3D Fluid-structure Interaction Models Research Articles

Sites of Rupture in Human Atherosclerotic Carotid Plaques Are Associated With High Structural Stresses

It has been hypothesized that high structural stress in atherosclerotic plaques at critical sites may contribute to plaque disruption. To test that hypothesis, 3D fluid-structure interaction models were constructed based on in vivo MRI data of human atherosclerotic carotid plaques to assess structural stress behaviors of plaques with and without rupture. In vivo MRI data of carotid plaques from 12 patients scheduled for endarterectomy were acquired for model reconstruction. Histology confirmed that 5 of the 12 plaques had rupture. Plaque wall stress (PWS) and flow maximum shear stress were extracted from all nodal points on the lumen surface of each plaque for analysis. A critical PWS (maximum of PWS values from all possible vulnerable sites) was determined for each plaque. Mean PWS from all ulcer nodes in ruptured plaques was 86% higher than that from all nonulcer nodes (123.0 versus 66.3 kPa, P<0.0001). Mean flow maximum shear stress from all ulcer nodes in ruptured plaques was 170% higher than that from all nonulcer nodes (38.9 versus 14.4 dyn/cm2, P<0.0001). Mean critical PWS from the 5 ruptured plaques was 126% higher than that from the 7 nonruptured ones (247.3 versus 108 kPa, P=0.0016 using log transformation). The results of this study show that plaques with prior ruptures are associated with higher critical stress conditions, both at ulcer sites and when compared with nonruptured plaques. With further validations, plaque stress analysis may provide additional stress indicators helpful for image-based plaque vulnerability assessment.

MRI-based biomechanical imaging: initial study on early plaque progression and vessel remodeling

The goal of the study is to develop a noninvasive magnetic resonance imaging (MRI)-based biomechanical imaging technique to address biomechanical pathways of atherosclerotic progression and regression in vivo using a 3D fluid-structure interaction (FSI) model. Initial in vivo study was carried out in an early plaque model in pigs that underwent balloon-overstretch injury to the left carotid arteries. Consecutive MRI scans were performed while the pigs were maintained on high cholesterol (progression) or normal chow (regression), with an injection of a plaque-targeted contrast agent, Gadofluorine M. At the end of study, the specimens of carotid arterial segments were dissected and underwent dedicated mechanical testing to determine their material properties. 3D FSI computational model was applied to calculate structure stress and strain distribution. The plaque structure resembles early plaque with thickened intima. Lower maximal flow shear stress correlates with the growth of plaque volume during progression, but not during regression. In contrast, maximal principle structure stress/stain (stress-P1 and strain-P1) were shown to correlate strongly with the change in the plaque dimension during regression, but moderately during progression. This MRI-based biomechanical imaging method may allow for noninvasive dynamic assessment of local hemodynamic forces on the development of atherosclerotic plaques in vivo.

Patient-specific artery shrinkage and 3D zero-stress state in multi-component 3D FSI models for carotid atherosclerotic plaques based on in vivo MRI data.

Image-based computational models for atherosclerotic plaques have been developed to perform mechanical analysis to quantify critical flow and stress/strain conditions related to plaque rupture which often leads directly to heart attack or stroke. An important modeling issue is how to determine zero stress state from in vivo plaque geometries. This paper presents a method to quantify human carotid artery axial and inner circumferential shrinkages by using patient-specific ex vivo and in vivo MRI images. A shrink-stretch process based on patient-specific in vivo plaque morphology and shrinkage data was introduced to shrink the in vivo geometry first to find the zero-stress state (opening angle was ignored to reduce the complexity), and then stretch and pressurize to recover the in vivo plaque geometry with computed initial stress, strain, flow pressure and velocity conditions. Effects of the shrink-stretch process on plaque stress/strain distributions were demonstrated based on patient-specific data using 3D models with fluid-structure interactions (FSI). The average artery axial and inner circumferential shrinkages were 25% and 7.9%, respectively, based on a data set obtained from 10 patients. Maximum values of maximum principal stress and strain increased 349.8% and 249% respectively with 33% axial stretch. Influence of inner circumferential shrinkage (7.9%) was not very noticeable under 33% axial stretch, but became more noticeable under smaller axial stretch. Our results indicated that accurate knowledge of artery shrinkages and the shrink-stretch process will considerably improve the accuracy of computational predictions made based on results from those in vivo MRI-based FSI models.

