, London SW3 6PY, UK.
Giulio FalasconiArrhythmia Department, Teknon Heart Institute, Teknon Medical Center, 08022 Barcelona, Spain.ORCID 0000-0001-7128-9911
Giacomo TiniCardiology Unit, Department of Clinical and Molecular Medicine, Sant'Andrea University Hospital, Sapienza University, 00189 Rome, Italy.
Beatrice MusumeciCardiology Unit, Department of Clinical and Molecular Medicine, Sant'Andrea University Hospital, Sapienza University, 00189 Rome, Italy.ORCID 0000-0003-4872-7981
Diego PenelaArrhythmia Department, Teknon Heart Institute, Teknon Medical Center, 08022 Barcelona, Spain.
Andrea SagliettoDivision of Cardiology, Cardiovascular and Thoracic Department, "Citta Della Salute e Della Scienza" Hospital, 10126 Turin, Italy.ORCID 0000-0001-9475-1507
Luca ArcariCardiology Unit, Madre Giuseppina Vannini Hospital, 00177 Rome, Italy.ORCID 0000-0003-1410-6845
Chiara Bucciarelli-DucciRoyal Brompton and Harefield Hospitals, Guy's and St Thomas' NHS Foundation Trust, London SW3 6PY, UK.
Emanuele BarbatoCardiology Unit, Department of Clinical and Molecular Medicine, Sant'Andrea University Hospital, Sapienza University, 00189 Rome, Italy.
Antonio BerruezoArrhythmia Department, Teknon Heart Institute, Teknon Medical Center, 08022 Barcelona, Spain.
Pietro FranciaCardiology Unit, Department of Clinical and Molecular Medicine, Sant'Andrea University Hospital, Sapienza University, 00189 Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sudden cardiac death (SCD), the most devastating complication of hypertrophic cardiomyopathy (HCM), is primarily triggered by ventricular tachycardia or fibrillation. Despite advances in knowledge, the mechanisms driving ventricular arrhythmia in HCM remain incompletely understood, stemming from an interplay of multiple pro-arrhythmic factors. Myocyte disarray and myocardial fibrosis form a structural substrate favorable to re-entrant arrhythmias by altering myocardial electrophysiological properties, while cellular abnormalities predominate in patients without evident structural remodeling. Traditional SCD risk prediction models rely on clinical risk factors and regression-based risk estimation, often overlooking specific arrhythmic substrates. Emerging techniques now allow for the direct assessment of these substrates, providing deeper insights into the arrhythmogenic mechanisms and paving the way for more personalized SCD risk stratification. This review explores the contribution of cellular, structural, and electrophysiological substrates to arrhythmic risk in HCM, emphasizing their distinct roles. Furthermore, it highlights the potential of substrate-based approaches to refining SCD prevention strategies and improving outcomes for patients with HCM.

Indexed as

afterdepolarizationscardiovascular magnetic resonanceelectrophysiological studyhypertrophic cardiomyopathysubstratessudden cardiac deathventricular fibrillationventricular tachycardia

Identifiers

PMID40004861
PMCPMC11857077

What OpenQuestion holds

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Registered trials

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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.