A biomechanical model of coronary artery remodeling and atherosclerotic plaque growth

• Iterative 12-year mechanobiological simulation of coronary artery remodeling • Low WSS regions shift, driving plaque progression downstream and upstream • Geometry evolution modifies flow patterns and shear stress distribution • Emerging hemodynamics identify novel plaque-prone regions Atherosclerosis is a prevalent cardiovascular disease initiated by lipid infiltration into the arterial wall, leading to plaque formation and narrowing of the vascular lumen. This process significantly increases the risk of myocardial infarction and stroke, especially in complex geometries such as coronary bifurcations. In this study, a mechanobiological model is developed to simulate the bidirectional interaction between blood flow and atherosclerotic plaque growth within a 3D coronary bifurcation geometry. Hemodynamic parameters are calculated using experimental boundary conditions to determine shear stress distribution. LDL transport across the arterial wall is modeled using a three-pore theory, and concentration equations for LDL, OxLDL, monocytes, macrophages, and foam cells are solved within the wall. Lipid accumulation and wall geometry changes are then calculated and incorporated into the model in an iterative 12-year simulation. Our results indicate that plaque accumulation not only narrows the lumen and disturbs wall shear stress patterns, but also causes new plaque-prone areas to emerge. For instance, the downstream of LCX and LAD branches reach 59% and 49% occlusion, respectively, while the upstream regions, initially unaffected by low shear stress, show 45% occlusion over time. These geometric changes significantly impact disease progression and highlight the importance of accounting for the evolution of arterial morphology in predictive models. This study emphasizes the need for incorporating dynamic vascular remodeling into computational simulations to enhance diagnostic and therapeutic strategies for atherosclerosis.