ReviewProgress in biophysics and molecular biology2016
The link between abnormal calcium handling and electrical instability in acquired long QT syndrome--Does calcium precipitate arrhythmic storms?
Review 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 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 41 citations in OpenAlex.
- DENND3-p.R534S disrupts dyadic microdomain architecture to drive potentially pro-arrhythmic calcium and electrophysiologic instability.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
- Optical mapping: pioneering the frontier of preclinical antiarrhythmic drug evaluation.iScience · 2026Review
- Nedaplatin induced QT prolongation with polymorphic ventricular tachyarrhythmia: clinical experience and review of literature.Cardio-oncology (London, England) · 2026Article
- Arrhythmia Inducibility in the CAVB Dog Model, A Critical Analysis on Underlying Factors.Cardiovascular toxicology · 2025Article
- Interpretable manifold learning for T-wave alternans assessment with electrocardiographic imaging.Engineering applications of artificial intelligence · 2025Article
- X-Chromosome-Linked miRNAs Regulate Sex Differences in Cardiac Physiology.Circulation research · 2025Article
- An hiPSC-CM approach for electrophysiological phenotyping of a patient-specific case of short-coupled TdP.Stem cell research & therapy · 2024Article
- Myocardial SERCA2 Protects Against Cardiac Damage and Dysfunction Caused by Inhaled Bromine.The Journal of pharmacology and experimental therapeutics · 2024Article
- Primary Electrical Heart Disease-Principles of Pathophysiology and Genetics.International journal of molecular sciences · 2024Review
- Estimating the probability of early afterdepolarizations and predicting arrhythmic risk associated with long QT syndrome type 1 mutations.Biophysical journal · 2023Article
- Mechanistic insights into spontaneous transition from cellular alternans to ventricular fibrillation.Physiological reports · 2023Article
- Understanding Calmodulin Variants Affecting Calcium-Dependent Inactivation of L-Type Calcium Channels through Whole-Cell Simulation of the Cardiac Ventricular Myocyte.Biomolecules · 2022Article
- Dual loss of regulator of G protein signaling 2 and 5 exacerbates ventricular myocyte arrhythmias and disrupts the fine-tuning of GJournal of molecular and cellular cardiology · 2022Article
- Thyroid hormones regulate cardiac repolarization and QT-interval related gene expression in hiPSC cardiomyocytes.Scientific reports · 2022Article
- Simultaneous imaging of calcium and contraction in the beating heart of zebrafish larvae.Theranostics · 2022Article
- Cardiomyocyte NaBasic research in cardiology · 2021Article
- Genetic and Molecular Aspects of Drug-Induced QT Interval Prolongation.International journal of molecular sciences · 2021Review
- Potential Role of Serum S-100β Protein as a Predictor of Cardiotoxicity and Clinical Poor Outcome in Acute Amphetamine Intoxication.Cardiovascular toxicology · 2021Article
- Mapping Calcium Dynamics in the Heart of Zebrafish Embryos with Ratiometric Genetically Encoded Calcium Indicators.International journal of molecular sciences · 2020Article
- Two-variable nullcline analysis of ionic general equilibrium predicts calcium homeostasis in ventricular myocytes.PLoS computational biology · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Release of Ca(2+) ions from sarcoplasmic reticulum (SR) into myocyte cytoplasm and their binding to troponin C is the final signal form myocardial contraction. Synchronous contraction of ventricular myocytes is necessary for efficient cardiac pumping function. This requires both shuttling of Ca(2+) between SR and cytoplasm in individual myocytes, and organ-level synchronization of this process by means of electrical coupling among ventricular myocytes. Abnormal Ca(2+) release from SR causes arrhythmias in the setting of CPVT (catecholaminergic polymorphic ventricular tachycardia) and digoxin toxicity. Recent optical mapping data indicate that abnormal Ca(2+) handling causes arrhythmias in models of both repolarization impairment and profound bradycardia. The mechanisms involve dynamic spatial heterogeneity of myocardial Ca(2+) handling preceding arrhythmia onset, cell-synchronous systolic secondary Ca(2+) elevation (SSCE), as well as more complex abnormalities of intracellular Ca(2+) handling detected by subcellular optical mapping in Langendorff-perfused hearts. The regional heterogeneities in Ca(2+) handling cause action potential (AP) heterogeneities through sodium-calcium exchange (NCX) activation and eventually overwhelm electrical coupling of the tissue. Divergent Ca(2+) dynamics among different myocardial regions leads to temporal instability of AP duration and - on the patient level - in T wave lability. Although T-wave alternans has been linked to cardiac arrhythmias, non-alternans lability is observed in pre-clinical models of the long QT syndrome (LQTS) and CPVT, and in LQTS patients. Analysis of T wave lability may provide a real-time window on the abnormal Ca(2+) dynamics causing specific arrhythmias such as Torsade de Pointes (TdP).
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Registered trials
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.