A Stochastic Individual-Based Model of the Progression of Atrial Fibrillation in Individuals and Populations.

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 m...

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Main Authors: Eugene T Y Chang, Yen Ting Lin, Tobias Galla, Richard H Clayton, Julie Eatock
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2016-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4829251?pdf=render
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spelling doaj-bee9f27a1cba492a8432b5d121ef6c392020-11-25T00:42:32ZengPublic Library of Science (PLoS)PLoS ONE1932-62032016-01-01114e015234910.1371/journal.pone.0152349A Stochastic Individual-Based Model of the Progression of Atrial Fibrillation in Individuals and Populations.Eugene T Y ChangYen Ting LinTobias GallaRichard H ClaytonJulie EatockModels 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.http://europepmc.org/articles/PMC4829251?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Eugene T Y Chang
Yen Ting Lin
Tobias Galla
Richard H Clayton
Julie Eatock
spellingShingle Eugene T Y Chang
Yen Ting Lin
Tobias Galla
Richard H Clayton
Julie Eatock
A Stochastic Individual-Based Model of the Progression of Atrial Fibrillation in Individuals and Populations.
PLoS ONE
author_facet Eugene T Y Chang
Yen Ting Lin
Tobias Galla
Richard H Clayton
Julie Eatock
author_sort Eugene T Y Chang
title A Stochastic Individual-Based Model of the Progression of Atrial Fibrillation in Individuals and Populations.
title_short A Stochastic Individual-Based Model of the Progression of Atrial Fibrillation in Individuals and Populations.
title_full A Stochastic Individual-Based Model of the Progression of Atrial Fibrillation in Individuals and Populations.
title_fullStr A Stochastic Individual-Based Model of the Progression of Atrial Fibrillation in Individuals and Populations.
title_full_unstemmed A Stochastic Individual-Based Model of the Progression of Atrial Fibrillation in Individuals and Populations.
title_sort stochastic individual-based model of the progression of atrial fibrillation in individuals and populations.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2016-01-01
description 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.
url http://europepmc.org/articles/PMC4829251?pdf=render
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