ArticleComputational and mathematical methods in medicine2017
Simulation of Atrial Fibrosis Using Coupled Myocyte-Fibroblast Cellular and Human Atrial Models.
Article in Computational and mathematical methods in medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Computational modeling of cardiac electrophysiology and arrhythmogenesis: toward clinical translation.Physiological reviews · 2024Review
- Patchy fibrosis promotes trigger-substrate interactions that both generate and maintain atrial fibrillation.Interface focus · 2023Article
- Screening and functional analysis of differentially expressed lncRNAs in rapid atrial pacing dog atrial tissue.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2021Article
- 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
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Atrial fibrosis is characterized by expansion of extracellular matrix and increase in the number of fibroblasts which has been associated with the development and maintenance of atrial arrhythmias. However, the mechanisms how the fibrosis contributes to atrial arrhythmia remain incompletely understood. In this study, we used a proposed fibroblast model coupled with the human atrial myocyte to investigate the effects of fibrosis on atrial excitability and repolarization at both cellular and macroscopic levels. The 12-lead electrocardiogram (ECG) was also simulated to explore the index of clinical diagnosis for fibrosis. The simulation results showed that the fibrosis can modify action potential morphology of human atrial myocyte, slow down wave propagation, and have rate adaptation, thus causing the atrial electrical heterogeneity. The fibrosis alone was sufficient to cause arrhythmia, induce reentry wave, and result in low amplitude and wide P waves at normal heart rate and significant prolonged and inverse P waves at high heart rate. All these symptoms aggravated when the level of fibrosis increased. Our simulations demonstrated that fibrosis is the substrate of atrial arrhythmia and thereby may be a potential target in the treatment of atrial arrhythmias.
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