ArticlePloS one2013
Rotor termination is critically dependent on kinetic properties of I kur inhibitors in an in silico model of chronic atrial fibrillation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Digital Twin Models in Atrial Fibrillation: Charting the Future of Precision Therapy?Journal of personalized medicine · 2025Review
- How synergy between mechanistic and statistical models is impacting research in atrial fibrillation.Frontiers in physiology · 2022Review
- The role of personalized atrial modeling in understanding atrial fibrillation mechanisms and improving treatment.International journal of cardiology · 2019Review
- Understanding AF Mechanisms Through Computational Modelling and Simulations.Arrhythmia & electrophysiology review · 2019Review
- 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
- Computational Modeling of Electrophysiology and Pharmacotherapy of Atrial Fibrillation: Recent Advances and Future Challenges.Frontiers in physiology · 2018Review
- In silico assessment of genetic variation in KCNA5 reveals multiple mechanisms of human atrial arrhythmogenesis.PLoS computational biology · 2017Article
- Rate-Dependent Role of IBiophysical journal · 2017Article
- Synergistic Anti-arrhythmic Effects in Human Atria with Combined Use of Sodium Blockers and Acacetin.Frontiers in physiology · 2017Article
- Atrial Heterogeneity Generates Re-entrant Substrate during Atrial Fibrillation and Anti-arrhythmic Drug Action: Mechanistic Insights from Canine Atrial Models.PLoS computational biology · 2016Article
- Comparison of Detailed and Simplified Models of Human Atrial Myocytes to Recapitulate Patient Specific Properties.PLoS computational biology · 2016Article
- Isoenzyme-specific regulation of cardiac Kv1.5/Kvβ1.2 ion channel complex by protein kinase C: central role of PKCβII.Naunyn-Schmiedeberg's archives of pharmacology · 2014Article
- Mathematical approaches to understanding and imaging atrial fibrillation: significance for mechanisms and management.Circulation research · 2014Review
- Human atrial cell models to analyse haemodialysis-related effects on cardiac electrophysiology: work in progress.Computational and mathematical methods in medicine · 2014Review
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Authors and funding
8 authors.
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Abstract
Inhibition of the atrial ultra-rapid delayed rectifier potassium current (I Kur) represents a promising therapeutic strategy in the therapy of atrial fibrillation. However, experimental and clinical data on the antiarrhythmic efficacy remain controversial. We tested the hypothesis that antiarrhythmic effects of I Kur inhibitors are dependent on kinetic properties of channel blockade. A mathematical description of I Kur blockade was introduced into Courtemanche-Ramirez-Nattel models of normal and remodeled atrial electrophysiology. Effects of five model compounds with different kinetic properties were analyzed. Although a reduction of dominant frequencies could be observed in two dimensional tissue simulations for all compounds, a reduction of spiral wave activity could be only be detected in two cases. We found that an increase of the percent area of refractory tissue due to a prolongation of the wavelength seems to be particularly important. By automatic tracking of spiral tip movement we find that increased refractoriness resulted in rotor extinction caused by an increased spiral-tip meandering. We show that antiarrhythmic effects of I Kur inhibitors are dependent on kinetic properties of blockade. We find that an increase of the percent area of refractory tissue is the underlying mechanism for an increased spiral-tip meandering, resulting in the extinction of re-entrant circuits.
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