Patient-specific three-dimensional simulation of LDL accumulation in a human left coronary artery in its healthy and atherosclerotic states

2009 ◽  
Vol 296 (6) ◽  
pp. H1969-H1982 ◽  
Author(s):  
Ufuk Olgac ◽  
Dimos Poulikakos ◽  
Stefan C. Saur ◽  
Hatem Alkadhi ◽  
Vartan Kurtcuoglu
Keyword(s):  
Shear Stress ◽  
Coronary Artery ◽  
Left Coronary Artery ◽  
Three Dimensional ◽  
Arterial Blood Flow ◽  
Patient Specific ◽  
Computed Tomography Images ◽  
Arterial Blood ◽  
Diseased State ◽  
Stress Dependent

We calculate low-density lipoprotein (LDL) transport from blood into arterial walls in a three-dimensional, patient-specific model of a human left coronary artery. The in vivo anatomy data are obtained from computed tomography images of a patient with coronary artery disease. Models of the artery anatomy in its healthy and diseased states are derived after segmentation of the vessel lumen, with and without the detected plaque, respectively. Spatial shear stress distribution at the endothelium is determined through the reconstruction of the arterial blood flow field using computational fluid dynamics. The arterial endothelium is represented by a shear stress-dependent, three-pore model, taking into account blood plasma and LDL passage through normal junctions, leaky junctions, and the vesicular pathway. Intraluminal pressures of 70 and 120 mmHg are employed as the normal and hypertensive operating pressures, respectively. By applying our model to both the healthy and diseased states, we show that the location of the plaque in the diseased state corresponds to one of the two sites with predicted high-LDL concentration in the healthy state. We further show that, in the diseased state, the site with high-LDL concentration has shifted distal to the plaque, which is in agreement with the clinical observation that plaques generally grow in the downstream direction. We also demonstrate that hypertension leads to increased number of regions with high-LDL concentration, elucidating one of the ways in which hypertension may promote atherosclerosis.

scholarly journals Fluid–structure interactions (FSI) based study of low-density lipoproteins (LDL) uptake in the left coronary artery

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xueping Chen ◽  
Jian Zhuang ◽  
Huanlei Huang ◽  
Yueheng Wu
Keyword(s):  
Shear Stress ◽  
Coronary Artery ◽  
Left Coronary Artery ◽  
Arterial Wall ◽  
Low Density Lipoproteins ◽  
Patient Specific ◽  
Low Density ◽  
Fluid Structure ◽  
Flowing Blood ◽  
Stress Dependent

AbstractThe purpose of this study is to compare the effect of the different physical factors on low-density lipoproteins (LDL) accumulation from flowing blood to the arterial wall of the left coronary arteries. The three-dimensional (3D) computational model of the left coronary arterial tree is reconstructed from a patient-specific computed tomography angiography (CTA) image. The endothelium of the coronary artery is represented by a shear stress dependent three-pore model. Fluid–structure interaction ($$FSI$$ FSI ) based numerical method is used to study the LDL transport from vascular lumen into the arterial wall. The results show that the high elastic property of the arterial wall decreases the complexity of the local flow field in the coronary bifurcation system. The places of high levels of LDL uptake coincide with the regions of low wall shear stress. In addition, hypertension promotes LDL uptake from flowing blood in the arterial wall, while the thickened arterial wall decreases this process. The present computer strategy combining the methods of coronary CTA image 3D reconstruction, $$FSI$$ FSI simulation, and three-pore modeling was illustrated to be effective on the simulation of the distribution and the uptake of LDL. This may have great potential for the early prediction of the local atherosclerosis lesion in the human left coronary artery.

