Experimental validation of a time-domain-based wave propagation model of blood flow in viscoelastic vessels

Time-domain-based one-dimensional wave propagation models of the arterial system are preferable over one-dimensional wave propagation models in the frequency domain since the latter neglect the non-linear convection forces present in the physiological situation, especially when the vessel is tapered. Moreover, one-dimensional wave propagation models of the arterial system can be used to provide boundary conditions for fully three-dimensional fluid-structure interaction computations that are usually defined in the time domain. In this study, a time-domain-based one-dimensional wave propagation model in a cross-sectional area, flow and pressure (A,q,p)-formulation is developed. Using this formulation, a constitutive law that includes viscoelasticity based on the mechanical behaviour of a Kelvin body, is introduced. The resulting pressure and flow waves travelling through a straight and tapered vessel are compared to experimental data obtained from measurements in an in vitro setup. The model presented shows to be well suited to predict wave propagation through these straight and tapered vessels with viscoelastic wall properties and hereto can serve as a time-domain-based method to model wave propagation in the human arterial system.     

Comparative study of viscoelastic arterial wall models in nonlinear one-dimensional finite element simulations of blood flow

It is well known that blood vessels exhibit viscoelastic properties, which are modeled in the literature with different mathematical forms and experimental bases. The wide range of existing viscoelastic wall models may produce significantly different blood flow, pressure, and vessel deformation solutions in cardiovascular simulations. In this paper, we present a novel comparative study of two different viscoelastic wall models in nonlinear one-dimensional (1D) simulations of blood flow. The viscoelastic models are from papers by Holenstein et al. in 1980 (model V1) and Valdez-Jasso et al. in 2009 (model V2). The static elastic or zero-frequency responses of both models are chosen to be identical. The nonlinear 1D blood flow equations incorporating wall viscoelasticity are solved using a space-time finite element method and the implementation is verified with the Method of Manufactured Solutions. Simulation results using models V1, V2 and the common static elastic model are compared in three application examples: (i) wave propagation study in an idealized vessel with reflection-free outflow boundary condition; (ii) carotid artery model with nonperiodic boundary conditions; and (iii) subject-specific abdominal aorta model under rest and simulated lower limb exercise conditions. In the wave propagation study the damping and wave speed were largest for model V2 and lowest for the elastic model. In the carotid and abdominal aorta studies the most significant differences between wall models were observed in the hysteresis (pressure-area) loops, which were larger for V2 than V1, indicating that V2 is a more dissipative model. The cross-sectional area oscillations over the cardiac cycle were smaller for the viscoelastic models compared to the elastic model. In the abdominal aorta study, differences between constitutive models were more pronounced under exercise conditions than at rest. Inlet pressure pulse for model V1 was larger than the pulse for V2 and the elastic model in the exercise case. In this paper, we have successfully implemented and verified two viscoelastic wall models in a nonlinear 1D finite element blood flow solver and analyzed differences between these models in various idealized and physiological simulations, including exercise. The computational model of blood flow presented here can be utilized in further studies of the cardiovascular system incorporating viscoelastic wall properties.     

Validation of a patient-specific one-dimensional model of the systemic arterial tree

The aim of this study is to develop and validate a patient-specific distributed model of the systemic arterial tree. This model is built using geometric and hemodynamic data measured on a specific person and validated with noninvasive measurements of flow and pressure on the same person, providing thus a patient-specific model and validation. The systemic arterial tree geometry was obtained from MR angiographic measurements. A nonlinear viscoelastic constitutive law for the arterial wall is considered. Arterial wall distensibility is based on literature data and adapted to match the wave propagation velocity of the main arteries of the specific subject, which were estimated by pressure waves traveling time. The intimal shear stress is modeled using the Witzig-Womersley theory. Blood pressure is measured using applanation tonometry and flow rate using transcranial ultrasound and phase-contrast-MRI. The model predicts pressure and flow waveforms in good qualitative and quantitative agreement with the in vivo measurements, in terms of wave shape and specific wave features. Comparison with a generic one-dimensional model shows that the patient-specific model better predicts pressure and flow at specific arterial sites. These results obtained let us conclude that a patient-specific one-dimensional model of the arterial tree is able to predict well pressure and flow waveforms in the main systemic circulation, whereas this is not always the case for a generic one-dimensional model.     