2101 Role of hemodynamic forces on plaque development: non-invasive assessment with MRI methods

Purpose Fluid shear stress was thought to lead to atherosclerotic plaque progression, but such measurement procedures are often invasive. The goal of the present study is to address the biomechanical pathways of atherosclerosis progression and regression with our non-invasive MRI methods and a 3D fluid-structure interaction (FSI) model. The study was performed in a large animal atherosclerotic model.

On the stability of the coupling of 3D and 1D fluid-structure interaction models for blood flow simulations

We consider the coupling between three-dimensional (3D) and one-dimensional (1D) fluid-structure interaction (FSI) models describing blood flow inside compliant vessels. The 1D model is a hyperbolic system of partial differential equations. The 3D model consists of the Navier-Stokes equations for incompressible Newtonian fluids coupled with a model for the vessel wall dynamics. A non standard formulation for the Navier-Stokes equations is adopted to have suitable boundary conditions for the coupling of the models. With this we derive an energy estimate for the fully 3D-1D FSI coupling. We consider several possible models for the mechanics of the vessel wall in the 3D problem and show how the 3D-1D coupling depends on them. Several comparative numerical tests illustrating the coupling are presented.

Fluid-structure modeling of flow-induced alveolar epithelial cell deformation

Fluid buildup in the small pulmonary airways can exert injurious stresses on the epithelial cells which line airway walls. Under these conditions, the amount of deformation-induced cell injury may depend on the magnitude of the hydrodynamic stresses and the cells’ mechanical properties. In this study, we present 2D and 3D fluid-structure interaction models of flow-induced cell deformation. We report wall shear stress on the cells and cell membrane strain for a range of cell and membrane stiffness values. Results indicate that more compliant cells experience lower wall shear stresses but higher membrane strains. We correlate our results to experimental studies of cellular injury under airway reopening conditions and validate our computational method by comparison to an analytical solution of flow over a rigid protrusion in a channel.

In Vivo/Ex Vivo MRI-Based 3D Non-Newtonian FSI Models for Human Atherosclerotic Plaques Compared with Fluid/Wall-Only Models.

It has been recognized that fluid-structure interactions (FSI) play an important role in cardiovascular disease initiation and development. However, in vivo MRI multi-component FSI models for human carotid atherosclerotic plaques with bifurcation and quantitative comparisons of FSI models with fluid-only or structure-only models are currently lacking in the literature. A 3D non-Newtonian multi-component FSI model based on in vivo/ex vivo MRI images for human atherosclerotic plaques was introduced to investigate flow and plaque stress/strain behaviors which may be related to plaque progression and rupture. Both artery wall and plaque components were assumed to be hyperelastic, isotropic, incompressible and homogeneous. Blood flow was assumed to be laminar, non-Newtonian, viscous and incompressible. In vivo/ex vivo MRI images were acquired using histologically-validated multi-spectral MRI protocols. The 3D FSI models were solved and results were compared with those from a Newtonian FSI model and wall-only/fluid-only models. A 145% difference in maximum principal stresses (Stress-P(1)) between the FSI and wall-only models and 40% difference in flow maximum shear stress (MSS) between the FSI and fluid-only models were found at the throat of the plaque using a severe plaque sample (70% severity by diameter). Flow maximum shear stress (MSS) from the rigid wall model is much higher (20-40% in maximum MSS values, 100-150% in stagnation region) than those from FSI models.