ArticleInternational journal of cardiology. Heart & vasculature2024
Whole-heart computational modelling provides further mechanistic insights into ST-elevation in Brugada syndrome.
Article in International journal of cardiology. Heart & vasculature, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The functional impact of myofiber macroscopic organization and disarray in computational models of the murine heart.PLoS computational biology · 2026Article
- Electrophysiological Modeling and Molecular Dynamics Simulations of Cardiac Sodium Channels in Brugada Syndrome.BioMed research international · 2026Article
- Hypernatremia Enhances Transient Outward Potassium and Late Sodium Currents in a Mouse Model of Long QT Syndrome Type 3.bioRxiv : the preprint server for biology · 2025Article
- High-density atrial mapping, P-wave analysis, and computational simulations in Brugada syndrome: Enhancing the understanding of atrial fibrillation.Heart rhythm O2 · 2025Article
- Digital Twins of Biological Systems: A Narrative Review.IEEE open journal of engineering in medicine and biology · 2024Article
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Authors and funding
8 authors.
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Abstract
Background: Brugada syndrome (BrS) is characterized by dynamic ST-elevations in right precordial leads and increased risk of ventricular fibrillation and sudden cardiac death. As the mechanism underlying ST-elevation and malignant arrhythmias is controversial computational modeling can aid in exploring the disease mechanism. Thus we aim to test the main competing hypotheses ('delayed depolarization' vs. 'early repolarization') of BrS in a whole-heart computational model. Methods: In a 3D whole-heart computational model, delayed epicardial RVOT activation with local conduction delay was simulated by reducing conductivity in the epicardial RVOT. Early repolarization was simulated by instead increasing the transient outward potassium current (I Results: Delayed depolarization with local conduction delay in the computational model resulted in coved-type ST-elevation with negative T-waves in the precordial surface ECG leads. 'Saddleback'-shaped ST-elevation was obtained with reduced substrate extent or thickness. Increased I Conclusions: In this whole-heart BrS computational model of both major hypotheses, realistic coved-type ECG resulted only from delayed epicardial RVOT depolarization with local conduction delay but not early repolarizing ion channel modifications. These simulations provide further support for the depolarization hypothesis as electrophysiological mechanism underlying BrS.
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