Zynq SoC based acceleration of the lattice Boltzmann method

Cerebral aneurysm is a life‐threatening condition. It is a weakness in a blood vessel that may enlarge and bleed into the surrounding area. In order to understand the surrounding environmental conditions during the interventions or surgical procedures, a simulation of blood flow in cerebral arteries is needed. One of the effective simulation approaches is to use the lattice Boltzmann (LB) method. Due to the computational complexity of the algorithm, the simulation is usually performed on high performance computers. In this paper, efficient hardware architectures of the LB method on a Zynq system‐on‐chip (SoC) are designed and implemented. The proposed architectures have first been simulated in Vivado HLS environment and later implemented on a ZedBoard using the software‐defined SoC (SDSoC) development environment. In addition, a set of evaluations of different hardware architectures of the LB implementation is discussed in this paper. The experimental results show that the proposed implementation is able to accelerate the processing speed by a factor of 52 compared to a dual‐core ARM processor‐based software implementation

High fidelity blood flow in a patient-specific arteriovenous fistula

An arteriovenous fistula, created by artificially connecting segments of a patient's vasculature, is the preferred way to gain access to the bloodstream for kidney dialysis. The increasing power and availability of supercomputing infrastructure means that it is becoming more realistic to use simulations to help identify the best type and location of a fistula for a specific patient. We describe a 3D fistula model that uses the lattice Boltzmann method to simultaneously resolve blood flow in patient-specific arteries and veins. The simulations conducted here, comprising vasculatures of the whole forearm, demonstrate qualified validation against clinical data. Ongoing research to further encompass complex biophysics on realistic time scales will permit the use of human-scale physiological models for basic and clinical medicine

Multi-scale computational modeling of coronary blood flow: application to fractional flow reserve.

Introduction. Fractional flow reserve (FFR) is presently an invasive coronary clinical index. Non-invasive CT imaging combined with computational coronary flow modelling may reduce the patient’s burden of undergoing invasive testing. Research statement. The ability to obtain information of the hemodynamic significance of detected lesions would streamline decision making in escalation to invasive angiography. Methods. A reduced order (lumped parameter) model of the coronary vasculature was further developed. The model was used in the assessment of the roles of structure and function on the FFR. Sophisticated methods were used to elicit numerical solutions. Further, CT imaging (n = 10) provided multiple porcine geometries based upon algorithms encoded within an existing scientific platform. Results. It was found that the length of large vessel stenosis and presence of microvascular disease are primary regulators of FFR. Further, the CT data provided a basis to investigate relationships between coronary geometry (structure) and blood flow (function) attributes. Discussion. The presented model, upon personalization, may compliment and streamline ongoing imaging efforts by guiding FFR assessment. It is likely to assist in preliminary data generation for future projects. The computational geometries will contribute to an open source service that will be made available to our University’s researchers

Towards Blood Flow in the Virtual Human: Efficient Self-Coupling of HemeLB

Many scientific and medical researchers are working towards the creation of a virtual human - a personalised digital copy of an individual - that will assist in a patient's diagnosis, treatment and recovery. The complex nature of living systems means that the development of this remains a major challenge. We describe progress in enabling the HemeLB lattice Boltzmann code to simulate 3D macroscopic blood flow on a full human scale. Significant developments in memory management and load balancing allow near linear scaling performance of the code on hundreds of thousands of computer cores. Integral to the construction of a virtual human, we also outline the implementation of a self-coupling strategy for HemeLB. This allows simultaneous simulation of arterial and venous vascular trees based on human-specific geometries.Comment: 30 pages, 10 figures, To be published in Interface Focus (https://royalsocietypublishing.org/journal/rsfs

Parametric analysis of an efficient boundary condition to control outlet flow rates in large arterial networks