Investigation of two-way fluid-structure interaction of blood flow in a patient-specific left coronary artery

2021 ◽  
pp. 1-18
Author(s):  
Abdulgaphur Athani ◽  
N.N.N. Ghazali ◽  
Irfan Anjum Badruddin ◽  
Sarfaraz Kamangar ◽  
Ali E. Anqi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Coronary Artery ◽  
Wall Shear Stress ◽  
Left Coronary Artery ◽  
Fluid Structure Interaction ◽  
Patient Specific ◽  
Hemodynamic Parameters ◽  
Fluid Structure ◽  
Structure Interaction

BACKGROUND: The blood flow in the human artery has been a subject of sincere interest due to its prime importance linked with human health. The hemodynamic study has revealed an essential aspect of blood flow that eventually proved to be paramount to make a correct decision to treat patients suffering from cardiac disease. OBJECTIVE: The current study aims to elucidate the two-way fluid-structure interaction (FSI) analysis of the blood flow and the effect of stenosis on hemodynamic parameters. METHODS: A patient-specific 3D model of the left coronary artery was constructed based on computed tomography (CT) images. The blood is assumed to be incompressible, homogenous, and behaves as Non-Newtonian, while the artery is considered as a nonlinear elastic, anisotropic, and incompressible material. Pulsatile flow conditions were applied at the boundary. Two-way coupled FSI modeling approach was used between fluid and solid domain. The hemodynamic parameters such as the pressure, velocity streamline, and wall shear stress were analyzed in the fluid domain and the solid domain deformation. RESULTS: The simulated results reveal that pressure drop exists in the vicinity of stenosis and a recirculation region after the stenosis. It was noted that stenosis leads to high wall stress. The results also demonstrate an overestimation of wall shear stress and velocity in the rigid wall CFD model compared to the FSI model.

scholarly journals Two-Phase Non-Newtonian Pulsatile Blood Flow Simulations in a Rigid and Flexible Patient-Specific Left Coronary Artery (LCA) Exhibiting Multi-Stenosis

2021 ◽  
Vol 11 (23) ◽  
pp. 11361
Author(s):  
Abdulgaphur Athani ◽  
Nik Nazri Nik Ghazali ◽  
Irfan Anjum Badruddin ◽  
Abdullah Y. Usmani ◽  
Sarfaraz Kamangar ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Left Coronary Artery ◽  
Solid Wall ◽  
Three Dimensional ◽  
Patient Specific ◽  
Maximum Pressure ◽  
Three Dimensional Model ◽  
Two Phase ◽  
Pressure Drops

Coronary artery disease (CAD) is stated as one of the most common causes of death all over the world. This article explores the influence of multi stenosis in a flexible and rigid left coronary artery (LCA) model using a multiphase blood flow system which has not yet been studied. Two-way fluid–solid interaction (FSI) is employed to achieve flow within the flexible artery model. A realistic three-dimensional model of multi-stenosed LCA was reconstructed based on computerized tomography (CT) images. The fluid domain was solved using a finite volume-based commercial software (FLUENT 2020). The fluid (blood) and solid (wall) domains were fully coupled by using the ANSYS Fluid-Structure Interaction solver. The maximum pressure drops, and wall shear stress was determined across the sever stenosis (90% AS). The higher region of displacement occurs at the pre-stenosis area compared to the other area of the left coronary artery model. An increase in blood flow velocity across the restricted regions (stenosis) in the LCA was observed, whereas the recirculation zone at the post-stenosis and bifurcation regions was noted. An overestimation of hemodynamic descriptors for the rigid models was found as compared to the FSI models.

