ArticleEuropean heart journal2024
NaV1.5 autoantibodies in Brugada syndrome: pathogenetic implications.
Article in European heart journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Late IMedicinal research reviews · 2026Review
- The Immune System as a Proarrhythmic Mediator: A Novel Paradigm for the Development of New Antiarrhythmic Therapy.The Canadian journal of cardiology · 2026Review
- hERG epitope mimic-decoy peptide corrects autoimmune-long QT syndrome in guinea pigs.Communications medicine · 2026Article
- Contemporary Perspectives on J-Wave Syndromes: An Expert Consensus Statement.Journal of arrhythmia · 2026Article
- Editorial: Past, present, and future of Brugada syndrome: a comprehensive framework.Frontiers in cardiovascular medicine · 2026Article
- Epigenetic regulation of electromechanical continuity might determine phenotypic heterogeneity in SCN5A mutation carriers in Brugada syndrome.Scientific reports · 2025Article
- Clinical presentation and outcomes of patients with biallelicHeart rhythm O2 · 2025Article
- Autoimmune cardiac channelopathies and heart rhythm disorders: A contemporary review.Heart rhythm · 2025Review
- Brugada syndrome.Nature reviews. Disease primers · 2025Review
- Brugada syndrome diagnosed in a young woman occurring postpartum: case report and literature review.Frontiers in cardiovascular medicine · 2025Article
- Anti-Ro/SSA antibodies in adult arrhythmias: pathogenesis, clinical implications, and therapeutic strategies.Frontiers in immunology · 2025Review
- Mechanistic Relevance of Ventricular Arrhythmias in Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2024Review
- Brugada syndrome update.Frontiers in physiology · 2024Review
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Authors and funding
25 authors.
Funding
Abstract
BACKGROUND AND
aimsPatients suffering from Brugada syndrome (BrS) are predisposed to life-threatening cardiac arrhythmias. Diagnosis is challenging due to the elusive electrocardiographic (ECG) signature that often requires unconventional ECG lead placement and drug challenges to be detected. Although NaV1.5 sodium channel dysfunction is a recognized pathophysiological mechanism in BrS, only 25% of patients have detectable SCN5A variants. Given the emerging role of autoimmunity in cardiac ion channel function, this study explores the presence and potential impact of anti-NaV1.5 autoantibodies in BrS patients.
methodsUsing engineered HEK293A cells expressing recombinant NaV1.5 protein, plasma from 50 BrS patients and 50 controls was screened for anti-NaV1.5 autoantibodies via western blot, with specificity confirmed by immunoprecipitation and immunofluorescence. The impact of these autoantibodies on sodium current density and their pathophysiological effects were assessed in cellular models and through plasma injection in wild-type mice.
resultsAnti-NaV1.5 autoantibodies were detected in 90% of BrS patients vs. 6% of controls, yielding a diagnostic area under the curve of .92, with 94% specificity and 90% sensitivity. These findings were consistent across varying patient demographics and independent of SCN5A mutation status. Electrophysiological studies demonstrated a significant reduction specifically in sodium current density. Notably, mice injected with BrS plasma showed Brugada-like ECG abnormalities, supporting the pathogenic role of these autoantibodies.
conclusionsThe study demonstrates the presence of anti-NaV1.5 autoantibodies in the majority of BrS patients, suggesting an immunopathogenic component of the syndrome beyond genetic predispositions. These autoantibodies, which could serve as additional diagnostic markers, also prompt reconsideration of the underlying mechanisms of BrS, as evidenced by their role in inducing the ECG signature of the syndrome in wild-type mice. These findings encourage a more comprehensive diagnostic approach and point to new avenues for therapeutic research.
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