Bulletin of the American Physical Society
69th Annual Meeting of the APS Division of Fluid Dynamics
Volume 61, Number 20
Sunday–Tuesday, November 20–22, 2016; Portland, Oregon
Session M15: Bio: Red Blood Cells and Thrombosis Formation |
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Chair: Shawn Shadden, University of California, Berkeley Room: E143/144 |
Tuesday, November 22, 2016 8:00AM - 8:13AM |
M15.00001: An immersed-boundary method for modeling flow of deformable blood cells in complex geometry Peter Balogh, Prosenjit Bagchi We present a computational methodology for simulating blood flow at the cellular scale in highly complex geometries, such as microvascular networks. Immersed boundary methods provide the foundation for our approach, as they allow modeling flows in arbitrary geometries, in addition to resolving the large deformation and dynamics of individual blood cell with high fidelity. Different simulation components are seamlessly integrated into the present methodology that can simultaneously model stationary rigid boundaries of arbitrary and complex shape, moving rigid bodies, and highly deformable interfaces of blood cells that are governed by non-linear elasticity. This permits physiologically realistic simulations of blood cells flowing in complex microvascular networks characterized by multiple bifurcating and merging vessels. The methodology is validated against analytical theory, experimental data, and previous numerical results. We then demonstrate the capabilities of the methodology by simulating deformable blood cells and heterogeneous cell suspensions flowing in both physiologically realistic microvascular networks and geometrically intricate microfluidic devices. The methodology offers the potential of scaling up to large microvascular networks at organ levels. [Preview Abstract] |
Tuesday, November 22, 2016 8:13AM - 8:26AM |
M15.00002: Axial dispersion in flowing red blood cell suspensions Thomas Podgorski, Sylvain Losserand, Gwennou Coupier A key parameter in blood microcirculation is the transit time of red blood cells (RBCs) through an organ, which can influence the efficiency of gas exchange and oxygen availability. A large dispersion of this transit time is observed in vivo and is partly due to the axial dispersion in the flowing suspension. In the classic Taylor-Aris example of a solute flowing in a tube, the combination of molecular diffusion and parabolic velocity profile leads to enhanced axial dispersion. In suspensions of non-Brownian deformable bodies such as RBCs, axial dispersion is governed by a combination of shear induced migration and shear-induced diffusion arising from hydrodynamic interactions. We revisit this problem in the case of RBC pulses flowing in a microchannel and show that the axial dispersion of the pulse eventually saturates with a final extension that depends directly on RBC mechanical properties. The result is especially interesting in the dilute limit since the final pulse length depends only on the channel width, exponent of the migration law and dimensionless migration velocity. In continuous flow, the dispersion of transit times is the result of complex cell-cell and cell-wall interactions and is strongy influenced by the polydispersity of the blood sample. [Preview Abstract] |
Tuesday, November 22, 2016 8:26AM - 8:39AM |
M15.00003: Modeling malaria infected cells in microcirculation Amir Hossein Raffiee, Sadegh Dabiri, Arezoo Motavalizadeh Ardekani Plasmodim (P.) falciparum is one of the deadliest types of malaria species that invades healthy red blood cells (RBC) in human blood flow. This parasite develops through 48-hour intra-RBC process leading to significant morphological and mechanical (e.g., stiffening) changes in RBC membrane. These changes have remarkable effects on blood circulation such as increase in flow resistance and obstruction in microcirculation. In this work a computational framework is developed to model RBC suspension in blood flow using front-tracking technique. The present study focuses on blood flow behavior under normal and infected circumstances and predicts changes in blood rheology for different levels of parasitemia and hematocrit. This model allows better understanding of blood flow circulation up to a single cell level and provides us with realistic and deep insight into hematologic diseases such as malaria. [Preview Abstract] |
Tuesday, November 22, 2016 8:39AM - 8:52AM |