Theoretical analysis of pressure pulse propagation in arterial vessels.

An original mathematical model of viscous fluid motion in a tapered and distensible tube is presented. The model equations are deduced by assuming a two-dimensional flow and taking into account the nonlinear terms in the fluid motion equations, as well as the nonlinear deformation of the tube wall. One distinctive feature of the model is the formal integration with respect to the radial coordinate of the Navier-Stokes equations by power series expansion. The consequent computational frame allows an easy, accurate evaluation of the effects produced by changing the values of all physical and geometrical tube parameters. The model is employed to study the propagation along an arterial vessel of a pressure pulse produced by a single flow pulse applied at the proximal vessel extremity. In particular, the effects of the natural taper angle of the arterial wall on pulse propagation are investigated. The simulation results show that tapering considerably influences wave attenuation but not wave velocity. The substantially different behavior of pulse propagation, depending upon whether it travels towards the distal extremity or in the opposite direction, is observed: natural tapering causes a continuous increase in the pulse amplitude as it moves towards the distal extremity; on the contrary, the reflected pulse, running in the opposite direction, is greatly damped. For a vessel with physical and geometrical properties similar to those of a canine femoral artery and 0.1 degree taper angle, the forward amplification is about 0.9 m-1 and the backward attenuation is 1.4 m-1, so that the overall tapering effect gives a remarkably damped pressure response. For a natural taper angle of 0.14 degrees the perturbation is almost extinct when the pulse wave returns to the proximal extremity.     

Influence of the distensibility of large arteries on the longitudinal impedance: application for the development of non-invasive techniques to the diagnosis of arterial diseases

Background

This study shows that the arterial longitudinal impedance constitutes a hemodynamic parameter of interest for performance characterization of large arteries in normal condition as well as in pathological situations. For this purpose, we solved the Navier?CStokes equations for an incompressible flow using the finite element analysis method and the Arbitrary Lagrangian Eulerian (ALE) formulation. The mathematical model assumes a two-dimensional flow and takes into account the nonlinear terms in the equations of fluid motion that express the convective acceleration, as well as the nonlinear deformation of the arterial wall. Several numerical simulations of the blood flow in large vessels have been performed to study the propagation along an arterial vessel of a pressure gradient pulse and a rate flow pulse. These simulations include various deformations of the wall artery leading to parietal displacements ranging from 0 (rigid wall) to 15% (very elastic wall) in order to consider physiological and pathological cases.

Results

The results show significant changes of the rate flow and the pressure gradient wave as a function of aosc, the relative variation in the radius of the artery over a cardiac cycle. These changes are notable beyond a critical value of aosc equal to 0.05. This critical value is also found in the evolution of the longitudinal impedance. So, above a variation of radius of 5%, the convective acceleration, created by the fluid-wall interactions, have an influence on the flow detectable on the longitudinal impedance.

Conclusions

The interpretation of the evolution of the longitudinal impedance shows that it could be a mean to test the performance of large arteries and can contribute to the diagnosis of parietal lesions of large arteries. For a blood vessel with a wall displacement higher than 5% similar to those of large arteries like the aorta, the longitudinal impedance is substantially greater than that obtained in the absence of wall displacement. This study also explains the effects of convective acceleration, on the shape of the decline of the pressure gradient wave and shows that they should not be neglected when the variation in radius is greater than 5%.     

Wave Propagation through a Viscous Incompressible Fluid Contained in an Initially Stressed Elastic Tube

To have a better understanding of the flow of blood in arteries a theoretical analysis of the pressure wave propagation through a viscous incompressible fluid contained in an initially stressed tube is considered. The fluid is assumed to be Newtonian. The tube is taken to be elastic and isotropic. The analysis is restricted to tubes with thin walls and to waves whose wavelengths are very large compared with the radius of the tube. It is further assumed that the amplitude of the pressure disturbance is sufficiently small so that nonlinear terms of the inertia of the fluid are negligible compared with linear ones. Both circumferential and longitudinal initial stresses are considered; however, their origins are not specified. Initial stresses enter equations as independent parameters. A frequency equation, which is quadratic in the square of the propagation velocity is obtained. Two out of four roots of this equation give the velocity of propagation of two distinct outgoing waves. The remaining two roots represent incoming waves corresponding to the first two waves. One of the waves propagates more slowly than the other. As the circumferential and/or longitudinal stress of the wall increases, the velocity of propagation and transmission per wavelength of the slower wave decreases. The response of the fast wave to a change in the initial stress is on the opposite direction.     