Substantial effort is being invested in the creation of a virtual human-a model which will improve our understanding of human physiology and diseases and assist clinicians in the design of personalised medical treatments. A central challenge of achieving blood flow simulations at full-human scale is the development of an efficient and accurate approach to imposing boundary conditions on many outlets. A previous study proposed an efficient method for implementing the two-element Windkessel model to control the flow rate ratios at outlets. Here we clarify the general role of the resistance and capacitance in this approach and conduct a parametric sweep to examine how to choose their values for complex geometries. We show that the error of the flow rate ratios decreases exponentially as the resistance increases. The errors fall below 4% in a simple five-outlets model and 7% in a human artery model comprising ten outlets. Moreover, the flow rate ratios converge faster and suffer from weaker fluctuations as the capacitance decreases. Our findings also establish constraints on the parameters controlling the numerical stability of the simulations. The findings from this work are directly applicable to larger and more complex vascular domains encountered at full-human scale

Transport in complex systems : a lattice Boltzmann approach

Celem niniejszej pracy jest zbadanie możliwości efektywnego modelowania procesów transportu w złożonych systemach z zakresu dynamiki płynów za pomocą metody siatkowej Boltzmanna (LBM). Złożoność systemu została potraktowana wieloaspektowo i konkretne układy, które poddano analizie pokrywały szeroki zakres zagadnień fizycznych, m.in. przepływy wielofazowe, hemodynamikę oraz turbulencje. We wszystkich przypadkach szczególna uwaga została zwrócona na aspekty numeryczne — dokładność używanych modeli, jak również szybkość z jaką pozwalają one uzyskać zadowalające rozwiązanie. W ramach pracy rozwinięty został pakiet oprogramowania Sailfish, będący otwarta implementacja metody siatkowej Boltzmanna na procesory kart graficznych (GPU). Po analizie szybkości jego działania, walidacji oraz omówieniu założeń projektowych, pakiet ten został użyty do symulacji trzech typów przepływów. Pierwszym z nich były przepływy typu Brethertona/Taylora w dwu- i trójwymiarowych geometriach, do symulacji których zastosowano model energii swobodnej. Analiza otrzymanych wyników pokazała dobra zgodność z danymi dostępnymi w literaturze, zarówno eksperymentalnymi, jak i otrzymanymi za pomocą innych metod numerycznych. Drugim badanym problemem były przepływy krwi w realistycznych geometriach tętnic dostarczających krew do ludzkiego mózgu. Wyniki symulacji zostały dokładnie porównane z rozwiązaniem otrzymanym metoda objętości skończonych z wykorzystaniem pakietu OpenFOAM, przyspieszonego komercyjna biblioteka pozwalająca na wykonywanie obliczeń na GPU. Otrzymano dobra zgodność między badanymi metodami oraz pokazano, że metoda siatkowa Boltzmanna pozwala na wykonywanie symulacji do ok. 20 razy szybciej. Trzecim przeanalizowanym zagadnieniem były turbulentne przepływy w prostych geometriach. Po zwalidowaniu wszystkich zaimplementowanych modeli relaksacji na przypadku wiru Kidy, zbadano przepływy w pustym kanale oraz w obecności przeszkód. Do symulacji wykorzystano zarówno siatki zapewniające pełną rozdzielczość aż do skal Kolmogorova, jak i siatki o mniejszej rozdzielczości. Również w tym kontekście pokazano dobrą zgodność wyników otrzymanych metodą siatkową Boltzmanna z wynikami innych symulacji oraz badaniami eksperymentalnymi. Pokazano również, że implementacja LBM w pakiecie Sailfish zapewnia większą stabilność obliczeń niż ta opisana w literaturze dla tych samych przepływów i modeli relaksacji

