Endovascular repair of type B aortic dissection: a study by computational fluid dynamics

Aortic dissection is a dangerous pathological condi-tion where blood intrudes into the layers of the arte-rial walls, creating an artificial channel (false lumen). In the absence of thrombosis or surgical intervention, blood will enter the false lumen through the proximal tear, and join the true lumen again through a distal tear. Rupture of the weakened outer wall will result in extremely high mortality rates. Type B thoracic aortic dissection (TAD), occurring along the de-scending aorta, can be repaired surgically by the de-ployment of an endovascular stent graft, concealing the proximal entry tear. Blood might still flow into the false lumen (FL) through the distal tear. The do-main of such flow should be minimized, as complete thrombosis of the FL is generally believed to be more beneficial for the patient. The dependence on the area ratios of the lumens and size of these tears is studied by computational fluid dynamics.published_or_final_versio

Efects of non‑Newtonian viscosity on arterial and venous fow and transport

It is well known that blood exhibits non-Newtonian viscosity, but it is generally modeled as a Newtonian fluid. However, in situations of low shear rate, the validity of the Newtonian assumption is questionable. In this study, we investigated differences between Newtonian and non-Newtonian hemodynamic metrics such as velocity, vorticity, and wall shear stress. In addition, we investigated cardiovascular transport using two different approaches, Eulerian mass transport and Lagrangian particle tracking. Non-Newtonian solutions revealed important differences in both hemodynamic and transport metrics relative to the Newtonian model. Most notably for the hemodynamic metrics, in-plane velocity and vorticity were consistently larger in the Newtonian approximation for both arterial and venous flows. Conversely, wall shear stresses were larger for the non-Newtonian case for both the arterial and venous models. Our results also indicate that for the Lagrangian metrics, the history of accumulated shear was consistently larger for both arterial and venous flows in the Newtonian approximation. Lastly, our results also suggest that the Newtonian model produces larger near wall and luminal mass transport values compared to the non-Newtonian model, likely due to the increased vorticity and recirculation. These findings demonstrate the importance of accounting for non-Newtonian behavior in cardiovascular flows exhibiting significant regions of low shear rate and recirculation

Development and application of lattice Boltzmann method for complex axisymmetric flows

The lattice Boltzmann method (LBM) has become an effective numerical technique for computational fluid dynamics (CFD) in recent years. It has many advantages over the conventional computational methods like finite element and finite difference methods. The method is characterised by simplicity, easy treatment of boundary conditions and parallel feature in programming that makes it ideal for solving large-scale real-life problems. This thesis presents the development and applications of a lattice Boltzmann model for both steady and unsteady two-dimensional axisymmetric flows. The axisymmetric flows are described by three-dimensional (3D) Navier-Stokes equations, which can be solved by three-dimensional (3D) lattice Boltzmann method. If cylindrical coordinates are applied, such 3D equations become 2D axisymmetric flow equations. However, they cannot be solved using the 2D standard LBM. In order to study more complicated axisymmetric flow problems by 2D LBM, in this thesis, firstly, the revised axisymmetric lattice Boltzmann D2Q9 model (AxLAB®) is applied and tested for some benchmark for axisymmetric laminar flows and more complicated flows including 3D Womersley flow and forced axisymmetric cold-flow jets, and flows with swirl such as the cylindrical cavity flows and the swirling flow in a closed cylinder with rotating top and bottom. Secondly, the AxLAB® is extended to simulate turbulent flows and non-Newtonian fluid flows. A well-known power-law scheme is incorporated into the AxLAB® to simulate the non-Newtonian fluid flow: the Taylor Couette flows for Newtonian and non-Newtonian fluids are simulated and compared. The combined effects of the Reynolds number, the radius ratio, and the power-law index on the flow characteristics are analysed and compared with other literatures. All the numerical results are also compared with the existing numerical results or experimental data reported in the literature to demonstrate the accuracy of the model. Thirdly, a further developed AxLAB® is presented to simulate the turbulent flows. The turbulent flow is efficiently and naturally simulated through incorporation of the standard subgrid-scale stress (SGS) model into the axisymmetric lattice Boltzmann equation in a consistent manner with the lattice gas dynamics. The model is verified by applying it to several typical cases in engineering: (i) pipe flow through an abrupt axisymmetric constriction, (ii) axisymmetric separated and reattached flow and (iii) pulsatile flows in a stenotic vessel. All the numerical results obtained using the present methods are compared with experimental data and other available numerical solutions, indicating good agreements. This shows that the improved AxLAB® is simple and is able to predict axisymmetric turbulent, non-Newtonian complicated flows at good accuracy

Frequency composition of wall shear stress in animal models of atherosclerosis

Atherosclerosis and plaque rupture are widely known as multifactorial problems. To isolate the significance of wall shear stress in these problems, the work of this thesis explores the hypothesis that the frequency composition of the wall shear stress signal is associated with the different plaque compositions and disease characteristics in animal models of atherosclerosis. In this thesis, a lattice Boltzmann simulation tool was developed to test the hypothesis with the basic functionality of an existing code being enhanced for blood flow simulation and wall shear stress calculation. The wall shear stress signals computed from the simulation tool were analysed in terms of the frequency composition to recover the harmonic amplitude and phase information. This information was then used in comparing the different animal models. Compared to the healthy, non-diseased vessel, disease models are known to result in a decrease in the time-averaged wall shear stress from the reduction in blood flow rate and local complex flow patterns. Further to this, the simulation of these models showed a decrease in the first harmonic amplitude along the length of the vessel. This is a key result of this thesis as the decreased first harmonic amplitude is associated with an increase in the expression of adhesion molecules and proinflammatory factors in endothelial cells. The uniformity in wall shear stress in regions of different plaque type, however, suggests the dominance of circumferential stretch effects over wall shear stress effects in the disease process. Blood flow simulations in the mouse, rabbit and human vessels were also performed to deduce scaling relationships of the zeroth and first harmonic amplitudes between mammals. The body mass exponent of the first harmonic amplitude was found to be higher than that of the zeroth harmonic amplitude. This suggests an increased significance of the first harmonic component in the wall shear stress signal relative to the zeroth harmonic amplitude in larger mammals. The absence of plaque rupture in the atherosclerotic minipig, however, also suggests the dominance of genomic effects over wall shear stress effects in the disease process. A key issue in atherosclerosis research is the absence of plaque rupture in the mouse model. The apparent dominance of circumferential stretch and genomic differences shown here suggests that the wall shear stress alone cannot explain the lack of plaque rupture in atherosclerotic mice. How these differences affect plaque composition would be key in understanding the absence of plaque rupture in mouse models and how studies in mice can be applied to benefit human treatments