ArticlePloS one2016
A Stochastic Individual-Based Model of the Progression of Atrial Fibrillation in Individuals and Populations.
Article in PloS one, 2016. 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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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
5 citing papers in PubMed.
- Computational models of atrial fibrillation: achievements, challenges, and perspectives for improving clinical care.Cardiovascular research · 2021Review
- Computational modeling: What does it tell us about atrial fibrillation therapy?International journal of cardiology · 2019Review
- Is human atrial fibrillation stochastic or deterministic?-Insights from missing ordinal patterns and causal entropy-complexity plane analysis.Chaos (Woodbury, N.Y.) · 2018Article
- Mechanisms of stochastic onset and termination of atrial fibrillation studied with a cellular automaton model.Journal of the Royal Society, Interface · 2017Article
- Myocardial architecture and patient variability in clinical patterns of atrial fibrillation.Physical review. E · 2016Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Models that represent the mechanisms that initiate and sustain atrial fibrillation (AF) in the heart are computationally expensive to simulate and therefore only capture short time scales of a few heart beats. It is therefore difficult to embed biophysical mechanisms into both policy-level disease models, which consider populations of patients over multiple decades, and guidelines that recommend treatment strategies for patients. The aim of this study is to link these modelling paradigms using a stylised population-level model that both represents AF progression over a long time-scale and retains a description of biophysical mechanisms. We develop a non-Markovian binary switching model incorporating three different aspects of AF progression: genetic disposition, disease/age related remodelling, and AF-related remodelling. This approach allows us to simulate individual AF episodes as well as the natural progression of AF in patients over a period of decades. Model parameters are derived, where possible, from the literature, and the model development has highlighted a need for quantitative data that describe the progression of AF in population of patients. The model produces time series data of AF episodes over the lifetimes of simulated patients. These are analysed to quantitatively describe progression of AF in terms of several underlying parameters. Overall, the model has potential to link mechanisms of AF to progression, and to be used as a tool to study clinical markers of AF or as training data for AF classification algorithms.
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