M15.00004: Blood flow simulation on a role for red blood cells in platelet adhesion. Kazuya Shimizu, Kazuyasu Sugiyama, Shu Takagi Large-scale blood flow simulations were conducted and a role for red blood cells in platelet adhesion was discussed. The flow conditions and hematocrit values were set to the same as corresponding experiments, and the numerical results were compared with the measurements. Numerical results show the number of platelets adhered on the wall is increased with the increase in hematocrit values. The number of adhered platelets estimated from the simulation was approximately 28 (per 0.01 square millimeter per minute) for the hematocrit value of 20 {\%}. These results agree well with the experimental results qualitatively and quantitatively, which proves the validity of the present numerical model including the interaction between fluid and many elastic bodies and the modeling of platelet adhesion. Numerical simulation also reproduces the behavior of red blood cells in the blood flow and their role in platelet adhesion. Red blood cells deform to a flat shape and move towards channel center region. In contrast, platelets are pushed out and have many chances to contact with the wall. As a result, the large number of adhered platelets is observed as hematocrit values becomes high. This result indicates the presence of red blood cells plays a crucial role in platelet adhesion. [Preview Abstract] |
Tuesday, November 22, 2016 8:52AM - 9:05AM |
M15.00005: Seamless particle-based modeling of blood clotting Alireza Yazdani, George Karniadakis We propose a new multiscale framework that seamlessly integrate four key components of blood clotting namely, blood rheology, cell mechanics, coagulation kinetics and transport of species and platelet adhesive dynamics. We use transport dissipative particle dynamics (tDPD) which is an extended form of original DPD as the base solver to model both blood flow and the reactive transport of chemical species in the coagulation cascade. Further, we use a coarse-grained representation of blood cell's membrane that accounts for its mechanics; both red blood cells and platelets are resolved at sub-cellular resolution, and stochastic bond formation/dissociation are included to account for platelet adhesive dynamics at the site of injury. Our results show good qualitative agreement with in vivo experiments. The numerical framework allows us to perform systematic analysis on different mechanisms of blood clotting. In addition, this new multiscale particle-based methodology can open new directions in addressing different biological processes from sub-cellular to macroscopic scales. [Preview Abstract] |
Tuesday, November 22, 2016 9:05AM - 9:18AM |
M15.00006: Computational reconstruction and fluid dynamics of in vivo thrombi from the microcirculation Mehran Mirramezani, Maurizio Tomaiuolo, Timothy Stalker, Shawn Shadden Blood flow and mass transfer can have significant effects on clot growth, composition and stability during the hemostatic response. We integrate in vivo data with CFD to better understand transport processes during clot formation. By utilizing electron microscopy, we reconstructed the 3D thrombus structure formed after a penetrating laser injury in a mouse cremaster muscle. Random jammed packing is used to reconstruct the microenvironment of the platelet aggregate, with platelets modeled as ellipsoids. In our 3D model, Stokes flow is simulated to obtain the velocity field in the explicitly meshed gaps between platelets and the lumen surrounding the thrombus. Based on in vivo data, a clot is composed of a core of highly activated platelets covered by a shell of loosely adherent platelets. We studied the effects of clot size (thrombus growth), gap distribution (consolidation), and vessel blood flow rate on mean intrathrombus velocity. The results show that velocity is smaller in the core as compared to the shell, potentially enabling higher concentration of agonists in the core contributing to its activation. In addition, our results do not appear to be sensitive to the geometry of the platelets, but rather gap size plays more important role on intrathrombus velocity and transport. [Preview Abstract] |
Tuesday, November 22, 2016 9:18AM - 9:31AM |
M15.00007: A Fictitious Domain Method for Resolving the Interaction of Blood Flow with Clot Growth Debanjan Mukherjee, Shawn Shadden Thrombosis and thrombo-embolism cause a range of diseases including heart attack and stroke. Closer understanding of clot and blood flow mechanics provides valuable insights on the etiology, diagnosis, and treatment of thrombotic diseases. Such mechanics are complicated, however, by the discrete and multi-scale phenomena underlying thrombosis, and the complex interactions of unsteady, pulsatile hemodynamics with a clot of arbitrary shape and microstructure. We have developed a computational technique, based on a fictitious domain based finite element method, to study these interactions. The method can resolve arbitrary clot geometries, and dynamically couple fluid flow with static or growing clot boundaries. Macroscopic thrombus-hemodynamics interactions were investigated within idealized vessel geometries representative of the common carotid artery, with realistic unsteady flow profiles as inputs. The method was also employed successfully to resolve micro-scale interactions using a model driven by in-vivo morphology data. The results provide insights into the flow structures and hemodynamic loading around an arbitrarily grown clot at arterial length-scales, as well as flow and transport within the interstices of platelet aggregates composing the clot. [Preview Abstract] |
