Effect of a Lipid Pool on Stress/Strain Distributions in Stenotic Arteries: 3-D Fluid-Structure Interactions (FSI) Models

Tang, Dalin; Yang, Chun; Kobayashi, Shunichi; Ku, David N.

doi:10.1115/1.1762898

Cited by 119 publications

(77 citation statements)

References 27 publications

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“…Figures 3 -5 show that global maximal stress often appears at healthy parts of the vessel where either vessel wall is thinner than the diseased plaque side or vessel curvature is large. [35][36][37] Indeed, stress distributions in atherosclerotic plaques are affected by many factors which include (but are not limited to) (a) Blood pressure which is the driving force of flow and vessel deformation. (b) Vessel and plaque geometry.…”

Section: Assessing Plaque Vulnerability: Css Methods and Cpvimentioning

confidence: 99%

Local Maximal Stress Hypothesis and Computational Plaque Vulnerability Index for Atherosclerotic Plaque Assessment

et al. 2005

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It is believed that atherosclerotic plaque rupture may be related to maximal stress conditions in the plaque. More careful examination of stress distributions in plaques reveals that it may be the local stress/strain behaviors at critical sites such as very thin plaque cap and locations with plaque cap weakness that are more closely related to plaque rupture risk. A "local maximal stress hypothesis" and a stress-based computational plaque vulnerability index (CPVI) are proposed to assess plaque vulnerability. A critical site selection (CSS) method is proposed to identify critical sites in the plaque and critical stress conditions which are be used to determine CPVI values. Our initial results based on 34 2D MRI slices from 14 human coronary plaque samples indicate that CPVI plaque assessment has an 85% agreement rate (91% if the square root of stress values is used) with assessment given by histopathological analysis. Large-scale and long-term patient studies are needed to further validate our findings for more accurate quantitative plaque vulnerability assessment.

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Section: Assessing Plaque Vulnerability: Css Methods and Cpvimentioning

confidence: 99%

Local Maximal Stress Hypothesis and Computational Plaque Vulnerability Index for Atherosclerotic Plaque Assessment

et al. 2005

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“…The results indicate that the stress values from both the blood flow and the vessel wall are affected by many factors such as stenosis severity, lipid core size, plaque cap thickness, and fluid-structure interactions [67] ; they may also contribute to continued plaque progression [69] . The anisotropic material property is also considered to improve the accuracies of plaque stress predictions [68;82] .…”

Section: Models For Biomechanicsmentioning

confidence: 99%

Mathematical modeling and simulation of the evolution of plaques in blood vessels

et al. 2015

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The formation of plaques is one of the main causes for the blockage of arteries. This can lead to ischaemic brain or myocardial infarctions as well as other cardiovascular diseases. Possible biochemical and biomechanical processes contribute to the development of plaque growth and rupture. The main biochemical processes are the penetration of monocytes and the accumulation of foam cells in the vessel wall, leading to the formation and growth of plaques. The biomechanical forces can be measured by observing stresses in the blood flow and the vessel wall, which may lead to the rupture of plaques.In this thesis, we formulate an appropriate model to describe the evolution of plaques. The model consists of both the interaction between the blood flow and the vessel wall, and the growth of plaques due to the penetration of monocytes from the blood flow into the vessel wall. The Navier-Stokes equations and the elastic structure equations are used to describe the dynamics of fluid (blood flow) and the mechanics of structure (vessel wall). The motion of monocytes is described by the convection-diffusion-reaction equation, coupled with an equation for the accumulation of foam cells. Finally the metric of growth is introduced to accurately determine the stress tensor, and its evolution equation is derived. The variational formulation of the model is transformed into the ALE (Arbitrary Lagrangian-Eulerian) formulation, and all the equations are rewritten in the fixed domain. Temporal discretization is achieved with finite differences and spatial discretization is based on the Galerkin finite element method. The nonlinear systems are linearized and solved by the Newton method.Based on the model and the numerical methods above, numerical simulations are performed by using the software Gascoigne. The obtained numerical results make an agreement with the observation, and support the assumption that the penetration of monocytes and the accumulation of foam cells lead to the formation and growth of plaques, and that the evolution of plaques induces the increase of stresses in the vessel wall, which is an indicator of plaque rupture. Zusammenfassung

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“…The fully coupled fluid and structure models were solved by a commercial finiteelement package ADINA (ADINA R & D, Inc., Watertown, MA, USA) which has been tested by hundreds of real-life applications [2] and has been used by Tang in the last several years [6,7]. ADINA uses unstructured finite element methods for both fluid and solid models.…”

Section: Solution Methodsmentioning

confidence: 99%

“…In this paper, the following values were chosen to match experimental data and existing literature [3,6,8] …”

Section: The Solid and Fluid Modelsmentioning

confidence: 99%

See 1 more Smart Citation

3D Computational Mechanical Analysis for Human Atherosclerotic Plaques Using MRI-Based Models with Fluid-Structure Interactions

Tang

Yang

Zheng

et al. 2004

Medical Image Computing and Computer-Assisted Intervention – MICCAI 2004

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Abstract. Atherosclerotic plaques may rupture without warning and cause acute cardiovascular syndromes such as heart attack and stroke. It is believed that mechanical forces play an important role in plaque progression and rupture. A three-dimensional (3D) MRI-based finite-element model with multicomponent plaque structure and fluid-structure interactions (FSI) is introduced to perform mechanical analysis for human atherosclerotic plaques and identify critical flow and stress/strain conditions which may be related to plaque rupture. The coupled fluid and structure models are solved by ADINA, a well-tested finite-element package. Our results indicate that pressure conditions, plaque structure, component size and location, material properties, and model assumptions all have considerable effects on flow and plaque stress/strain behaviors. Large-scale patient studies are needed to validate the computational findings. This FSI model provides more complete stress/strain analysis and better interpretation of information from MR images and may lead to more accurate plaque vulnerability assessment and rupture predictions.

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Effect of a Lipid Pool on Stress/Strain Distributions in Stenotic Arteries: 3-D Fluid-Structure Interactions (FSI) Models

Cited by 119 publications

References 27 publications

Local Maximal Stress Hypothesis and Computational Plaque Vulnerability Index for Atherosclerotic Plaque Assessment

Local Maximal Stress Hypothesis and Computational Plaque Vulnerability Index for Atherosclerotic Plaque Assessment

Mathematical modeling and simulation of the evolution of plaques in blood vessels

3D Computational Mechanical Analysis for Human Atherosclerotic Plaques Using MRI-Based Models with Fluid-Structure Interactions

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