Bulletin of the American Physical Society
68th Annual Meeting of the APS Division of Fluid Dynamics
Volume 60, Number 21
Sunday–Tuesday, November 22–24, 2015; Boston, Massachusetts
Session L23: Biofluids: Cardiovascular Disease I: Aneurysms |
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Chair: Noelia Gutierrez, Stanford University Room: 300 |
Monday, November 23, 2015 4:05PM - 4:18PM |
L23.00001: Assessment Of Coronary Artery Aneurysms Using Transluminal Attenuation Gradient And Computational Modeling In Kawasaki Disease Patients Noelia Grande Gutierrez, Andrew Kahn, Olga Shirinsky, Nina Gagarina, Galina Lyskina, Ryuji Fukazawa, Shunichi Owaga, Jane Burns, Alison Marsden Kawasaki Disease (KD) can result in coronary artery aneurysms (CAA) in up to 25{\%} of patients, putting them at risk of thrombus formation, myocardial infarction and sudden death. Clinical guidelines recommend CAA diameter \textgreater 8 mm as the arbitrary criterion for initiating systemic anticoagulation. KD patient specific modeling and flow simulations suggest that hemodynamic data can predict regions at increased risk of thrombosis. Transluminal Attenuation Gradient (TAG) is determined from the change in radiological attenuation per vessel length and has been proposed as a non-invasive method for characterizing coronary stenosis from CT Angiography. We hypothesized that CAA abnormal flow could be quantified using TAG. We computed hemodynamics for patient specific coronary models using a stabilized finite element method, coupled numerically to a lumped parameter network to model the heart and vascular boundary conditions. TAG was quantified in the major coronary arteries. We compared TAG for aneurysmal and normal arteries and we analyzed TAG correlation with hemodynamic and geometrical parameters. Our results suggest that TAG may provide hemodynamic data not available from anatomy alone. TAG represents a possible extension to standard CTA that could help to better evaluate the risk of thrombus formation in KD. [Preview Abstract] |
Monday, November 23, 2015 4:18PM - 4:31PM |
L23.00002: Wall shear stress manifolds and near wall flow topology in aneurysms Amirhossein Arzani, Alberto M. Gambaruto, Guoning Chen, Shawn C. Shadden Transport of atherogenic and thrombogenic chemicals near the vessel wall highly influences atherosclerosis and thrombosis. The high Schmidt number of these species leads to a thin concentration boundary layer near the wall. The wall shear stress (WSS) vector field can be scaled to obtain the near wall velocity in this region, thus providing first order approximation to near wall transport. In this study, the complex blood flow in patient-specific abdominal aortic aneurysms was considered. Lagrangian tracking of surface-bound tracers representing near wall species was employed to identify Lagrangian coherent structures (LCS) for the WSS surface vector field. The WSS LCS matched the stable and unstable manifolds of saddle type fixed points of the time-average WSS vector field, due to the quasi-steady nature of these near wall transport processes. A WSS exposure time measure is introduced to quantify the concentration of near wall species. The effect of diffusion and normal flow on these structures is investigated. The WSS LCS highly influence the concentration of near wall species, and provide a template for near-wall transport. [Preview Abstract] |
Monday, November 23, 2015 4:31PM - 4:44PM |
L23.00003: One-dimensional model for the intracranial pulse morphological analysis during hyperventilation and CO$_{2}$ inhalation tests Jaiyoung Ryu, Xiao Hu, Shawn C. Shadden The brain's CO$_{2}$ reactivity mechanism is coupled with cerebral autoregulation and other unique features of cerebral hemodynamics. We developed a one-dimensional nonlinear model of blood flow in the cerebral arteries coupled to lumped parameter (LP) networks. The LP networks incorporate cerebral autoregulation, CO$_{2}$ reactivity, intracranial pressure, cerebrospinal fluid, and cortical collateral blood flow models. The model was used to evaluate hemodynamic variables (arterial deformation, blood velocity and pressure) in the cerebral vasculature during hyperventilation and CO$_{2}$ inhalation test. Tests were performed for various arterial blood pressure (ABP) representing normal and hypotensive conditions. The increase of the cerebral blood flow rates agreed well with the published measurements for various ABP measurements taken during clinical CO$_{2}$ reactivity tests. The changes in distal vasculature affected the reflected pulse wave energy, which caused the waveform morphological changes at the middle cerebral, common and internal carotid arteries. The pulse morphological analysis demonstrated agreement with previous clinical measurements for cerebral vasoconstriction and vasodilation. [Preview Abstract] |
Monday, November 23, 2015 4:44PM - 4:57PM |
