ArticleBiomedical engineering online2017
Effects of amiodarone on short QT syndrome variant 3 in human ventricles: a simulation study.
Article in Biomedical engineering online, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 21 citations in OpenAlex.
- Machine learning approach to evaluate TdP risk of drugs using cardiac electrophysiological model including inter-individual variability.Frontiers in physiology · 2023Article
- Computational prediction of drug response in short QT syndrome type 1 based on measurements of compound effect in stem cell-derived cardiomyocytes.PLoS computational biology · 2021Article
- Review
- Molecular Insights into the Short QT Syndrome.The Journal of innovations in cardiac rhythm management · 2018Article
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Authors and funding
3 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundShort QT syndrome (SQTS) is a newly identified clinical disorder associated with atrial and/or ventricular arrhythmias and increased risk of sudden cardiac death (SCD). The SQTS variant 3 is linked to D172N mutation to the KCNJ2 gene that causes a gain-of-function to the inward rectifier potassium channel current (I
methodsThe ten Tusscher et al. model for the human ventricular action potentials (APs) was modified to incorporate I
resultsAmiodarone prolonged the ventricular cell APD and decreased the maximal voltage heterogeneity (δV) among three difference cells types across transmural ventricular wall, leading to a decreased transmural heterogeneity of APD along a 1D model of ventricular transmural strand. Amiodarone increased cellular ERP, prolonged QT interval and decreased the T-wave amplitude. It reduced tissue's temporal susceptibility to the initiation of re-entry and increased the minimum substrate size necessary to sustain re-entry in the 2D tissue.
conclusionsAt the therapeutic-relevant concentration of amiodarone, the APD and ERP at the single cell level were increased significantly. The QT interval in pseudo-ECG was prolonged and the re-entry in tissue was prevented. This study provides further evidence that amiodarone may be a potential pharmacological agent for preventing arrhythmogenesis for SQT3 patients.
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