Computational Model of Coronary Arteries with In-Stent Restenosis: Mutual Influence of Hemodynamics, Growth Mechanics and Pharmacokinetics

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 collectively modulate restenosis progression, offering a promising tool for enhancing clinical decison-making and patient-specific treatment.