L23.00004: Mathematical modelling of blood-brain barrier failure and edema Sarah Waters, Georgina Lang, Dominic Vella, Alain Goriely Injuries such as traumatic brain injury and stroke can result in increased blood-brain barrier permeability. This increase may lead to water accumulation in the brain tissue resulting in vasogenic edema. Although the initial injury may be localised, the resulting edema causes mechanical damage and compression of the vasculature beyond the original injury site. We employ a biphasic mixture model to investigate the consequences of blood-brain barrier permeability changes within a region of brain tissue and the onset of vasogenic edema. We find that such localised changes can indeed result in brain tissue swelling and that the type of damage that results (stress damage or strain damage) depends on the ability of the brain to clear edema fluid. [Preview Abstract] |
Monday, November 23, 2015 4:57PM - 5:10PM |
L23.00005: Modelling Brain Temperature and Perfusion for Cerebral Cooling Stephen Blowers, Prashant Valluri, Ian Marshall, Peter Andrews, Bridget Harris, Michael Thrippleton Brain temperature relies heavily on two aspects: i) blood perfusion and porous heat transport through tissue and ii) blood flow and heat transfer through embedded arterial and venous vasculature. Moreover brain temperature cannot be measured directly unless highly invasive surgical procedures are used. A 3D two-phase fluid-porous model for mapping flow and temperature in brain is presented with arterial and venous vessels extracted from MRI scans. Heat generation through metabolism is also included. The model is robust and reveals flow and temperature maps in unprecedented 3D detail. However, the Karmen-Kozeny parameters of the porous (tissue) phase need to be optimised for expected perfusion profiles. In order to optimise the K-K parameters a reduced order two-phase model is developed where 1D vessels are created with a tree generation algorithm embedded inside a 3D porous domain. Results reveal that blood perfusion is a strong function of the porosity distribution in the tissue. We present a qualitative comparison between the simulated perfusion maps and those obtained clinically. We also present results studying the effect of scalp cooling on core brain temperature and preliminary results agree with those observed clinically. [Preview Abstract] |
Monday, November 23, 2015 5:10PM - 5:23PM |
L23.00006: A dimensionless parameter for classifying hemodynamics in intracranial. Hafez Asgharzadeh, Iman Borazjani Rupture of an intracranial aneurysm (IA) is a disease with high rates of mortality. Given the risk associated with the aneurysm surgery, quantifying the likelihood of aneurysm rupture is essential. There are many risk factors that could be implicated in the rupture of an aneurysm. However, the most important factors correlated to the IA rupture are hemodynamic factors such as wall shear stress (WSS) and oscillatory shear index (OSI) which are affected by the IA flows. Here, we carry out three-dimensional high resolution simulations on representative IA models with simple geometries to test a dimensionless number (first proposed by Le et al., ASME J Biomech Eng, 2010), denoted as An number, to classify the flow mode. An number is defined as the ratio of the time takes the parent artery flow transports across the IA neck to the time required for vortex ring formation. Based on the definition, the flow mode is vortex if An\textgreater 1 and it is cavity if An\textless 1. We show that the specific definition of Le et al works for sidewall but needs to be modified for bifurcation aneurysms. In addition, we show that this classification works on three-dimensional geometries reconstructed from three-dimensional rotational angiography of human subjects. Furthermore, we verify the correlation of IA flow mode and WSS/OSI on the human subject IA. [Preview Abstract] |
Monday, November 23, 2015 5:23PM - 5:36PM |
L23.00007: Numerical simulations of post-surgical flow and thrombosis in basilar artery aneurysms Santhosh Seshadhri, Michael Lawton, Loic Boussel, David Saloner, Vitaliy Rayz Surgical treatment of basilar artery aneurysms presents a major challenge since it is crucial to preserve the flow to the vital brainstem perforators branching of the basilar artery. In some cases, basilar aneurysms can be treated by clipping vessels in order to induce flow reduction and aneurysm thrombosis. Patient-specific CFD models can provide guidance to clinicians by simulating postoperative flows resulting from alternative surgeries. Several surgical options were evaluated for four basilar aneurysm patients. Patient-specific models were generated from preoperative MR angiography and MR velocimetry data and modified to simulate different procedures. The Navier-Stokes equations were solved with a finite-volume solver Fluent. Virtual contrast injections were simulated by solving the advection-diffusion equation in order to estimate the flow residence time and determine thrombus-prone regions. The results indicated on procedures that reduce intra-aneurysmal velocities and flow regions which are likely to become thrombosed. Thus CFD modeling can help improve the outcome of surgeries altering the flow in basilar aneurysms. [Preview Abstract] |
