Direct numerical simulation of transitional flow in a stenosed carotid bifurcation.

The blood flow dynamics of a stenosed, subject-specific, carotid bifurcation were numerically simulated using the spectral element method. Pulsatile inlet conditions were based on in vivo color Doppler ultrasound measurements of blood velocity. The results demonstrated the transitional or weakly turbulent state of the blood flow, which featured rapid velocity and pressure fluctuations in the post-stenotic region of the internal carotid artery (ICA) during systole and laminar flow during diastole. High-frequency vortex shedding was greatest downstream of the stenosis during the deceleration phase of systole. Velocity fluctuations had a frequency within the audible range of 100-300Hz. Instantaneous wall shear stress (WSS) within the stenosis was relatively high during systole ( approximately 25-45Pa) compared to that in a healthy carotid. In addition, high spatial gradients of WSS were present due to flow separation on the inner wall. Oscillatory flow reversal and low pressure were observed distal to the stenosis in the ICA. This study predicts the complex flow field, the turbulence levels and the distribution of the biomechanical stresses present in vivo within a stenosed carotid artery.

Modeling transition to turbulence in eccentric stenotic flows.

Mean flow predictions obtained from a host of turbulence models were found to be in poor agreement with recent direct numerical simulation results for turbulent flow distal to an idealized eccentric stenosis. Many of the widely used turbulence models, including a large eddy simulation model, were unable to accurately capture the poststenotic transition to turbulence. The results suggest that efforts toward developing more accurate turbulence models for low-Reynolds number, separated transitional flows are necessary before such models can be used confidently under hemodynamic conditions where turbulence may develop.

Importance of flow division on transition to turbulence within an arteriovenous graft.

Transitional blood flow in an arteriovenous graft under various conditions of flow division was examined through direct numerical simulation. This junction consists of an inlet vessel (prosthetic graft) connected to a host vessel (vein) at an acute angle (21.6 degrees ). Inlet Reynolds numbers, based on mean velocity and graft inlet diameter, ranged from 800 to 1400. Various flow divisions between the two ends of the host vessel (i.e., the proximal venous segment, PVS, and distal venous segment, DVS) were considered (PVS:DVS ratios of 100:0, 85:15, 70:30 and 115:(15)). The numerical technique employed the spectral element method which is a high-order discretization ideally suited to the simulation of transitional flows in complex domains. High velocity and pressure fluctuations were observed for the PVS:DVS=70:30 and 85:15 cases and absent from the 100:0 and 115:(15) cases; the results indicate the importance of flow division on the development of turbulence in this junction. Transition to turbulence was observed at Reynolds numbers as low as 1000 and 800 under flow divisions of 85:15 and 70:30, respectively, significantly lower than the critical value of 2100. The frequency spectra of velocity fluctuations indicated a significant intensity within the frequency range of approximately 300Hz downstream of the junction. An adverse pressure gradient developed in the PVS when graft inflow divided into opposite directions in the junction. This pressure gradient had a destabilizing effect on the flow and enhanced transition to turbulence in the PVS. These findings suggest that measurements of in vivo flow rates at the inlet and outlets are critical for the accurate prediction of arteriovenous hemodynamics. A potential clinical application of these results might be to close off the DVS during graft construction to ensure a 100:0 flow division.

Eliminating parasitic currents in the lattice Boltzmann equation method for nonideal gases.

A formulation of the intermolecular force in the nonideal-gas lattice Boltzmann equation method is examined. Discretization errors in the computation of the intermolecular force cause parasitic currents. These currents can be eliminated to roundoff if the potential form of the intermolecular force is used with compact isotropic discretization. Numerical tests confirm the elimination of the parasitic currents.

Transitional flow at the venous anastomosis of an arteriovenous graft: potential activation of the ERK1/2 mechanotransduction pathway.

We present experimental and computational results that describe the level, distribution, and importance of velocity fluctuations within the venous anastomosis of an arteriovenous graft. The motivation of this work is to understand better the importance of biomechanical forces in the development of intimal hyperplasia within these grafts. Steady-flow in vitro studies (Re = 1060 and 1820) were conducted within a graft model that represents the venous anastomosis to measure velocity by means of laser Doppler anemometry. Numerical simulations with the same geometry and flow conditions were conducted by employing the spectral element technique. As flow enters the vein from the graft, the velocity field exhibits flow separation and coherent structures (weak turbulence) that originate from the separation shear layer. We also report results of a porcine animal study in which the distribution and magnitude of vein-wall vibration on the venous anastomosis were measured at the time of graft construction. Preliminary molecular biology studies indicate elevated activity levels of the extracellular regulatory kinase ERK1/2, a mitogen-activated protein kinase involved in mechanotransduction, at regions of increased vein-wall vibration. These findings suggest a potential relationship between the associated turbulence-induced vein-wall vibration and the development of intimal hyperplasia in arteriovenous grafts. Further research is necessary, however, in order to determine if a correlation exists and to differentiate the vibration effect from that of flow related effects.