Wave Propagation in a Viscous Fluid Contained in an Orthotropic Elastic Tube

The problem of pressure wave propagation through a viscous fluid contained in an orthotropic elastic tube is considered in connection with arterial blood flow. Solutions to the fluid flow and elasticity equations are obtained for the presence of a reflected wave. Numerical results are presented for both isotropic and orthotropic elastic tubes. In particular, the pressure pulse, flow rate, axial fluid velocity, and wall displacements are plotted vs. time at various stations along the ascending aorta of man. The results indicate an increase in the peak value of the pressure pulse and a decrease in the flow rate as the pulse propagates away from the heart. Finally, the velocity of wave propagation depends mainly on the tangential modulus of elasticity of the arterial wall, and anisotropy of the wall accounts in part for the reduction of longitudinal movements and an increase in the hydraulic resistance.     

Fluid–structure interaction in a fully coupled three-dimensional mitral–atrium–pulmonary model

This paper aims to investigate detailed mechanical interactions between the pulmonary haemodynamics and left heart function in pathophysiological situations (e.g. atrial fibrillation and acute mitral regurgitation). This is achieved by developing a complex computational framework for a coupled pulmonary circulation, left atrium and mitral valve model. The left atrium and mitral valve are modelled with physiologically realistic three-dimensional geometries, fibre-reinforced hyperelastic materials and fluid–structure interaction, and the pulmonary vessels are modelled as one-dimensional network ended with structured trees, with specified vessel geometries and wall material properties. This new coupled model reveals some interesting results which could be of diagnostic values. For example, the wave propagation through the pulmonary vasculature can lead to different arrival times for the second systolic flow wave (S2 wave) among the pulmonary veins, forming vortex rings inside the left atrium. In the case of acute mitral regurgitation, the left atrium experiences an increased energy dissipation and pressure elevation. The pulmonary veins can experience increased wave intensities, reversal flow during systole and increased early-diastolic flow wave (D wave), which in turn causes an additional flow wave across the mitral valve (L wave), as well as a reversal flow at the left atrial appendage orifice. In the case of atrial fibrillation, we show that the loss of active contraction is associated with a slower flow inside the left atrial appendage and disappearances of the late-diastole atrial reversal wave (AR wave) and the first systolic wave (S1 wave) in pulmonary veins. The haemodynamic changes along the pulmonary vessel trees on different scales from microscopic vessels to the main pulmonary artery can all be captured in this model. The work promises a potential in quantifying disease progression and medical treatments of various pulmonary diseases such as the pulmonary hypertension due to a left heart dysfunction.

     

A thick walled viscoelastic model for the mechanics of arteries

A knowledge of the mechanics of arteries is of importance in the determination of vessel rheological properties and in the studies of blood flow and certain arterial diseases. Most existing arterial models treat only wave motions; however, other types of motion, in particular those associated with flow development and other end effects, occur in the vascular system. Thus, a model is needed which can be applied to a variety of possible types of motion.

An arterial model is described which includes the effects of thick walls, linear viscoelasticity, and wall tethering. The forms of the displacements and stresses are found independently of the exact form of the applied fluid stresses; thus, the results are applicable to a range of possible dynamical conditions. Displacements and stress states can then be found from experimental or theoretical knowledge of the blood pressure and flow. The results are applied to flow development and wave propagation regions in the arteries.     

Mechanics of blood flow

The historical development of the mechanics of blood flow can be traced from ancient times, to Leonardo da Vinci and Leonhard Euler and up to the present times with increasing biological knowledge and mathematical analysis. In the last two decades, quantitative and numerical methods have steadily given more complete and precise understanding. In the arterial system wave propagation computations based on nonlinear one-dimensional modeling have given the best representation of pulse wave propagation. In the veins, the theory of unsteady flow in collapsible tubes has recently been extensively developed. In the last decade, progress has been made in describing the blood flow at junctions, through stenoses, in bends and in capillary blood vessels. The rheological behavior of individual red blood cells has been explored. A working model consists of an elastic membrane filled with viscous fluid. This model forms a basis for understanding the viscous and viscoelastic behavior of blood.     

