Fluid‐Structure Interaction Study of Coronary Artery Disease Biomechanics

Abstract

Coronary artery disease (CAD) kills 1 in 7 in the United States. Atherosclerosis and thrombosis are both disease states that are impacted by biomechanical conditions in the blood vessels. Platelets and vascular endothelial cells are known to respond to their mechanical environments, which can be altered around a coronary stenosis. Certain pertinent mechanical parameters, such as vascular wall shear stress and strain, can be difficult or impossible to measure directly in vivo.Computational fluid dynamics (CFD) models and Fluid‐Structure Interaction (FSI) models are often used to assess coronary artery biomechanics. In this study, we developed three FSI models based on the computed tomography data from a patient: a normal model, a severe stenosis model with a 71% diameter occlusion (which would be a candidate for intervention), and a mild stenosis model (50% diameter occlusion, which would not be considered clinically severe). Our hypothesis was that the high‐resolution FSI model could reveal small changes in coronary biomechanics at the cellular level (microscopic scale), which may be used as a biomarker/indicator for endothelial cell and platelet activation at the early stage of disease development. FSI simulations were conducted in COMSOL Multiphysics. Time‐dependent velocity and pressure boundary conditions were applied at the inlet and outlet of the fluid domain, respectively. A five‐parameter Mooney‐Rivlin hyperelastic material model was used to model the material properties of the artery. A time‐dependent pressure boundary condition was applied to the outside of the vessel, mimicking squeezing of the cardiac muscle in areas of myocardial bridging. In the region of interest, a spatial resolution of less than 40 µm was achieved. This is comparable to the size of vascular endothelial cells (which can range in size from 20‐100 µm), allowing us to capture hemodynamic and solid mechanical behavior at the cellular level. In the normal geometry, wall shear stress (WSS) values peaked at 1.51 Pa. In the 71% stenosis throat, transient WSS could reach 200 Pa, while in the 50% stenosis throat, the maximum WSS was less than 5 Pa. In the recirculation zone of the 71% stenosis, WSS peaked at 4.66 Pa, while in the recirculation zone of the 50% stenosis WSS reduced to 0.83 Pa, which is pathologically low. Time‐averaged wall shear stress (TAWSS) was 0.62+0.002 Pa (average + standard error) in the normal model, 1.60+0.004 Pa in the 50% stenosis model, and 7.47+0.017 Pa in the 71% stenosis model. Time‐averaged wall shear stress gradient (TAWSSG) was 0.018+6.25*10‐5 N/m in the normal model, 0.150+3.4*10‐4 N/m in the 50% stenosis model, and 0.970+0.002 N/m in the 71% stenosis model. Radial strain in the normal, 71% stenosis throat, 50% stenosis throat, 71% recirculation zone, and 50% recirculation zone peaked at 7.5%, 4.0%, 6.3%, 0.5%, and 5.1% respectively, and the circumferential strain peaked at 8.9%, 4.4%, 6.6%, 0.6%, and 4.2% respectively. In summary, we were able to develop mesoscopic FSI models that can provide microscopic hemodynamic information at the cellular level. Such information can be used in the in vitro models to study biomechanical pathways associated with coronary artery atherosclerosis and thrombosis; it may also be used as biomarkers at the early stage of atherosclerosis development.