A New Hexahedral Mesher for a Numerically Efficient Patient Specific Analysis of Arterial Blood Flow and Wall Shear Stress

2010 ◽  
Author(s):  
G. De Santis ◽  
P. Mortier ◽  
M. De Beule ◽  
P. Segers ◽  
P. Verdonck ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Imaging Techniques ◽  
Arterial Blood Flow ◽  
Patient Specific ◽  
Arterial Tree ◽  
Arterial Blood ◽  
Current Measuring ◽  
Wall Shear

Atherosclerosis depends on systemic risk factors but manifests itself as geometrically focal plaques, which appear in regions of the arterial tree experiencing low and/or oscillating Wall Shear Stress (WSS) such as outer edges of vessels bifurcations and highly curved vessels. Because direct measurements of WSS (differential quantity) in vivo are difficult due to limited spatial resolution offered by current measuring technologies (ultrasound, phase contrast MRI), an indirect approach is often taken, integrating medical imaging techniques (biplane angiography, CT, MRI) with Computational Fluid Dynamics (CFD) for patient specific WSS profiling.

scholarly journals Shear-stress-induced von Willebrand factor binding to platelets causes the activation of tyrosine kinase(s)

1994 ◽  
Vol 302 (3) ◽  
pp. 681-686 ◽  
Author(s):  
K Razdan ◽  
J D Hellums ◽  
M H Kroll
Keyword(s):  
Shear Stress ◽  
Platelet Aggregation ◽  
Tyrosine Phosphorylation ◽  
Von Willebrand Factor ◽  
Arterial Blood Flow ◽  
Shear Stresses ◽  
Arterial Blood ◽  
Stress Dependent ◽  
Von Willebrand ◽  
Willebrand Factor

Pathological arterial blood flow generates fluid shear stresses that directly cause platelet aggregation. The mechanism of shear-induced platelet aggregation is incompletely understood, but involves von Willebrand factor (vWF) binding to platelet glycoprotein (GP) Ib and GP IIb-IIIa, leading to the transmembrane influx of Ca2+ and the activation of protein kinase C. To investigate this further, shear-stress-induced protein tyrosine phosphorylation (PTP) of washed platelets was studied in a cone-plate viscometer. A time- and shear-stress-dependent tyrosine phosphorylation of substrates with approx. M(r) 29,000-31,000, 36,000, 50,000, 58,000, 64,000, 76,000, 85,000 and 105,000 was observed. PTP in response to a threshold shear stress of 0.3 mN/cm2 (30 dyn/cm2) was enhanced in most cases by exogenous purified human vWF, and PTP in response to a pathological shear stress of 0.9 mN/cm2 (90 dyn/cm2) was inhibited in some cases by inhibiting vWF binding to GP Ib or GP IIb-IIIa, or by inhibiting Ca2+ responses with extracellular EGTA. Shear-induced PTP of a substrate of M(r) approximately 31,000 appeared to be independent of GP Ib, and PTP of a substrate(s) of M(r) approximately 29,000 was shear-stress-dependent but independent of extracellular Ca2+. Cytochalasin D, which inhibits GP Ib-cytoskeleton interactions, inhibits the PTP of a substrate of M(r) approximately 76,000. These results suggest that tyrosine phosphorylation may be involved in transmembrane signalling that mediates platelet adhesion and aggregation in response to pathological shear stresses generated at sites of arterial vaso-occlusion.

scholarly journals Decomposition of Velocity Field Along a Centerline Curve Using Frenet-Frames: Application to Arterial Blood Flow Simulations

2021 ◽  
Author(s):  
Benjámin Csippa ◽  
Levente Sándor ◽  
György Paál
Keyword(s):  
Blood Flow ◽  
Velocity Field ◽  
Cross Sections ◽  
Evaluation Method ◽  
Three Dimensional ◽  
Arterial Blood Flow ◽  
Patient Specific ◽  
Flow Simulations ◽  
Arterial Blood ◽  
Curvature And Torsion

This paper presents a novel method for the evaluation of three-dimensional blood-flow simulations based, on the decomposition of the velocity field into localized coordinate systems along the vessels centerline. The method is based on the computation of accurate centerlines with the Vascular Modeling Toolkit (VMTK) library, to calculate the localized Frenet-frames along the centerline and the morphological features, namely the curvature and torsion. Using the Frenet-frame unit vectors, the velocity field can be decomposed into axial, circumferential and radial components and visualized in a diagram along the centerline. This paper includes case studies with four idealized geometries resembling the carotid siphon and two patient-specific cases to demonstrate the capability of the method and the connection between morphology and flow. The proposed evaluation method presented in this paper can be easily extended to other derived quantities of the velocity fields, such as the wall shear stress field. Furthermore, it can be used in other fields of engineering with tubular cross-sections with complex torsion and curvature distribution.