Why is the subendocardium more vulnerable to ischemia? A new paradigm

Myocardial ischemia is transmurally heterogeneous where the subendocardium is at higher risk. Stenosis induces reduced perfusion pressure, blood flow redistribution away from the subendocardium, and consequent subendocardial vulnerability. We propose that the flow redistribution stems from the higher compliance of the subendocardial vasculature. This new paradigm was tested using network flow simulation based on measured coronary anatomy, vessel flow and mechanics, and myocardium-vessel interactions. Flow redistribution was quantified by the relative change in the subendocardial-to-subepicardial perfusion ratio under a 60-mmHg perfusion pressure reduction. Myocardial contraction was found to induce the following: 1) more compressive loading and subsequent lower transvascular pressure in deeper vessels, 2) consequent higher compliance of the subendocardial vasculature, and 3) substantial flow redistribution, i.e., a 20% drop in the subendocardial-to-subepicardial flow ratio under the prescribed reduction in perfusion pressure. This flow redistribution was found to occur primarily because the vessel compliance is nonlinear (pressure dependent). The observed thinner subendocardial vessel walls were predicted to induce a higher compliance of the subendocardial vasculature and greater flow redistribution. Subendocardial perfusion was predicted to improve with a reduction of either heart rate or left ventricular pressure under low perfusion pressure. In conclusion, subendocardial vulnerability to a acute reduction in perfusion pressure stems primarily from differences in vascular compliance induced by transmural differences in both extravascular loading and vessel wall thickness. Subendocardial ischemia can be improved by a reduction of heart rate and left ventricular pressure.     

Pulse wave propagation in a model human arterial network: Assessment of 1-D visco-elastic simulations against in vitro measurements

The accuracy of the nonlinear one-dimensional (1-D) equations of pressure and flow wave propagation in Voigt-type visco-elastic arteries was tested against measurements in a well-defined experimental 1:1 replica of the 37 largest conduit arteries in the human systemic circulation. The parameters required by the numerical algorithm were directly measured in the in vitro setup and no data fitting was involved. The inclusion of wall visco-elasticity in the numerical model reduced the underdamped high-frequency oscillations obtained using a purely elastic tube law, especially in peripheral vessels, which was previously reported in this paper [Matthys et al., 2007. Pulse wave propagation in a model human arterial network: Assessment of 1-D numerical simulations against in vitro measurements. J. Biomech. 40, 3476-3486]. In comparison to the purely elastic model, visco-elasticity significantly reduced the average relative root-mean-square errors between numerical and experimental waveforms over the 70 locations measured in the in vitro model: from 3.0% to 2.5% (p<0.012) for pressure and from 15.7% to 10.8% (p<0.002) for the flow rate. In the frequency domain, average relative errors between numerical and experimental amplitudes from the 5th to the 20th harmonic decreased from 0.7% to 0.5% (p<0.107) for pressure and from 7.0% to 3.3% (p<10(-6)) for the flow rate. These results provide additional support for the use of 1-D reduced modelling to accurately simulate clinically relevant problems at a reasonable computational cost.     

Linear propagation of pulsatile waves in viscoelastic tubes

An experimental and theoretical analysis is made of pulsatile wave propagation in deformable latex tubes as a model of the propagation of pressure pulses in arteries. A quasi one-dimensional linear model is used in which, in particular, attention is paid to the viscous phenomena in fluid and tube wall. The agreement between experimental and theoretical results is satisfactory. It appeared that the viscoelastic behaviour of the tube wall dominates the damping of the pressure pulse. Several linear models are used to describe the wall behaviour. No significant differences between the results of these models were found.     

