ArticleHeart rhythm2015
Complex excitation dynamics underlie polymorphic ventricular tachycardia in a transgenic rabbit model of long QT syndrome type 1.
Article in Heart rhythm, 2015. 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, 47 citations in OpenAlex.
- Variable expressivity in long QT syndrome type 2 rabbits defines a low threshold for therapeuticAmerican journal of physiology. Heart and circulatory physiology · 2026Article
- 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
- Loss of developmentally derived Irf8+ macrophages promotes hyperinnervation and arrhythmia in the adult zebrafish heart.bioRxiv : the preprint server for biology · 2024Article
- Myofibroblast senescence promotes arrhythmogenic remodeling in the aged infarcted rabbit heart.eLife · 2023Article
- One Billion hiPSC-Cardiomyocytes: Upscaling Engineered Cardiac Tissues to Create High Cell Density Therapies for Clinical Translation in Heart Regeneration.Bioengineering (Basel, Switzerland) · 2023Article
- Initiation of ventricular arrhythmia in the acquired long QT syndrome.Cardiovascular research · 2023Article
- Directed graph mapping shows rotors maintain non-terminating and focal sources maintain self-terminating Torsade de Pointes in canine model.Frontiers in physiology · 2023Article
- Conduction delays across the specialized conduction system of the heart: Revisiting atrioventricular node (AVN) and Purkinje-ventricular junction (PVJ) delays.Frontiers in cardiovascular medicine · 2023Article
- R-on-T and the initiation of reentry revisited: Integrating old and new concepts.Heart rhythm · 2022Article
- DG-Mapping: a novel software package for the analysis of any type of reentry and focal activation of simulated, experimental or clinical data of cardiac arrhythmia.Medical & biological engineering & computing · 2022Article
- Long-QT founder variant T309I-Kv7.1 with dominant negative pattern may predispose delayed afterdepolarizations under β-adrenergic stimulation.Scientific reports · 2021Article
- PKA phosphorylation underlies functional recruitment of sarcolemmal SK2 channels in ventricular myocytes from hypertrophic hearts.The Journal of physiology · 2020Article
- Transgenic Rabbit Models in Proarrhythmia Research.Frontiers in pharmacology · 2020Review
- Fragmented endocardial signals and early afterdepolarizations during torsades de pointes tachycardia.Cardiology journal · 2020Article
- Human Cardiac Fibroblast Number and Activation State Modulate Electromechanical Function of hiPSC-Cardiomyocytes in Engineered Myocardium.Stem cells international · 2020Article
- R-From-T as a Common Mechanism of Arrhythmia Initiation in Long QT Syndromes.Circulation. Arrhythmia and electrophysiology · 2019Article
- The Increment of Short-term Variability of Repolarisation Determines the Severity of the Imminent Arrhythmic Outcome.Arrhythmia & electrophysiology review · 2019Review
- Transient Outward KCirculation. Arrhythmia and electrophysiology · 2018Article
- Mechanisms linking T-wave alternans to spontaneous initiation of ventricular arrhythmias in rabbit models of long QT syndrome.The Journal of physiology · 2018Article
- Pharmacological Modulation of Mitochondrial CaFrontiers in physiology · 2018Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 1 country.
Funding
Abstract
backgroundLong QT syndrome type 1 (LQT1) is a congenital disease arising from a loss of function in the slowly activating delayed potassium current IKs, which causes early afterdepolarizations (EADs) and polymorphic ventricular tachycardia (pVT).
objectiveThe purpose of this study was to investigate the mechanisms underlying pVT using a transgenic rabbit model of LQT1.
methodsHearts were perfused retrogradely, and action potentials were recorded using a voltage-sensitive dye and CMOS cameras.
resultsBolus injection of isoproterenol (140 nM) induced pVT initiated by focal excitations from the right ventricle (RV; n = 16 of 18 pVTs). After the pVT was initiated, complex focal excitations occurred in both the RV and the left ventricle, which caused oscillations of the QRS complexes on ECG, consistent with the recent proposal of multiple shifting foci caused by EAD chaos. Moreover, the action potential upstroke in pVT showed a bimodal distribution, demonstrating the coexistence of 2 types of excitation that interacted to produce complex pVT: Na(+) current (INa)-mediated fast conduction and L-type Ca(2+) current (ICa)-mediated slow conduction coexist, manifesting as pVT. Addition of 2 μM tetrodotoxin to reduce INa converted pVT into monomorphic VT. Reducing late INa in computer simulation converted pVT into a single dominant reentry, agreeing with experimental results.
conclusionOur study demonstrates that pVT in LQT1 rabbits is initiated by focal excitations from the RV and is maintained by multiple shifting foci in both ventricles. Moreover, wave conduction in pVT exhibits bi-excitability, that is, fast wavefronts driven by INa and slow wavefronts driven by ICa co-exist during pVT.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.