ArticleProgress in biophysics and molecular biology2016
Early afterdepolarizations promote transmural reentry in ischemic human ventricles with reduced repolarization reserve.
Article in Progress in biophysics and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 86 citations in OpenAlex.
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- Initiation of ventricular arrhythmia in the acquired long QT syndrome.Cardiovascular research · 2023Article
- Prolonged repolarization in the early phase of ischemia is associated with ventricular fibrillation development in a porcine model.Frontiers in physiology · 2023Article
- Antiarrhythmic and Inotropic Effects of Selective NaInternational journal of molecular sciences · 2022Review
- R-on-T and the initiation of reentry revisited: Integrating old and new concepts.Heart rhythm · 2022Article
- KHz-rate volumetric voltage imaging of the whole Zebrafish heart.Biophysical reports · 2022Article
- Cardiac electro-mechanical activity in a deforming human cardiac tissue: modeling, existence-uniqueness, finite element computation and application to multiple ischemic disease.Journal of mathematical biology · 2022Article
- Life and death saddles in the heart.Physical review. E · 2021Article
- Model Systems for Addressing Mechanism of Arrhythmogenesis in Cardiac Repair.Current cardiology reports · 2021Review
- Electrophysiological and anatomical factors determine arrhythmic risk in acute myocardial ischaemia and its modulation by sodium current availability.Interface focus · 2021Article
- Mechanisms of Premature Ventricular Complexes Caused by QT Prolongation.Biophysical journal · 2021Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
aimsAcute ischemia is a major cause of sudden arrhythmic death, further promoted by potassium current blockers. Macro-reentry around the ischemic region and early afterdepolarizations (EADs) caused by electrotonic current have been suggested as potential mechanisms in animal and isolated cell studies. However, ventricular and human-specific arrhythmia mechanisms and their modulation by repolarization reserve remain unclear. The goal of this paper is to unravel multiscale mechanisms underlying the modulation of arrhythmic risk by potassium current (IKr) block in human ventricles with acute regional ischemia. METHODS AND
resultsA human ventricular biophysically-detailed model, with acute regional ischemia is constructed by integrating experimental knowledge on the electrophysiological ionic alterations caused by coronary occlusion. Arrhythmic risk is evaluated by determining the vulnerable window (VW) for reentry following ectopy at the ischemic border zone. Macro-reentry around the ischemic region is the main reentrant mechanism in the ischemic human ventricle with increased repolarization reserve due to the ATP-sensitive potassium current (IK(ATP)) activation. Prolongation of refractoriness by 4% caused by 30% IKr reduction counteracts the establishment of macro-reentry and reduces the VW for reentry (by 23.5%). However, a further decrease in repolarization reserve (50% IKr reduction) is less anti-arrhythmic despite further prolongation of refractoriness. This is due to the establishment of transmural reentry enabled by electrotonically-triggered EADs in the ischemic border zone. EADs are produced by L-type calcium current (ICaL) reactivation due to prolonged low amplitude electrotonic current injected during the repolarization phase.
conclusionsElectrotonically-triggered EADs are identified as a potential mechanism facilitating intramural reentry in a regionally-ischemic human ventricles model with reduced repolarization reserve.
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