ArticleBiophysical journal2012
Synchronization of early afterdepolarizations and arrhythmogenesis in heterogeneous cardiac tissue models.
Article in Biophysical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Population Modeling Approach for Human Cardiac Arrhythmia Risk Prediction.Circulation. Arrhythmia and electrophysiology · 2026Article
- Occupational stress, cardiovascular vulnerability and sudden cardiac death in police officers: mechanisms and the protective role of structured exercise.Frontiers in public health · 2026Review
- Intracellular ion accumulation in the genesis of complex action potential dynamics under cardiac diseases.Physical review. E · 2024Article
- Directed graph mapping shows rotors maintain non-terminating and focal sources maintain self-terminating Torsade de Pointes in canine model.Frontiers in physiology · 2023Article
- Article
- Computational modeling of aberrant electrical activity following remuscularization with intramyocardially injected pluripotent stem cell-derived cardiomyocytes.Journal of molecular and cellular cardiology · 2022Article
- Targeting late ICaL to close the window to ventricular arrhythmias.The Journal of general physiology · 2021Article
- Mechanisms of phase-3 early afterdepolarizations and triggered activities in ventricular myocyte models.Physiological reports · 2021Article
- Mechanisms underlying age-associated manifestation of cardiac sodium channel gain-of-function.Journal of molecular and cellular cardiology · 2021Article
- Circadian Rhythms of Early Afterdepolarizations and Ventricular Arrhythmias in a Cardiomyocyte Model.Biophysical journal · 2021Article
- Intercellular Sodium Regulates Repolarization in Cardiac Tissue with Sodium Channel Gain of Function.Biophysical journal · 2020Article
- In silico investigation of the mechanisms underlying atrial fibrillation due to impaired Pitx2.PLoS computational biology · 2020Article
- Multiple Dynamical Mechanisms of Phase-2 Early Afterdepolarizations in a Human Ventricular Myocyte Model:Frontiers in physiology · 2019Article
- Determinants of early afterdepolarization properties in ventricular myocyte models.PLoS computational biology · 2018Article
- Revealing the Concealed Nature of Long-QT Type 3 Syndrome.Circulation. Arrhythmia and electrophysiology · 2017Article
- Effects of early afterdepolarizations on excitation patterns in an accurate model of the human ventricles.PloS one · 2017Article
- Computational Cardiac Modeling Reveals Mechanisms of Ventricular Arrhythmogenesis in Long QT Syndrome Type 8:Frontiers in physiology · 2017Article
- Spatial Patterns of Excitation at Tissue and Whole Organ Level Due to Early Afterdepolarizations.Frontiers in physiology · 2017Review
- Ventricular arrhythmias and the His-Purkinje system.Nature reviews. Cardiology · 2016Review
- Early Drug Discovery Prediction of Proarrhythmia Potential and Its Covariates.The AAPS journal · 2015Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Early afterdepolarizations (EADs) are linked to both triggered arrhythmias and reentrant arrhythmias by causing premature ventricular complexes (PVCs), focal excitations, or heterogeneous tissue substrates for reentry formation. However, a critical number of cells that synchronously exhibit EADs are needed to result in arrhythmia triggers and substrates in tissue. In this study, we use mathematical modeling and computer simulations to investigate EAD synchronization and arrhythmia induction in tissue models with random cell-to-cell variations. Our major observations are as follows. Random cell-to-cell variations in action potential duration without EAD presence do not cause large dispersion of refractoriness in well-coupled tissue. In the presence of phase-2 EADs, the cells may synchronously exhibit the same number of EADs or no EADs with a very small dispersion of refractoriness, or synchronize regionally to result in large dispersion of refractoriness. In the presence of phase-3 EADs, regional synchronization leads to propagating EADs, forming PVCs in tissue. Interestingly, even though the uncoupled cells exhibit either no EAD or only a single EAD, when these cells are coupled to form a tissue, more than one PVC can occur. When the PVCs occur at different locations and time, multifocal arrhythmias are triggered, with the foci shifting in space and time in an irregular manner. The focal arrhythmias either spontaneously terminate or degenerate into reentrant arrhythmias due to heterogeneities and spatiotemporal chaotic dynamics of the foci.
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