Tuesday, November 22, 2016 9:31AM - 9:44AM |
M15.00008: Spatial dependence of thrombolysis Hari hara sudhan Lakshmanan, Jevgenia Zilberman-Rudenko, Owen McCarty, Jeevan Maddala Thrombolysis under hemodynamic conditions is affected by both transport processes and reactions, thus profoundly dependent on the geometry of blood vessels or vasculature. Although thrombosis has long been observed clinically, a systematic and quantitative understanding has not been established in complex geometries such as vasculature, where various factors would affect thrombogenesis and its stability. A thrombus's location determines the effect of hydrodynamic forces on it and rate of tPA diffusion, that would result in either embolization or formation of micro-aggregates. Preliminary experiments have shown that thrombolysis is not uniform across an entire network with different locations lysing at different rates. Numerical simulations of thrombolysis under hemodynamics in a microfluidic geometry such as a ladder network with a focus on parameters such as reaction rate, shear gradient, velocity and diffusion established the lysis's dependence on geometry. Finite element simulations of blood flow coupled with reactions have been performed in COMSOL and the results were used to develop quantifiable metrics for thrombolysis in a complex geometry. [Preview Abstract] |
Tuesday, November 22, 2016 9:44AM - 9:57AM |
M15.00009: Evaluating How Circle of Willis Topology Affects Embolus Distribution in the Brain Neel Jani, Debanjan Mukherjee, Shawn Shadden Embolic stroke occurs when fragmented cellular or acellular material (emboli) travels to the brain to occlude an artery. Understanding the transport of emboli across unsteady, pulsatile flow in complex arterial geometries is challenging and influenced by a range of factors, including patient anatomy. The work herein develops the modeling and mechanistic understanding of how embolus transport is affected by the arterial connections at the base of the brain known as the Circle of Willis (CoW). A majority of the human population has an incomplete CoW anatomy, with connections either missing or ill-developed. We employ numerical simulations combining image-based modeling, computational fluid dynamics, discrete particle dynamics, and a sampling based analysis to compare collateral flow through the most prevalent CoW topologies, to determine embolus distribution fractions among vessels in the CoW, and to investigate the role of inertial effects in causing differences in flow and embolus distribution. The computational framework developed enables characterization of the complex interplay of anatomy, hemodynamics, and embolus properties in the context of embolic stroke as well as statistical analysis of embolism risks across common CoW variations. [Preview Abstract] |
Tuesday, November 22, 2016 9:57AM - 10:10AM |
M15.00010: The influence of inflow cannula malposition and left ventricle size on intraventricular thrombosis risk for Left Ventricle Assist Device V. Keshav Chivukula, Patrick McGah, Anthony Prisco, Jennifer Beckman, Nanush Mokadam, Claudius Mahr, Alberto Aliseda Patients with left ventricular assist devices (LVAD) have high incidence of thrombosis and stroke. Patient-specific left ventricle 3D models were created with different LVAD inflow cannula angles with the ventricle axis (in increments of $\pm7^o$). Left ventricle sizes ranging from $4-7.5~cm$ in diameter were studied. The aim is optimizing inflow cannula selection and alignment in LVAD patients by understanding the roles that misalignment of the cannula and ventricle size variability play in platelet activation, residence time and agglomeration. Unsteady CFD simulations with patient-specific boundary conditions were performed, and particle tracking was conducted for 10 cardiac cycles to compute the residence time and shear stress histories of platelets for different configurations. Eulerian and Lagrangian metrics, as well as a newly-developed thrombogenic potential score were calculated and used to assess the thrombogenic risk associated with the inflow cannula. Results indicate that inflow cannula misalignment can significantly increase the risk of thrombosis. Cannula sizing without ventricle size consideration affects thrombogenecity for patients outside the normal range (5-6 cm). A methodology is outlined for minimization of thrombotic potential in LVAD implantation strategies [Preview Abstract] |
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