One-dimensional model for propagation of a pressure wave in a model of the human arterial network: comparison of theoretical and experimental results

Pulse wave evaluation is an effective method for arteriosclerosis screening. In a previous study, we verified that pulse waveforms change markedly due to arterial stiffness. However, a pulse wave consists of two components, the incident wave and multireflected waves. Clarification of the complicated propagation of these waves is necessary to gain an understanding of the nature of pulse waves in vivo. In this study, we built a one-dimensional theoretical model of a pressure wave propagating in a flexible tube. To evaluate the applicability of the model, we compared theoretical estimations with measured data obtained from basic tube models and a simple arterial model. We constructed different viscoelastic tube set-ups: two straight tubes; one tube connected to two tubes of different elasticity; a single bifurcation tube; and a simple arterial network with four bifurcations. Soft polyurethane tubes were used and the configuration was based on a realistic human arterial network. The tensile modulus of the material was similar to the elasticity of arteries. A pulsatile flow with ejection time 0.3 s was applied using a controlled pump. Inner pressure waves and flow velocity were then measured using a pressure sensor and an ultrasonic diagnostic system. We formulated a 1D model derived from the Navier-Stokes equations and a continuity equation to characterize pressure propagation in flexible tubes. The theoretical model includes nonlinearity and attenuation terms due to the tube wall, and flow viscosity derived from a steady Hagen-Poiseuille profile. Under the same configuration as for experiments, the governing equations were computed using the MacCormack scheme. The theoretical pressure waves for each case showed a good fit to the experimental waves. The square sum of residuals (difference between theoretical and experimental wave-forms) for each case was <10.0%. A possible explanation for the increase in the square sum of residuals is the approximation error for flow viscosity. However, the comparatively small values prove the validity of the approach and indicate the usefulness of the model for understanding pressure propagation in the human arterial network.     

Wall stress and flow dynamics in abdominal aortic aneurysms: finite element analysis vs. fluid–structure interaction

Abdominal aortic aneurysm (AAA) rupture is the clinical manifestation of an induced force exceeding the resistance provided by the strength of the arterial wall. This force is most frequently assumed to be the product of a uniform luminal pressure acting along the diseased wall. However fluid dynamics is a known contributor to the pathogenesis of AAAs, and the dynamic interaction of blood flow and the arterial wall represents the in vivo environment at the macro-scale. The primary objective of this investigation is to assess the significance of assuming an arbitrary estimated peak fluid pressure inside the aneurysm sac for the evaluation of AAA wall mechanics, as compared with the non-uniform pressure resulting from a coupled fluid–structure interaction (FSI) analysis. In addition, a finite element approach is utilised to estimate the effects of asymmetry and wall thickness on the wall stress and fluid dynamics of ten idealised AAA models and one non-aneurysmal control. Five degrees of asymmetry with uniform and variable wall thickness are used. Each was modelled under a static pressure-deformation analysis, as well as a transient FSI. The results show that the inclusion of fluid flow yields a maximum AAA wall stress up to 20% higher compared to that obtained with a static wall stress analysis with an assumed peak luminal pressure of 117 mmHg. The variable wall models have a maximum wall stress nearly four times that of a uniform wall thickness, and also increasing with asymmetry in both instances. The inclusion of an axial stretch and external pressure to the computational domain decreases the wall stress by 17%.     

A multiscale approach for modelling wave propagation in an arterial segment

A mathematical model of blood flow through an arterial vessel is presented and the wave propagation in it is studied numerically. Based on the assumption of long wavelength and small amplitude of the pressure waves, a quasi-one-dimensional (1D) differential model is adopted. It describes the non-linear fluid-wall interaction and includes wall deformation in both radial and axial directions. The 1D model is coupled with a six compartment lumped parameter model, which accounts for the global circulatory features and provides boundary conditions. The differential equations are first linearized to investigate the nature of the propagation phenomena. The full non-linear equations are then approximated with a numerical finite difference method on a staggered grid. Some numerical simulations show the characteristics of the wave propagation. The dependence of the flow, of the wall deformation and of the wave velocity on the elasticity parameter has been highlighted. The importance of the axial deformation is evidenced by its variation in correspondence of the pressure peaks. The wave disturbances consequent to a local stiffening of the vessel and to a compliance jump due to prosthetic implantations are finally studied.     