Models of coupled smooth muscleand endothelial cells

Impaired mass transfer characteristics of blood borne vasoactive species such as ATP in regions such as an arterial bifurcation have been hypothesized as a prospective mechanism in the aetiology of atherosclerotic lesions. Arterial endothelial (EC) and smooth muscle cells (SMC) respond differentially to altered local hemodynamics and produce coordinated macro-scale responses via intercellular communication. Using a computationally designed arterial segment comprising large populations of mathematically modelled coupled ECs & SMCs, we investigate their response to spatial gradients of blood borne agonist concentrations and the effect of micro-scale driven perturbation on the macro-scale. Altering homocellular (between same cell type) and heterocellular (between different cell types) intercellular coupling we simulated four cases of normal and pathological arterial segments experiencing an identical gradient in the concentration of the agonist. Results show that the heterocellular calcium (Ca2+) coupling between ECs and SMCs is important in eliciting a rapid response when the vessel segment is stimulated by the agonist gradient. In the absence of heterocellular coupling, homocellular Ca2+ coupling between smooth muscle cells is necessary for propagation of Ca2+ waves from downstream to upstream cells axially. Desynchronized intracellular Ca2+ oscillations in coupled smooth muscle cells are mandatory for this propagation. Upon decoupling the heterocellular membrane potential, the arterial segment looses the inhibitory effect of endothelial cells on the Ca2+ dynamics of underlying smooth muscle cells. The full system comprising hundreds of thousands of coupled nonlinear ordinary differential equations simulated on the massively parallel Blue Gene architecture. The use of massively parallel computational architectures shows the capability of this approach to address macro-scale phenomena driven by elementary micro-scale components of the system

Massively parallel simulations of coupled arterial cells : Ca2+ dynamics and atherosclerosis.

Ischaemic heart disease (IHD) is the most common cardiovascular disease, and is a major cause of mortality globally. The underlying process of IHD involves the development of atherosclerotic plaques on the arterial wall. These plaques can subsequently rupture and release thrombogenic species into circulation, or can occlude the vessel downstream following detachment. Such complications result in ischaemia—a restriction of blood supply to tissue that results in a shortage of vital cellular nutrients, such as oxygen and glucose. Recent publications hypothesise that cellular ionised calcium (Ca2+) concentrations play an important role in atherogenesis. There has been a significant amount of research on cardiovascular disease within multiple sub areas, including: in vivo and in vitro experimental work, computational fluid dynamics (CFD) simulations, and computational modelling of pathological behaviour. However, a combination of these fields will provide a greater understanding of the conditions that promote plaque development. The research presented in this thesis consists primarily of massively parallel simulations of arterial bifurcations which used CFD to generate the input agonist maps for each arterial mesh. Micro-scale dynamics of coupled endothelial cells (ECs) and smooth muscle cells (SMCs) were modelled in bifurcation surfaces containing over one million cells. In particular, the effect bifurcation angulation may have on atherosclerosis development was investigated. A number of improvements were introduced to the original coupled cells model to perform these simulations. A surface-mesh generation pipeline capable of creating geometrically varying 3-D surfaces, including EC and SMC layers, was implemented. These surfaces were used in CFD simulations to generate agonist input maps, and to define the EC and SMC layers on which the dynamics in our simulations are mapped. A detailed inositol triphosphate (IP3) pathway and gap-junction currents were introduced to the coupled cells model. These additions were to ensure our simulations present physiologically accurate results when compared to related experimental research and computational modelling. Finally, the parallel implementation that enabled our simulations to be conducted at the macro scale was improved by the introduction of Open-Multi-Processing (OpenMP). The massively parallel simulations displayed propagating Ca2+ waves in SMCs and steady-state concentrations of Ca2+ in ECs. Particularly complex SMC Ca2+ behaviour was observed in the lateral regions where the main stem meets the branches. Waves propagated in a slower, sporadic manner, and over significantly shorter distances. Further, we observed lower time-averaged Ca2+ concentrations in arterial geometries with wider bifurcation angles compared to those with narrower bifurcation angles. The regions of low EC and SMC Ca2+ concentrations correspond to the sites re- search utilising CFD agrees are those most likely to experience plaque development due to flow detachment. Furthermore, we noted the low Ca2+ concentrations in these areas are more prominent in arterial geometries with wider bifurcation angles. These results suggest bifurcation angulation may have a significant effect on the susceptibility of arterial regions to atherosclerosis development