Monday, November 23, 2015 5:36PM - 5:49PM |
L23.00008: Vortex Imprints at the Wall, But Not in the Bulk, Distinguish Ruptured from Unruptured Intracranial Aneurysms Nicole Varble, Hui Meng Intracranial aneurysms affect 3{\%} of the population. Risk stratification of aneurysms is important, as rupture often leads to death or permanent disability. Image-based CFD analyses of patient-specific aneurysms have identified low and oscillatory wall shear stress to predict rupture. These stresses are sensed biologically at the luminal wall, but the flow dynamics related to aneurysm rupture requires further understanding. We have conducted two studies: one examines vortex dynamics, and the other, high frequency flow fluctuations in patient-specific aneurysms. In the first study, based on Q-criterion vortex identification, we developed two measures to quantify regions within the aneurysm where rotational flow is dominate: the ratio of volume or surface area where Q \textgreater 0 vs. the \textit{total} aneurysmal volume or surface area, respectively termed volume vortex fraction (VVF) and surface vortex fraction (SVF). Statistical analysis of 204 aneurysms shows that SVF, but not VVF, distinguishes ruptured from unruptured aneurysms, suggesting that once again, the local flow patterns on the wall is directly relevant to rupture. In the second study, high-resolution CFD (high spatial and temporal resolutions and second-order discretization schemes) on 56 middle cerebral artery aneurysms shows the presence of temporal fluctuations in 8 aneurysms, but such flow instability bears no correlation with rupture. [Preview Abstract] |
Monday, November 23, 2015 5:49PM - 6:02PM |
L23.00009: Fluid-Structure Interaction Modeling of Intracranial Aneurysm Hemodynamics: Effects of Different Assumptions Hamidreza Rajabzadeh Oghaz, Robert Damiano, Hui Meng Intracranial aneurysms (IAs) are pathological outpouchings of cerebral vessels, the progression of which are mediated by complex interactions between the blood flow and vasculature. Image-based computational fluid dynamics (CFD) has been used for decades to investigate IA hemodynamics. However, the commonly adopted simplifying assumptions in CFD (e.g. rigid wall) compromise the simulation accuracy and mask the complex physics involved in IA progression and eventual rupture. Several groups have considered the wall compliance by using fluid-structure interaction (FSI) modeling. However, FSI simulation is highly sensitive to numerical assumptions (e.g. linear-elastic wall material, Newtonian fluid, initial vessel configuration, and constant pressure outlet), the effects of which are poorly understood. In this study, a comprehensive investigation of the sensitivity of FSI simulations in patient-specific IAs is investigated using a multi-stage approach with a varying level of complexity. We start with simulations incorporating several common simplifications: rigid wall, Newtonian fluid, and constant pressure at the outlets, and then we stepwise remove these simplifications until the most comprehensive FSI simulations. Hemodynamic parameters such as wall shear stress and oscillatory shear index are assessed and compared at each stage to better understand the sensitivity of in FSI simulations for IA to model assumptions. [Preview Abstract] |
Monday, November 23, 2015 6:02PM - 6:15PM |
L23.00010: ABSTRACT WITHDRAWN |
Monday, November 23, 2015 6:15PM - 6:28PM |
L23.00011: Coupled simulation of vascular growth and remodeling, hemodynamics and stress-mediated mechanotransduction Jiacheng Wu, Shawn C. Shadden A computational framework to couple vascular G{\&}R, blood flow simulation and stress-mediated mechanotransduction is derived for patient specific geometry. A hyperelastic constitutive relation is considered for vascular material and vessel wall is modeled via constrained mixture theory. The coupled simulation is divided into three time scales - G{\&}R (weeks-years), hemodynamics (seconds) and stress-mediated mechanotransduction (much less than 1 second). G{\&}R is simulated and vessel wall deformation (and tension) is computed to obtain the current vessel geometry, which defines the new boundary for blood flow. Hemodynamics are then simulated in the updated domain to calculate WSS field. A system of ODE's is derived based on conservation law and phenomenological models to describe the signaling pathways from mechanical stimuli (WSS, wall tension) to mass production rate of vascular constituents, which, in turn, changes the kinetics of G{\&}R. To reduce computation cost, blood flow is only simulated when G{\&}R causes significant change to geometry, and steady state response of the ODE system for mechanotransduction is used to characterize the influence of WSS and wall tension on G{\&}R, due to separation of three time scales. [Preview Abstract] |
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