Evidence map›Paper›PMID 27070920›Full record

ArticlePloS one2016

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

Eugene T Y Chang, Yen Ting Lin, Tobias Galla, Richard H Clayton, Julie Eatock

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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.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Eugene T Y ChangInsigneo Institute for in-silico Medicine and Department of Computer Science, The University of Sheffield, Sheffield S1 4DP, United Kingdom.
Yen Ting LinSchool of Physics and Astronomy, The University of Manchester, Manchester M13 9PL, United Kingdom.
Tobias GallaSchool of Physics and Astronomy, The University of Manchester, Manchester M13 9PL, United Kingdom.
Richard H ClaytonInsigneo Institute for in-silico Medicine and Department of Computer Science, The University of Sheffield, Sheffield S1 4DP, United Kingdom.
Julie EatockDepartment of Computer Science, Brunel University London, Uxbridge UB8 3PH, Middlesex, United Kingdom.ORCID http://orcid.org/0000-0002-8963-8312

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AdultAlgorithmsAtrial FibrillationDisease ProgressionElectrocardiographyHeart RateHumansMiddle Aged

Identifiers

PMID27070920
PMCPMC4829251

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.