Modeling pulsatile flow in aortic aneurysms: effect of non-Newtonian properties of blood

Pulsatile flow in an axisymmetric rigid-walled model of an abdominal aorta aneurysm was analyzed numerically for various aneurysm dilations using physiologically realistic resting waveform at time-averaged Reynolds number of 300 and peak Reynolds number of 1607. Discretization of the governing equations was achieved using a finite element scheme based on the Galerkin method of weighted residuals. Comparisons with previously published work on the basis of special cases were performed and found to be in excellent agreement. Our findings indicate that the velocity fields are significantly affected by non-Newtonian properties in pathologically altered configurations. Non-Newtonian fluid shear stress is found to be greater than Newtonian fluid shear stress during peak systole. Further, the maximum shear stress is found to occur near the distal end of AAA during peak systole. The impact of non-Newtonian blood flow characteristics on pressure compared to Newtonian model is found insignificant under resting conditions. Viscous and inertial forces associated with blood flow are responsible for the changes in the wall that result in thrombus deposition and dilation while rupture of AAA is more likely determined by much larger mechanical stresses imposed by pulsatile pressure on the wall of AAA.     

Newtonian and non-Newtonian blood flow in coiled cerebral aneurysms

Endovascular coiling aims to isolate the aneurysm from blood circulation by altering hemodynamics inside the aneurysm and triggering blood coagulation. Computational fluid dynamics (CFD) techniques have the potential to predict the post-operative hemodynamics and to investigate the complex interaction between blood flow and coils. The purpose of this work is to study the influence of blood viscosity on hemodynamics in coiled aneurysms. Three image-based aneurysm models were used. Each case was virtually coiled with a packing density of around 30%. CFD simulations were performed in coiled and untreated aneurysm geometries using a Newtonian and a Non-Newtonian fluid models. Newtonian fluid slightly overestimates the intra-aneurysmal velocity inside the aneurysm before and after coiling. There were numerical differences between fluid models on velocity magnitudes in coiled simulations. Moreover, the non-Newtonian fluid model produces high viscosity (>0.007$>0.007$ [Pa s]) at aneurysm fundus after coiling. Nonetheless, these local differences and high-viscous regions were not sufficient to alter the main flow patterns and velocity magnitudes before and after coiling. To evaluate the influence of coiling on intra-aneurysmal hemodynamics, the assumption of a Newtonian fluid can be used.     

Blood flow in abdominal aortic aneurysms: pulsatile flow hemodynamics

Numerical predictions of blood flow patterns and hemodynamic stresses in Abdominal Aortic Aneurysms (AAAs) are performed in a two-aneurysm, axisymmetric, rigid wall model using the spectral element method. Physiologically realistic aortic blood flow is simulated under pulsatile conditions for the range of time-averaged Reynolds numbers 50< or =Re(m)< or =300, corresponding to a range of peak Reynolds numbers 262.5< or =Re(peak) < or = 1575. The vortex dynamics induced by pulsatile flow in AAAs is characterized by a sequence of five different flow phases in one period of the flow cycle. Hemodynamic disturbance is evaluated for a modified set of indicator functions, which include wall pressure (p(w)), wall shear stress (tau(w)), and Wall Shear Stress Gradient (WSSG). At peak flow, the highest shear stress and WSSG levels are obtained downstream of both aneurysms, in a pattern similar to that of steady flow. Maximum values of wall shear stresses and wall shear stress gradients obtained at peak flow are evaluated as a function of the time-average Reynolds number resulting in a fourth order polynomial correlation. A comparison between predictions for steady and pulsatile flow is presented, illustrating the importance of considering time-dependent flow for the evaluation of hemodynamic indicators.     

Slowness of blood flow and resultant thrombus formation in cerebral aneurysms

It is not yet fully understood what causes cerebral aneurysms to rupture. Although no definitive conclusion has been reached, it is considered that there are haemodynamic, biochemical and physiological factors contributing to rupture. Numerical techniques seem promising for investigation of this multi-physical phenomenon. In fact, recent intensive numerical studies with computational fluid dynamics have revealed detailed haemodynamic features of the flow in cerebral aneurysms such as velocity, pressure and wall shear stress distributions. It is, therefore, expected that biochemical and physiological aspects of aneurysmal rupture will also be actively investigated using numerical approaches. Considering this background, the authors have been working on modelling of thrombus formation in cerebral aneurysms caused by stagnant blood flow, because many studies have suggested that slow blood flow and resulting low wall shear stress are connected with rupture. Firstly, in this review paper, slowness of the intra-aneurysmal flow is reviewed with an energy balance theory, and secondly, thrombus formation in cerebral bifurcation aneurysms is discussed from the viewpoint of numerical modelling. A computational result obtained by application of the authors’ platelet aggregation–adhesion model is also provided.     