Interaction of peristaltic flow with pulsatile flow in a circular cylindrical tube

The effect of pulsatile flow on peristaltic transport in a circular cylindrical tube is analysed. The flow of a Newtonian viscous incompressible fluid in a flexible circular cylindrical tube on which an axisymmetric travelling sinusoidal wave is imposed, is considered. The initial flow in the tube is induced by an arbitrary periodic pressure gradient. A perturbation solution with amplitude ratio (wave amplitude/tube radius) as a parameter is obtained when the frequency of the travelling wave and that of the imposed pressure gradient are equal. The interaction effects of periodic wall induced flow and periodic pressure imposed flow are visualized through the presence of substantially different components of steady and higher harmonic oscillating flow in the first order flow solution. Numerical results show a strong variation of steady state velocity profiles with boundary wave number and Reynolds number and a strong phase shift behaviour of the flow in the radial direction.     

Wall stress and flow dynamics in abdominal aortic aneurysms: finite element analysis vs. fluid-structure interaction

Abdominal aortic aneurysm (AAA) rupture is the clinical manifestation of an induced force exceeding the resistance provided by the strength of the arterial wall. This force is most frequently assumed to be the product of a uniform luminal pressure acting along the diseased wall. However fluid dynamics is a known contributor to the pathogenesis of AAAs, and the dynamic interaction of blood flow and the arterial wall represents the in vivo environment at the macro-scale. The primary objective of this investigation is to assess the significance of assuming an arbitrary estimated peak fluid pressure inside the aneurysm sac for the evaluation of AAA wall mechanics, as compared with the non-uniform pressure resulting from a coupled fluid-structure interaction (FSI) analysis. In addition, a finite element approach is utilised to estimate the effects of asymmetry and wall thickness on the wall stress and fluid dynamics of ten idealised AAA models and one non-aneurysmal control. Five degrees of asymmetry with uniform and variable wall thickness are used. Each was modelled under a static pressure-deformation analysis, as well as a transient FSI. The results show that the inclusion of fluid flow yields a maximum AAA wall stress up to 20% higher compared to that obtained with a static wall stress analysis with an assumed peak luminal pressure of 117 mmHg. The variable wall models have a maximum wall stress nearly four times that of a uniform wall thickness, and also increasing with asymmetry in both instances. The inclusion of an axial stretch and external pressure to the computational domain decreases the wall stress by 17%.     

Pulse wave velocity as a diagnostic index: the pitfalls of tethering versus stiffening of the arterial wall

Pulse wave velocity (PWV) is often used as a clinical index of aging, vascular disease, or age related hypertension. This practice is based on the assumption that a higher wave speed indicates vascular stiffening. This assumption is well grounded in the physics of pulsatile flow of an incompressible fluid where it is fully established that a pulse wave travels faster in a tube of stiffer wall, the wave speed becoming infinite in the mathematical limit of a rigid wall. However, in this paper we point out that the physical principal of higher pulse wave velocity in a stiffer tube is strictly valid only when the wall is free from outside constraints, which in the physiological setting is present in the form of tethering of the vessel wall. The use of PWV as an index of arterial stiffening may thus lose its validity if tethering is involved. A solution of the problem of vessel wall mechanics as they arise from the physiological pulsatile flow problem is presented for the purpose of resolving this issue. The vessel wall is considered to have finite thickness with or without tethering and with a range of mechanical properties ranging from viscoelastic to stiff. The results show that, indeed, while the wave speed becomes infinite in the mathematical limit of a rigid free wall, the opposite actually happens if the vessel wall is tethered. Here the wave speed actually diminishes as the degree of tethering increases. This dichotomy in the effects of tethering versus stiffening of the arterial wall may clearly lead to error in the interpretation of PWV as an index of vessel wall stiffness. In particular, a normal value of PWV may lead to the conclusion that vessel wall stiffening is absent while this value may in fact have been lowered by tethering. In other words, the diagnostic test may lead to a false negative diagnosis. Our results indicate that the reason for which PWV is lower in a tethered wall compared with that in a free wall of the same stiffness is that the radial movements of the wall are greatly reduced by tethering. More precisely, the results show that PWV depends strongly on the ratio of radial to axial displacements and that this ratio is much lower in a tethered wall than it is in a free wall of the same stiffness.