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  4. A computational model of coronary arteries with in-stent restenosis coupling hemodynamics and pharmacokinetics with growth mechanics
 
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A computational model of coronary arteries with in-stent restenosis coupling hemodynamics and pharmacokinetics with growth mechanics

Citation Link: https://doi.org/10.15480/882.16167
Publikationstyp
Journal Article
Date Issued
2025-11-10
Sprache
English
Author(s)
Ranno, Anna  
Manjunatha, Kiran  
Koritzius, Thore
Steinbrecher, Ivo
Hosters, Norbert
Nachtsheim, Maximilian
Nilcham, Pakhwan  
Schaaps, Nicole
Turoni-Glitz, Anne
Datz, Janina
Popp, Alexander  
Linka, Kevin  
Kontinuums- und Werkstoffmechanik M-15  
Vogt. Felix
Behr, Marek  
TORE-DOI
10.15480/882.16167
TORE-URI
https://hdl.handle.net/11420/58839
Journal
Scientific reports  
Volume
15
Issue
15
Article Number
39229
Citation
Scientific Reports 15: 39229: (2025)
Publisher DOI
10.1038/s41598-025-22291-w
Scopus ID
2-s2.0-105021274722
Publisher
Springer Science and Business Media LLC
Despite advances in stent technology, in-stent restenosis remains a critical challenge following percutaneous coronary intervention. In this work, we propose a comprehensive fluid-solid computational model to simulate restenosis after drug-eluting stent implantation. We develop a three-dimensional continuum-based framework that couples the complex interplay of hemodynamics, pharmacokinetics, and restenosis-induced arterial growth. Within the arterial wall, a continuum model of cell dynamics and tissue growth predicts neointimal thickening. Drug release is modeled by direct diffusion from the abluminal stent surface and one-way absorption of hydrophobic drug from the bloodstream at the lumen-wall interface. We incorporate blood flow influence into growth mechanics through the effect of non-physiological wall shear stresses on endothelial cells morphology. Due to the short time scale inherent in the fluid model, we adopt a quasi-steady approach that efficiently homogenizes hemodynamic-related quantities over clinically relevant time scales for restenosis and drug release. We verify the components of the computational model and the quasi-steady assumption using a test case with an idealized cylindrical artery and a one-ring stent. The framework is further extended to patient-specific geometries obtained from optical coherence tomography and virtual stent implantation. Our results showcase how stent design, drug elution, and hemodynamics can collectively modulate restenosis progression, and the proposed coupling framework could, in the long term, contribute to the development of clinical decision-support tools.
DDC Class
616: Diseases
620.1: Engineering Mechanics and Materials Science
Lizenz
https://creativecommons.org/licenses/by/4.0/
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