Structure of pulsatile flow in a model of elastic cerebral aneurysm

This study examines the effect of aneurysmal wall elasticity on the structure of flow within an elastic aneurysm during pulsatile flow. We visualized flow structure in a model of an elastic saccular aneurysm located at the bifurcation of the anterior cerebral artery and extending to the anterior communicating artery, and measured changes in the diameter of the aneurysm wall during pulsatile flow using particle imaging velocimetry (PIV). We similarly measured these features during steady flow by PIV and found that dilation of the aneurysmal wall absorbed the dynamic energy within the aneurysm. Accordingly, aneurysm wall elasticity functions as a biocompatible reaction that relieves wall shear stress acting on the vascular wall during pulsatile flow, and should thus inhibit the development and rupture of an aneurysm.     

Approximating hemodynamics of cerebral aneurysms with steady flow simulations

Computational fluid dynamics (CFD) simulations can be employed to gain a better understanding of hemodynamics in cerebral aneurysms and improve diagnosis and treatment. However, introduction of CFD techniques into clinical practice would require faster simulation times. The aim of this study was to evaluate the use of computationally inexpensive steady flow simulations to approximate the aneurysm's wall shear stress (WSS) field. Two experiments were conducted. Experiment 1 compared for two cases the time-averaged (TA), peak systole (PS) and end diastole (ED) WSS field between steady and pulsatile flow simulations. The flow rate waveform imposed at the inlet was varied to account for variations in heart rate, pulsatility index, and TA flow rate. Consistently across all flow rate waveforms, steady flow simulations accurately approximated the TA, but not the PS and ED, WSS field. Following up on experiment 1, experiment 2 tested the result for the TA WSS field in a larger population of 20 cases covering a wide range of aneurysm volumes and shapes. Steady flow simulations approximated the space-averaged WSS with a mean error of 4.3%. WSS fields were locally compared by calculating the absolute error per node of the surface mesh. The coefficient of variation of the root-mean-square error over these nodes was on average 7.1%. In conclusion, steady flow simulations can accurately approximate the TA WSS field of an aneurysm. The fast computation time of 6 min per simulation (on 64 processors) could help facilitate the introduction of CFD into clinical practice.     

Numerical and experimental studies on pulsatile flow in aneurysms arising laterally from a curved parent vessel at various angles

Both numerical and experimental studies have been performed to characterize the fluid flow inside the lateral aneurysms arising from the curved parent vessels at various angles gamma. The implicit solver was based on the time-dependent Navier-Stokes equations of incompressible laminar flow. Solutions were generated by a cell-center finite-volume method that used second order upwind and second order center flux difference splitting for the convection and diffusion term, respectively. The second order Crank-Nicolson method was used in the time integration term while the SIMPLEC algorithm was adopted to handle the pressure-velocity coupling. Complementarily, the particle tracking velocimetry (PTV) was used to measure the velocity fields. The conditions selected were to simulate an internal carotid artery with a diameter of 5 mm by similarity rules. The values of gamma explored were 0 degrees, 45 degrees, 90 degrees, and 135 degrees. Pulsatile flow with Wormersley number 3.9 and Reynolds numbers varying from 350 to 850 was considered. The computed results are firstly verified by the PTV measured ones. Discussion of the results is in terms of pulsatile main and secondary velocity vector fields, inflow rates into the aneurysm, and the distributions of wall shear stress and static pressure. It is found that among the angles examined gamma=45( composite function) is the riskiest angle from a fluid dynamics point of view and the aneurysmal dome is at risk.     

The effect of asymmetry in abdominal aortic aneurysms under physiologically realistic pulsatile flow conditions

