A fully coupled computational fluid dynamics – agent-based model of atherosclerotic plaque development: Multiscale modeling framework and parameter sensitivity analysis

Research output: Contribution to journalArticle

Anna Corti, Claudio Chiastra, Monika Colombo, Marc Garbey, Francesco Migliavacca, Stefano Casarin

Background: Peripheral Artery Disease (PAD) is an atherosclerotic disorder that leads to impaired lumen patency through intimal hyperplasia and the build-up of plaques, mainly localized in areas of disturbed flow. Computational models can provide valuable insights in the pathogenesis of atherosclerosis and act as a predictive tool to optimize current interventional techniques. Our hypothesis is that a reliable predictive model must include the atherosclerosis development history. Accordingly, we developed a multiscale modeling framework of atherosclerosis that replicates the hemodynamic-driven arterial wall remodeling and plaque formation. Methods: The framework was based on the coupling of Computational Fluid Dynamics (CFD) simulations with an Agent-Based Model (ABM). The CFD simulation computed the hemodynamics in a 3D artery model, while 2D ABMs simulated cell, Extracellular Matrix (ECM) and lipid dynamics in multiple vessel cross-sections. A sensitivity analysis was also performed to evaluate the oscillation of the ABM output to variations in the inputs and to identify the most influencing ABM parameters. Results: Our multiscale model qualitatively replicated both the physiologic and pathologic arterial configuration, capturing histological-like features. The ABM outputs were mostly driven by cell and ECM dynamics, largely affecting the lumen area. A subset of parameters was found to affect the final lipid core size, without influencing cell/ECM or lumen area trends. Conclusion: The fully coupled CFD-ABM framework described atherosclerotic morphological and compositional changes triggered by a disturbed hemodynamics.

Original languageEnglish (US)
Article number103623
JournalComputers in Biology and Medicine
Volume118
DOIs
StatePublished - Mar 1 2020

PMID: 31999550

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A fully coupled computational fluid dynamics – agent-based model of atherosclerotic plaque development : Multiscale modeling framework and parameter sensitivity analysis. / Corti, Anna; Chiastra, Claudio; Colombo, Monika; Garbey, Marc; Migliavacca, Francesco; Casarin, Stefano.

In: Computers in Biology and Medicine, Vol. 118, 103623, 01.03.2020.

Research output: Contribution to journalArticle

Harvard

Corti, A, Chiastra, C, Colombo, M, Garbey, M, Migliavacca, F & Casarin, S 2020, 'A fully coupled computational fluid dynamics – agent-based model of atherosclerotic plaque development: Multiscale modeling framework and parameter sensitivity analysis' Computers in Biology and Medicine, vol. 118, 103623. https://doi.org/10.1016/j.compbiomed.2020.103623

APA

Corti, A., Chiastra, C., Colombo, M., Garbey, M., Migliavacca, F., & Casarin, S. (2020). A fully coupled computational fluid dynamics – agent-based model of atherosclerotic plaque development: Multiscale modeling framework and parameter sensitivity analysis. Computers in Biology and Medicine, 118, [103623]. https://doi.org/10.1016/j.compbiomed.2020.103623

Vancouver

Corti A, Chiastra C, Colombo M, Garbey M, Migliavacca F, Casarin S. A fully coupled computational fluid dynamics – agent-based model of atherosclerotic plaque development: Multiscale modeling framework and parameter sensitivity analysis. Computers in Biology and Medicine. 2020 Mar 1;118. 103623. https://doi.org/10.1016/j.compbiomed.2020.103623

Author

Corti, Anna ; Chiastra, Claudio ; Colombo, Monika ; Garbey, Marc ; Migliavacca, Francesco ; Casarin, Stefano. / A fully coupled computational fluid dynamics – agent-based model of atherosclerotic plaque development : Multiscale modeling framework and parameter sensitivity analysis. In: Computers in Biology and Medicine. 2020 ; Vol. 118.

