ArticlePLoS computational biology2025
Systematic computational assessment of atrial function impairment due to fibrotic remodeling in electromechanical properties.
Article in PLoS computational biology, 2025. 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.
- Reconstructing AF-associated atrial fibrosis: Patient-specific iPSC models, fit-for-purpose atrial microphysiological systems, and nanomedicine.Materials today. Bio · 2026Review
- In silico optimization of regenerative cell therapy in the infarcted human ventricles to mitigate arrhythmic burden.Stem cell reports · 2026Article
- Mechanical characterization of human umbilical and chorionic plate arteries affected by fetal growth restriction.PNAS nexus · 2026Article
- Atrial FDG avidity is associated with reduced atrial strain and contractility independent of atrial fibrillation and cardiac sarcoidosis.European heart journal. Imaging methods and practice · 2026Article
- Systematic computational assessment of atrial function impairment due to fibrotic remodeling in electromechanical properties.PLoS computational biology · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
Cardiac fibrosis is a pathological condition associated with many cardiovascular diseases. Atrial fibrosis leads to reduced atrial function, resulting in diminished blood flow and an increased risk of stroke. This reduced function arises from altered myocardial electrophysiological and mechanical properties. Identifying the relative importance of these fibrosis-associated properties can reveal the most significant determinants of left atrial function impairment. In this study, we used a computational framework to investigate the relative importance of various fibrosis-associated properties. Our model, a 3D electromechanical framework coupled with a 0D circulatory model, incorporated patient-specific geometries and fibrosis distributions from clinical imaging data. Nine parameters related to fibrotic remodeling (conduction velocity, ion channel expression levels, cell- and tissue-scale contractility, and stiffness) were analyzed using two sensitivity analysis schemes: a one-factor-at-a-time setup, allowing for analysis of isolated effects, and a fractional factorial design, enabling examination of combined effects. As output, we tracked various metrics derived from model-predicted pressure-volume loops. Impairment of L-type calcium current (ICaL) was most detrimental (up to 64% reduction in A-loop area of the left atrial pressure-volume relationship, quantifying work performed during atrial contraction). Conversely, reduced inward rectifier current (IK1) led to improved atrial function (up to 27% increase in A-loop area). Detailed analysis of spatiotemporal distributions linked these effects to changes in intracellular calcium handling. Fractional factorial design analysis revealed that combination with other parameter changes blunted the impact of reduced ICaL but amplified the impact of reduced IK1. Future research focusing on IK1 and ICaL could be highly significant for clinical and scientific advances. Modeling work can help evaluate left atrial function among larger patient cohorts, focusing on strain analysis. Our work could also be extended to spatiotemporal simulations of blood flow and thrombosis, shedding light onto the mechanisms underlying atriogenic stroke.
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