In the abdominal segment of the human aorta under a patient's average resting conditions, pulsatile blood flow exhibits complex laminar patterns with secondary flows induced by adjacent branches and irregular vessel geometries. The flow dynamics becomes more complex when there is a pathological condition that causes changes in the normal structural composition of the vessel wall, for example, in the presence of an aneurysm. This work examines the hemodynamics of pulsatile blood flow in hypothetical three-dimensional models of abdominal aortic aneurysms (AAAs). Numerical predictions of blood flow patterns and hemodynamic stresses in AAAs are performed in single-aneurysm, asymmetric, rigid wall models using the finite element method. We characterize pulsatile flow dynamics in AAAs for average resting conditions by means of identifying regions of disturbed flow and quantifying the disturbance by evaluating flow-induced stresses at the aneurysm wall, specifically wall pressure and wall shear stress. Physiologically realistic abdominal aortic blood flow is simulated under pulsatile conditions for the range of time-average Reynolds numbers 50 < or = Rem < or = 300, corresponding to a range of peak Reynolds numbers 262.5 < or = Repeak < or = 1575. The vortex dynamics induced by pulsatile flow in AAAs is depicted by a sequence of four different flow phases in one period of the cardiac pulse. Peak wall shear stress and peak wall pressure are reported as a function of the time-average Reynolds number and aneurysm asymmetry. The effect of asymmetry in hypothetically shaped AAAs is to increase the maximum wall shear stress at peak flow and to induce the appearance of secondary flows in late diastole.     

Microcontinuum model for pulsatile blood flow through a stenosed tube

The effects of polar nature of blood and pulsatility on flow through a stenosed tube have been analysed by assuming blood as a micropolar fluid. Linearized solutions of basic equations are obtained through consecutive applications of finite Hankel and Laplace transforms. The analytical expressions for axial and particle angular velocities, wall shear stress, resistance to flow and apparent viscosity have been obtained. The axial velocity profiles for Newtonian and micropolar fluids have been compared. The interesting observation of this analysis is velocity, in certain parts of cycle, for micropolar fluid is higher than Newtonain fluid. Variation of apparent viscosity eta a with tube radius shows both inverse Fahraeus-Lindqvist and Fahraeus-Lindqvist effects. Finally, the resistance to flow and wall shear stress for normal and diseased blood have been computed and compared.     

Numerical simulations of pulsatile blood flow using a new constitutive model

In the present paper we use a new constitutive equation for whole human blood [R.G. Owens, A new microstructure-based constitutive model for human blood, J. Non-Newtonian Fluid Mech. (2006), to appear] to investigate the steady, oscillatory and pulsatile flow of blood in a straight, rigid walled tube at modest Womersley numbers. Comparisons are made with the experimental results of Thurston [Elastic effects in pulsatile blood flow, Microvasc. Res. 9 (1975), 145-157] for the pressure drop per unit length against volume flow rate and oscillatory flow rate amplitude. Agreement in all cases is very good. In the presentation of the numerical and experimental results we discuss the microstructural changes in the blood that account for its rheological behaviour in this simple class of flows. In this context, the concept of an apparent complex viscosity proves to be useful.     

Plasma viscosity and cerebral blood flow

We hypothesized that the response of cerebral blood flow (CBF) to changing viscosity would be dependent on "baseline" CBF, with a greater influence of viscosity during high-flow conditions. Plasma viscosity was adjusted to 1.0 or 3.0 cP in rats by exchange transfusion with red blood cells diluted in lactated Ringer solution or with dextran. Cortical CBF was measured by H(2) clearance. Two groups of animals remained normoxic and normocarbic and served as controls. Other groups were made anemic, hypercapnic, or hypoxic to increase CBF. Under baseline conditions before intervention, CBF did not differ between groups and averaged 49.4 +/- 10.2 ml. 100 g(-1). min(-1) (+/-SD). In control animals, changing plasma viscosity to 1. 0 or 3.0 cP resulted in CBF of 55.9 +/- 8.6 and 42.5 +/- 12.7 ml. 100 g(-1). min(-1), respectively (not significant). During hemodilution, hypercapnia, and hypoxia with a plasma viscosity of 1. 0 cP, CBF varied from 98 to 115 ml. 100 g(-1). min(-1). When plasma viscosity was 3.0 cP during hemodilution, hypercapnia, and hypoxia, CBF ranged from 56 to 58 ml. 100 g(-1). min(-1) and was significantly reduced in each case (P < 0.05). These results support the hypothesis that viscosity has a greater role in regulation of CBF when CBF is increased. In addition, because CBF more closely followed changes in plasma viscosity (rather than whole blood viscosity), we believe that plasma viscosity may be the more important factor in controlling CBF.     

Regional cerebral blood flow thresholds during cerebral ischemia.

The development of methods of determining regional cerebral blood flow (rCBF) has made possible the determination of thresholds for the appearance of cerebral ischemia. These thresholds vary depending on the method used for assessing cerebral ischemia. The following thresholds have been determined in man and nonhuman primates: 20 cc/100 g per min, electroencephalogram (EEG) and evoked cortical potential abnormalities appear, paralysis seen in waking monkeys; 15 cc/100 g per min. EEG and evoked cortical potential are lost; 12 cc/100 g per min, flows at this level in excess of 120 min produce infarction in waking animals; and 6 cc/100 g per min, massive loss of intracellular [K+]. The residual rCBF and the duration of ischemia determine the appearance of infarction in waking Macaca irus monkeys.     