BibTeX

@article{612c870dfa654757a0146cb0d5547a09,
title = "A fully coupled computational fluid dynamics – agent-based model of atherosclerotic plaque development: Multiscale modeling framework and parameter sensitivity analysis",
abstract = "Background: Peripheral Artery Disease (PAD) is an atherosclerotic disorder that leads to impaired lumen patency through intimal hyperplasia and the build-up of plaques, mainly localized in areas of disturbed flow. Computational models can provide valuable insights in the pathogenesis of atherosclerosis and act as a predictive tool to optimize current interventional techniques. Our hypothesis is that a reliable predictive model must include the atherosclerosis development history. Accordingly, we developed a multiscale modeling framework of atherosclerosis that replicates the hemodynamic-driven arterial wall remodeling and plaque formation. Methods: The framework was based on the coupling of Computational Fluid Dynamics (CFD) simulations with an Agent-Based Model (ABM). The CFD simulation computed the hemodynamics in a 3D artery model, while 2D ABMs simulated cell, Extracellular Matrix (ECM) and lipid dynamics in multiple vessel cross-sections. A sensitivity analysis was also performed to evaluate the oscillation of the ABM output to variations in the inputs and to identify the most influencing ABM parameters. Results: Our multiscale model qualitatively replicated both the physiologic and pathologic arterial configuration, capturing histological-like features. The ABM outputs were mostly driven by cell and ECM dynamics, largely affecting the lumen area. A subset of parameters was found to affect the final lipid core size, without influencing cell/ECM or lumen area trends. Conclusion: The fully coupled CFD-ABM framework described atherosclerotic morphological and compositional changes triggered by a disturbed hemodynamics.",
keywords = "Agent-based model, Atherosclerosis, Computer modeling, ECM, Hemodynamics, Lipid plaque, Multiscale model, Remodeling, SMC, Wall shear stress",
author = "Anna Corti and Claudio Chiastra and Monika Colombo and Marc Garbey and Francesco Migliavacca and Stefano Casarin",
year = "2020",
month = "3",
day = "1",
doi = "10.1016/j.compbiomed.2020.103623",
language = "English (US)",
volume = "118",
journal = "Computers in Biology and Medicine",
issn = "0010-4825",
publisher = "Elsevier Limited",

}

RIS

TY - JOUR

T1 - A fully coupled computational fluid dynamics – agent-based model of atherosclerotic plaque development

T2 - Computers in Biology and Medicine

AU - Corti, Anna

AU - Chiastra, Claudio

AU - Colombo, Monika

AU - Garbey, Marc

AU - Migliavacca, Francesco

AU - Casarin, Stefano

PY - 2020/3/1

Y1 - 2020/3/1

N2 - Background: Peripheral Artery Disease (PAD) is an atherosclerotic disorder that leads to impaired lumen patency through intimal hyperplasia and the build-up of plaques, mainly localized in areas of disturbed flow. Computational models can provide valuable insights in the pathogenesis of atherosclerosis and act as a predictive tool to optimize current interventional techniques. Our hypothesis is that a reliable predictive model must include the atherosclerosis development history. Accordingly, we developed a multiscale modeling framework of atherosclerosis that replicates the hemodynamic-driven arterial wall remodeling and plaque formation. Methods: The framework was based on the coupling of Computational Fluid Dynamics (CFD) simulations with an Agent-Based Model (ABM). The CFD simulation computed the hemodynamics in a 3D artery model, while 2D ABMs simulated cell, Extracellular Matrix (ECM) and lipid dynamics in multiple vessel cross-sections. A sensitivity analysis was also performed to evaluate the oscillation of the ABM output to variations in the inputs and to identify the most influencing ABM parameters. Results: Our multiscale model qualitatively replicated both the physiologic and pathologic arterial configuration, capturing histological-like features. The ABM outputs were mostly driven by cell and ECM dynamics, largely affecting the lumen area. A subset of parameters was found to affect the final lipid core size, without influencing cell/ECM or lumen area trends. Conclusion: The fully coupled CFD-ABM framework described atherosclerotic morphological and compositional changes triggered by a disturbed hemodynamics.

AB - Background: Peripheral Artery Disease (PAD) is an atherosclerotic disorder that leads to impaired lumen patency through intimal hyperplasia and the build-up of plaques, mainly localized in areas of disturbed flow. Computational models can provide valuable insights in the pathogenesis of atherosclerosis and act as a predictive tool to optimize current interventional techniques. Our hypothesis is that a reliable predictive model must include the atherosclerosis development history. Accordingly, we developed a multiscale modeling framework of atherosclerosis that replicates the hemodynamic-driven arterial wall remodeling and plaque formation. Methods: The framework was based on the coupling of Computational Fluid Dynamics (CFD) simulations with an Agent-Based Model (ABM). The CFD simulation computed the hemodynamics in a 3D artery model, while 2D ABMs simulated cell, Extracellular Matrix (ECM) and lipid dynamics in multiple vessel cross-sections. A sensitivity analysis was also performed to evaluate the oscillation of the ABM output to variations in the inputs and to identify the most influencing ABM parameters. Results: Our multiscale model qualitatively replicated both the physiologic and pathologic arterial configuration, capturing histological-like features. The ABM outputs were mostly driven by cell and ECM dynamics, largely affecting the lumen area. A subset of parameters was found to affect the final lipid core size, without influencing cell/ECM or lumen area trends. Conclusion: The fully coupled CFD-ABM framework described atherosclerotic morphological and compositional changes triggered by a disturbed hemodynamics.

KW - Agent-based model

KW - Atherosclerosis

KW - Computer modeling

KW - ECM

KW - Hemodynamics

KW - Lipid plaque

KW - Multiscale model

KW - Remodeling

KW - SMC

KW - Wall shear stress

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U2 - 10.1016/j.compbiomed.2020.103623

DO - 10.1016/j.compbiomed.2020.103623

M3 - Article

VL - 118

JO - Computers in Biology and Medicine

JF - Computers in Biology and Medicine

SN - 0010-4825

M1 - 103623

ER -

ID: 57257435