ArticlePhysiological reports2021
Mechanisms of phase-3 early afterdepolarizations and triggered activities in ventricular myocyte models.
Article in Physiological reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 11 citations in OpenAlex.
- Interplay between variability in intrinsic cellular properties and heart failure-associated remodeling in a simulated population with human heart failure.Journal of molecular and cellular cardiology · 2026Article
- Methadone Blockade of Inward Rectifier Potassium Current Promotes Both Early and Delayed Repolarization Arrhythmias: Mechanistic Insights From Computational Modeling.Journal of the American Heart Association · 2025Article
- Nicorandil as a promising therapeutic option for ventricular arrhythmia: A case report and review of literature.World journal of cardiology · 2024Article
- Curvature-mediated source and sink effects on the genesis of premature ventricular complexes in long QT syndrome.American journal of physiology. Heart and circulatory physiology · 2024Article
- Modeling incomplete penetrance in long QT syndrome type 3 through ion channel heterogeneity: an in silico population study.American journal of physiology. Heart and circulatory physiology · 2023Article
- Mechanisms of phase-3 early afterdepolarizations and triggered activities in ventricular myocyte models.Physiological reports · 2021Article
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2 authors at 1 institution in 1 country.
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Abstract
Early afterdepolarizations (EADs) are abnormal depolarizations during the repolarizing phase of the action potential, which are associated with cardiac arrhythmogenesis. EADs are classified into phase-2 and phase-3 EADs. Phase-2 EADs occur during phase 2 of the action potential, with takeoff potentials typically above -40 mV. Phase-3 EADs occur during phase 3 of the action potential, with takeoff potential between -70 and -50 mV. Since the amplitude of phase-3 EADs can be as large as that of a regular action potential, they are also called triggered activities (TAs). This also makes phase-3 EADs and TAs much more arrhythmogenic than phase-2 EADs since they can propagate easily in tissue. Although phase-2 EADs have been widely observed, phase-3 EADs and TAs have been rarely demonstrated in isolated ventricular myocytes. Here we carry out computer simulations of three widely used ventricular action potential models to investigate the mechanisms of phase-3 EADs and TAs. We show that when the T-type Ca
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