ArticleFrontiers in physiology2013
In silico investigation of the short QT syndrome, using human ventricle models incorporating electromechanical coupling.
Article in Frontiers in physiology, 2013. 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, 48 citations in OpenAlex.
- Mechano-electrical feedback in transgenic rabbit models of long QT syndrome Type 2 and short QT syndrome Type 1.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
- Cardiac arrhythmogenesis: roles of ion channels and their functional modification.Frontiers in physiology · 2024Review
- Advancing clinical translation of cardiac biomechanics models: a comprehensive review, applications and future pathways.Frontiers in physics · 2023Article
- Pro-arrhythmic effects of gain-of-function potassium channel mutations in the short QT syndrome.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Computational analysis of arrhythmogenesis in KCNH2 T618I mutation-associated short QT syndrome and the pharmacological effects of quinidine and sotalol.NPJ systems biology and applications · 2022Article
- Electromechanical reciprocity and arrhythmogenesis in long-QT syndrome and beyond.European heart journal · 2022Review
- A computational method for identifying an optimal combination of existing drugs to repair the action potentials of SQT1 ventricular myocytes.PLoS computational biology · 2021Article
- Investigation of the Effects of the Short QT Syndrome D172N Kir2.1 Mutation on Ventricular Action Potential Profile Using Dynamic Clamp.Frontiers in pharmacology · 2021Article
- Proarrhythmogenic Effect of the L532P and N588KJournal of Korean medical science · 2020Article
- Computational Study to Identify the Effects of the KCNJ2 E299V Mutation in Cardiac Pumping Capacity.Computational and mathematical methods in medicine · 2020Article
- Understanding the Beat-to-Beat Variations of P-Waves Morphologies in AF Patients During Sinus Rhythm: A Scoping Review of the Atrial Simulation Studies.Frontiers in physiology · 2019Article
- Molecular Insights into the Short QT Syndrome.The Journal of innovations in cardiac rhythm management · 2018Article
- Article
- Organ-level validation of a cross-bridge cycling descriptor in a left ventricular finite element model: effects of ventricular loading on myocardial strains.Physiological reports · 2017Article
- In silico investigation of a KCNQ1 mutation associated with short QT syndrome.Scientific reports · 2017Article
- Atrial arrhythmogenicity of KCNJ2 mutations in short QT syndrome: Insights from virtual human atria.PLoS computational biology · 2017Article
- A two dimensional electromechanical model of a cardiomyocyte to assess intra-cellular regional mechanical heterogeneities.PloS one · 2017Article
- Electro-mechanical dynamics of spiral waves in a discrete 2D model of human atrial tissue.PloS one · 2017Article
- Murine Electrophysiological Models of Cardiac Arrhythmogenesis.Physiological reviews · 2017Review
- Depth Attenuation Degree Based Visualization for Cardiac Ischemic Electrophysiological Feature Exploration.BioMed research international · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionGenetic forms of the Short QT Syndrome (SQTS) arise due to cardiac ion channel mutations leading to accelerated ventricular repolarization, arrhythmias and sudden cardiac death. Results from experimental and simulation studies suggest that changes to refractoriness and tissue vulnerability produce a substrate favorable to re-entry. Potential electromechanical consequences of the SQTS are less well-understood. The aim of this study was to utilize electromechanically coupled human ventricle models to explore electromechanical consequences of the SQTS. METHODS AND
resultsThe Rice et al. mechanical model was coupled to the ten Tusscher et al. ventricular cell model. Previously validated K(+) channel formulations for SQT variants 1 and 3 were incorporated. Functional effects of the SQTS mutations on [Ca(2+)] i transients, sarcomere length shortening and contractile force at the single cell level were evaluated with and without the consideration of stretch-activated channel current (I sac). Without I sac, at a stimulation frequency of 1Hz, the SQTS mutations produced dramatic reductions in the amplitude of [Ca(2+)] i transients, sarcomere length shortening and contractile force. When I sac was incorporated, there was a considerable attenuation of the effects of SQTS-associated action potential shortening on Ca(2+) transients, sarcomere shortening and contractile force. Single cell models were then incorporated into 3D human ventricular tissue models. The timing of maximum deformation was delayed in the SQTS setting compared to control.
conclusionThe incorporation of I sac appears to be an important consideration in modeling functional effects of SQT 1 and 3 mutations on cardiac electro-mechanical coupling. Whilst there is little evidence of profoundly impaired cardiac contractile function in SQTS patients, our 3D simulations correlate qualitatively with reported evidence for dissociation between ventricular repolarization and the end of mechanical systole.
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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.