Casson fluid model for pulsatile flow of blood under periodic body acceleration

Pulsatile flow of a Casson fluid under the influence of a periodic body acceleration has been studied in this paper. An implicit finite difference numerical procedure has been used to analyze the flow. Applicability of this method has been checked by comparing the obtained results with the analytical solution for Newtonian flow and explicit scheme solution. The agreement between the implicit and explicit scheme solutions and the analytical solution is good (error less than 1%). Flow variables have been computed at three locations in cardiovascular system (wide (femoral) and narrow (arteriole and coronary) tubes). Effects of yield stress, tube radius and pressure gradient combined, body acceleration amplitude and frequency etc., on flow have been studied. The following observations have been made: (i) Initial transient time It changes with yield stress in narrow tubes are insignificant, whereas in wide tubes It decreases with yield stress; (ii) The axial velocity and fluid acceleration variations with yield stress are uniform (changes only quantitatively, profiles shape remain same) in narrow tubes, whereas in wide tubes these variations are non-uniform (profiles change qualitatively as well as quantitatively); (iii) Yield stress effects on wall shear amplitude are insignificant in narrow tubes (congruent to 0.3% in arteriole and congruent to 6% in femoral); and (iv) For Newtonian fluid, mean flow rate does not change with body acceleration amplitude a0 and frequency fb but it increases (decreases) with a0(fb) for Casson fluid.     

Microwave method of determining cerebral blood flow

A noninvasive method of quantitative assessment of cerebral blood flow based on heat clearance from brain tissues is described. The rate of heat clearance depends essentially on the blood flow. The employment of microwave techniques permits to warm the investigated brain zone and to record the temperature decrease extracranially. As a thermometer, a microwave radiometer was used. The experiments were carried out on cats. The method was tested by current vasoactive drugs.     

Linear and nonlinear analyses of pulsatile blood flow in a cylindrical tube

A non-Newtonian shear-thinning constitutive relation is proposed to study pulsatile flow of whole blood in a cylindrical tube. The constitutive relation, which satisfies the principle of material frame indifference, is derived from viscometric data obtained from whole blood over a range of hematocrits. Assuming axisymmetric flow in a rigid cylindrical tube of constant diameter, a second-order, nonlinear partial differential equation governing the axial velocity component is obtained. Imposing a periodic pressure gradient, the governing equation was solved numerically using finite difference methods over a range of Stokes values and hematocrits. For a forcing frequency of 1 Hz, results are presented over tube diameters ranging between 0.1 and 2 cm and over hematocrits ranging between 10 and 80%. For a given hematocrit, velocity profiles predicted for the non-Newtonian model under sinusoidal forcing reveal attenuated volume flow rate and enhanced vorticity transport over the tube cross-section relative to a Newtonian fluid having a viscosity corresponding to the high shear-rate limit. For moderate to high Stokes numbers, consistent with flow in large arteries, our results revealed a viscosity distribution that was nearly time invariant. An analytic solution was obtained for a fluid having arbitrarily prescribed radially varying, temporally invariant viscosity and density distributions under arbitrary periodic pressure forcing. Close agreement was observed between our numerical and analytical results when the imposed viscosity distribution was chosen to approximate the time-averaged viscosity distribution predicted by the shear-thinning non-Newtonian model. For St > or approximately= 100, the disparity between our results and those of a Newtonian fluid of constant viscosity grows with a decreasing ratio of the DC to AC components of the pressure-gradient amplitude below 50%. In particular, for any purely oscillatory pressure-gradient (vanishing DC component), the Womersley solution is a particularly poor predictor of the amplitude and phase of wall shear rate for over half of the flow cycle. Under such circumstances, the analytical models presented here provide a simple and accurate means of estimating instantaneous wall shear rate, knowing only the pressure gradient and hematocrit.     

Stress analysis in a layered aortic arch model under pulsatile blood flow

Background  

Many cardiovascular diseases, such as aortic dissection, frequently occur on the aortic arch and fluid-structure interactions play an important role in the cardiovascular system. Mechanical stress is crucial in the functioning of the cardiovascular system; therefore, stress analysis is a useful tool for understanding vascular pathophysiology. The present study is concerned with the stress distribution in a layered aortic arch model with interaction between pulsatile flow and the wall of the blood vessel.