scholarly journals Application of subject-specific adaptive mechanical loading for bone healing in a mouse tail vertebral defect

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Angad Malhotra ◽  
Matthias Walle ◽  
Graeme R. Paul ◽  
Gisela A. Kuhn ◽  
Ralph Müller
Keyword(s):  
Mechanical Loading ◽  
Bone Defect ◽  
Bone Healing ◽  
Three Dimensional ◽  
Patient Specific ◽  
Dependent Manner ◽  
Micro Computed Tomography ◽  
Computed Tomography Images ◽  
Bone Defect Healing ◽  
Subject Specific

AbstractMethods to repair bone defects arising from trauma, resection, or disease, continue to be sought after. Cyclic mechanical loading is well established to influence bone (re)modelling activity, in which bone formation and resorption are correlated to micro-scale strain. Based on this, the application of mechanical stimulation across a bone defect could improve healing. However, if ignoring the mechanical integrity of defected bone, loading regimes have a high potential to either cause damage or be ineffective. This study explores real-time finite element (rtFE) methods that use three-dimensional structural analyses from micro-computed tomography images to estimate effective peak cyclic loads in a subject-specific and time-dependent manner. It demonstrates the concept in a cyclically loaded mouse caudal vertebral bone defect model. Using rtFE analysis combined with adaptive mechanical loading, mouse bone healing was significantly improved over non-loaded controls, with no incidence of vertebral fractures. Such rtFE-driven adaptive loading regimes demonstrated here could be relevant to clinical bone defect healing scenarios, where mechanical loading can become patient-specific and more efficacious. This is achieved by accounting for initial bone defect conditions and spatio-temporal healing, both being factors that are always unique to the patient.

A model of anemic tissue perfusion after blood transfusion shows critical role of endothelial response to shear stress stimuli

2021 ◽  
Author(s):  
Weiyu Li ◽  
Amy G. Tsai ◽  
Marcos Intaglietta ◽  
Daniel M. Tartakovsky
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Blood Transfusion ◽  
Critical Role ◽  
Cardiovascular Responses ◽  
Arterial Blood Flow ◽  
Microvascular Blood Flow ◽  
No Production ◽  
Arterial Blood ◽  
Transfusion Requirements

­­ ­Although some of the cardiovascular responses to changes in hematocrit (Hct) are not fully quantified experimentally, available information is sufficient to build a mathematical model of the consequences of treating anemia by introducing RBCs into the circulation via blood transfusion. We present such a model, which describes how the treatment of normovolemic anemia with blood transfusion impacts oxygen (O2) delivery (DO2, the product of blood O2 content and arterial blood flow) by the microcirculation. Our analysis accounts for the differential response of the endothelium to the wall shear stress (WSS) stimulus, changes in nitric oxide (NO) production due to modification of blood viscosity caused by alterations of both hematocrit (Hct) and cell free layer thickness, as well as for their combined effects on microvascular blood flow and DO2. Our model shows that transfusions of 1- and 2-unit of blood have a minimal effect on DO2 if the microcirculation is unresponsive to the WSS stimulus for NO production that causes vasodilatation increasing blood flow and DO2. Conversely, in a fully WSS responsive organism, blood transfusion significantly enhances blood flow and DO2, because increased viscosity stimulates endothelial NO production causing vasodilatation. This finding suggests that evaluation of a patients' pre-transfusion endothelial WSS responsiveness should be beneficial in determining the optimal transfusion requirements for treating anemic patients.

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