ArticleCardiovascular research2023
Initiation of ventricular arrhythmia in the acquired long QT syndrome.
Article in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Modeling ventricular tachycardia in genetic long QT syndrome using engineered cardiac tissues.Bioactive materials · 2026Article
- C-terminal long-QT type 1 R562S-Kv7.1 variant, the first variant in helix C impairing β-adrenergic response of the slow delayed rectifier K+ channel.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026Article
- Uncertainty quantification of conduction velocity in models of cardiac spread of activation.Medical & biological engineering & computing · 2026Article
- Personalized in vitro models reveal functional impact of aHeart rhythm O2 · 2026Article
- Case Report: Amiodarone-triggered refractory ventricular fibrillation storm in septic cardiomyopathy with pre-existing QT prolongation: termination using lidocaine and anisodamine.Frontiers in medicine · 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
- Global Knowledge Map and Emerging Research Trends in Induced Pluripotent Stem Cells and Hereditary Diseases: A CiteSpace-based Visualization and Analysis.Stem cell reviews and reports · 2025Review
- Arrhythmic events pertinent with antidepressants: a Bayesian disproportional analysis mining the FDA Adverse Event Reporting System database.Frontiers in psychiatry · 2025Article
- From genes to clinical management: A comprehensive review of long QT syndrome pathogenesis and treatment.Heart rhythm O2 · 2024Review
- 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
- Opioids-Induced Long QT Syndrome: A Challenge to Cardiac Health.Cardiovascular toxicology · 2024Review
- Primary Electrical Heart Disease-Principles of Pathophysiology and Genetics.International journal of molecular sciences · 2024Review
- Quercetin is a foe in the heart by targeting the hERG potassium channel.Iranian journal of basic medical sciences · 2024Article
- Risk factors for ventricular arrhythmias after emergency percutaneous coronary intervention in elderly patients with acute myocardial infarction.American journal of translational research · 2024Article
- Advancements in the diagnosis and management of premature ventricular contractions in pediatric patients.Frontiers in pediatrics · 2024Review
- Mechanisms of torsades de pointes: an update.Frontiers in cardiovascular medicine · 2024Review
- Contractility measurements for cardiotoxicity screening with ventricular myocardial slices of pigs.Cardiovascular research · 2023Article
- A simple approach for image-based modelling of the heart that enables robust simulation of highly heterogeneous electrical excitation.Scientific reports · 2023Article
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6 authors at 2 institutions in 1 country.
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Abstract
aimsLong QT syndrome (LQTS) carries a risk of life-threatening polymorphic ventricular tachycardia (Torsades de Pointes, TdP) and is a major cause of premature sudden cardiac death. TdP is induced by R-on-T premature ventricular complexes (PVCs), thought to be generated by cellular early-afterdepolarisations (EADs). However, EADs in tissue require cellular synchronisation, and their role in TdP induction remains unclear. We aimed to determine the mechanism of TdP induction in rabbit hearts with acquired LQTS (aLQTS). METHODS AND
resultsOptical mapping of action potentials (APs) and intracellular Ca2+ was performed in Langendorff-perfused rabbit hearts (n = 17). TdP induced by R-on-T PVCs was observed during aLQTS (50% K+/Mg++ & E4031) conditions in all hearts (P < 0.0001 vs. control). Islands of AP prolongation bounded by steep voltage gradients (VGs) were consistently observed before arrhythmia and peak VGs were more closely related to the PVC upstroke than EADs, both temporally (7 ± 5 ms vs. 44 ± 27 ms, P < 0.0001) and spatially (1.0 ± 0.7 vs. 3.6 ± 0.9 mm, P < 0.0001). PVCs were initiated at estimated voltages of ∼ -40 mV and had upstroke dF/dtmax and Vm-Ca2+ dynamics compatible with ICaL activation. Computational simulations demonstrated that PVCs could arise directly from VGs, through electrotonic triggering of ICaL. In experiments and the model, sub-maximal L-type Ca2+ channel (LTCC) block (200 nM nifedipine and 90% gCaL, respectively) abolished both PVCs and TdP in the continued presence of aLQTS.
conclusionThese data demonstrate that ICaL activation at sites displaying steep VGs generates the PVCs which induce TdP, providing a mechanism and rationale for LTCC blockers as a novel therapeutic approach in LQTS.
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