Three-Dimensional Multiphysics Modelling of Restenosis in Stented Coronary Arteries Incorporating Hemodynamics and Pharmacokinetics

Background: Ischemic heart disease (IHD) is one of the most common and potentially fatal human diseases, caused mainly by atherosclerosis and treated by percutaneous coronary intervention with intravascular stent placement to restore blood flow to the heart. Despite advances in stent technology, restenosis (neointima) remains a critical problem after coronary intervention. Methods: A computational model of restenosis after stenting was developed, integrating 12 equations describing the dynamics of lipoproteins, cells, cytokines, statins, collagen, and smooth muscle cells. Simulations over 180 days compared various geometries: 2D vs. 3D, fixed vs. moving mesh, single-layer vs. three-layer, and straight vs. curved artery. Three values of arterial wall porosity (0.983, 0.8025, and 0.68) were investigated. Results: Mathematical modelling revealed that 2D simulations overestimate neointima growth by 30.93–31.27% compared to 3D models that resolve the actual stent geometry. Statin therapy reduced plaque growth by 4.98–5.42% over 180 days. Within the investigated porosity range, plaque growth increased as porosity decreased: maximum restenosis rose from 9.7–9.9% to 20.9–21.4% in the straight and curved artery models, respectively, because reduced free volume intensifies biochemical reactions and foam cell accumulation. Fixed and moving mesh models showed minimal differences (up to 2.6% in 3D, 6.14% in 2D), confirming that fixed meshes are preferable for up to 180-day simulations due to computational efficiency and result consistency. Conclusions: The developed model includes 12 factors involved in the pathogenesis of restenosis and neointima formation and allows localising the areas most significant for understanding the mechanisms of this process.