ArticleJournal of the American College of Cardiology2015
Fibrosis, Connexin-43, and Conduction Abnormalities in the Brugada Syndrome.
Article in Journal of the American College of Cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 156 papers, 2 of them syntheses that pooled it.
What it found
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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.
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.
Ablation in Brugada Syndrome for Prevention of VF - A Randomized, Multi-center Study of Epicardial Ablation in Brugada Syndrome Patients to Prevent Arrhythmia Recurrence
Mapping of Ventricular Fibrillation (VF) Substrates and VF Arrhythmogenic Sources/Reentrant Circuits in Patients With Brugada and Early Repolarization Syndromes
Who cites it
156 citing papers in PubMed, 2 syntheses or guidelines pooled it, 367 citations in OpenAlex.
- Efficacy and safety of catheter ablation for Brugada syndrome: an updated systematic review.Clinical research in cardiology : official journal of the German Cardiac Society · 2023Pooled it
- SCN5A mutation status increases the risk of major arrhythmic events in Asian populations with Brugada syndrome: systematic review and meta-analysis.Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc · 2019Pooled it
- Artificial Intelligence Enabled Dielectric Fingerprinting of Arrhythmogenic Substrates: A Precision Paradigm for Tissue Characterization Guided Cardiac Electrophysiology.Sensors (Basel, Switzerland) · 2026Review
- Brugada Syndrome: an exemplar for the genomic basis of sudden death.European journal of human genetics : EJHG · 2026Review
- RYR1 Pathogenic Variant in a Patient With Overlapping Features of Brugada Syndrome and Arrhythmogenic Cardiomyopathy.JACC. Case reports · 2026Article
- Contemporary Perspectives on J-Wave Syndromes: An Expert Consensus Statement.Journal of arrhythmia · 2026Article
- Electromechanical and structural phenotypes from cardiac imaging and epicardial mapping in inherited arrhythmia syndromes.Frontiers in cardiovascular medicine · 2026Review
- Brugada Phenocopies: A Review of Mechanisms, Clinical Implications and Prognostic Considerations.Arrhythmia & electrophysiology review · 2026Review
- Time-dependent S-wave areas by 24-hour ECG are correlated with a high risk of sudden cardiac death: ECG prediction model development and validation for SCD risk.Cardiovascular diagnosis and therapy · 2025Article
- Epigenetic regulation of electromechanical continuity might determine phenotypic heterogeneity in SCN5A mutation carriers in Brugada syndrome.Scientific reports · 2025Article
- Uncommon and Accessory Electrocardiographic Findings in Brugada Syndrome: A Review.Journal of clinical medicine · 2025Review
- The Utility of Notched P-Wave on the Occurrence of Ventricular Fibrillation in Patients With Brugada Syndrome.Journal of arrhythmia · 2025Article
- Assessment of activation delay in the right ventricular outflow tract as a potential complementary diagnostic tool for Brugada Syndrome.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 · 2025Article
- Accumulating evidence for epicardial ablation in malignant forms of Brugada syndrome: summary of two randomized clinical trials.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 · 2025Article
- Hybrid mini-thoracotomy for Brugada syndrome: epicardial substrate characterization and ablation-results from UNCOVER(BrS) study.Frontiers in cardiovascular medicine · 2025Article
- Brugada syndrome in the forensic field: what do we know to date?Frontiers in cardiovascular medicine · 2025Review
- Editorial: Insights in cardiac rhythmology 2023.Frontiers in cardiovascular medicine · 2025Article
- Epicardial Ablation for Arrhythmogenic Disorders in Patients with Brugada Syndrome.Biomedicines · 2024Review
- Morphological phenotype of right ventricular outflow tract is associated with cardiovascular outcomes and premature death.Scientific reports · 2024Article
- NaV1.5 autoantibodies in Brugada syndrome: pathogenetic implications.European heart journal · 2024Article
96 more citing papers are in PubMed but not listed here.
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Authors and funding
20 authors at 10 institutions in 6 countries.
Funding
Abstract
backgroundThe right ventricular outflow tract (RVOT) is acknowledged to be responsible for arrhythmogenesis in Brugada syndrome (BrS), but the pathophysiology remains controversial.
objectivesThis study assessed the substrate underlying BrS at post-mortem and in vivo, and the role for open thoracotomy ablation.
methodsSix whole hearts from male post-mortem cases of unexplained sudden death (mean age 23.2 years) with negative specialist cardiac autopsy and familial BrS were used and matched to 6 homograft control hearts by sex and age (within 3 years) by random risk set sampling. Cardiac autopsy sections from cases and control hearts were stained with picrosirius red for collagen. The RVOT was evaluated in detail, including immunofluorescent stain for connexin-43 (Cx43). Collagen and Cx43 were quantified digitally and compared. An in vivo study was undertaken on 6 consecutive BrS patients (mean age 39.8 years, all men) during epicardial RVOT ablation for arrhythmia via thoracotomy. Abnormal late and fractionated potentials indicative of slowed conduction were identified, and biopsies were taken before ablation.
resultsCollagen was increased in BrS autopsy cases compared with control hearts (odds ratio [OR]: 1.42; p = 0.026). Fibrosis was greatest in the RVOT (OR: 1.98; p = 0.003) and the epicardium (OR: 2.00; p = 0.001). The Cx43 signal was reduced in BrS RVOT (OR: 0.59; p = 0.001). Autopsy and in vivo RVOT samples identified epicardial and interstitial fibrosis. This was collocated with abnormal potentials in vivo that, when ablated, abolished the type 1 Brugada electrocardiogram without ventricular arrhythmia over 24.6 ± 9.7 months.
conclusionsBrS is associated with epicardial surface and interstitial fibrosis and reduced gap junction expression in the RVOT. This collocates to abnormal potentials, and their ablation abolishes the BrS phenotype and life-threatening arrhythmias. BrS is also associated with increased collagen throughout the heart. Abnormal myocardial structure and conduction are therefore responsible for BrS.
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Registered trials
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.