Elastic Arterial Wall Research Articles

Non-Newtonian pulsatile blood flow through the stenosed arteries: comparison between the viscoelastic and elastic arterial wall in response to the alterations

:In this study, we investigate the impact of aortic stenosis on the hemodynamics of pulsatile blood flow within a 3D aortic model. Employing a non-Newtonian Casson model with a hematocrit of 45%, our study introduces a preliminary hypothesis to simulate blood flow dynamics, incorporating both linear elastic and viscoelastic models to define the mechanical characteristics of the artery. Through simulations conducted with Ansys-Cfx (version 15), we utilize a 2-way fluid-structure interaction (FSI) approach, employing a Lagrangian-Eulerian formulation with second-order accuracy. We explore the influence of stenosis severity on variables including velocity profiles, pressure distribution, shear stress, wall displacement, and changes in the OSI parameter. Our investigation encompasses arteries with both elastic and viscoelastic walls. The key findings that arise from our results highlight the viscoelastic model’s demonstration of reduced radial wall displacement when compared to the linear elastic model. Additionally, we observe that elevated arterial stenosis percentages lead to the elongation of vortex length, heightened wall shear stress, and increased slope of velocity profiles downstream of the stenosed region. Furthermore, bulky obstruction of viscoelastic arteries as opposed to elastic, resulted in a maximum 5 percent increase in velocity profile and a 29.6% decrease in radial displacement. The zenith of shear stress occurs concomitantly with the velocity’s peak within the stenosed area. Viscoelastic arterial wall shear stress at the stenosis site escalates due to the rapid expansion of the stenosis. The viscoelastic wall, responding with a blend of viscous and elastic characteristics to applied stress, undergoes slight deformation in shape. Following stress reduction, the wall gradually reverts to its original form, thus alleviating some of the applied stress. In contrast, the elastic wall retains its altered shape due to stress preservation within the material. Additionally, we ascertain an augmentation in radial displacement corresponding with increased artery stenosis.

Influence of Rigid-Elastic Artery Wall of Carotid and Coronary Stenosis on Hemodynamics.

Cardiovascular system abnormalities can result in serious health complications. By using the fluid-structure interaction (FSI) procedure, a comprehensive realistic approach can be employed to accurately investigate blood flow coupled with arterial wall response. The hemodynamics was investigated in both the coronary and carotid arteries based on the arterial wall response. The hemodynamics was estimated based on the numerical simulation of a comprehensive three-dimensional non-Newtonian blood flow model in elastic and rigid arteries. For stenotic right coronary artery (RCA), it was found that the maximum value of wall shear stress (WSS) for the FSI case is higher than the rigid wall. On the other hand, for the stenotic carotid artery (CA), it was found that the maximum value of WSS for the FSI case is lower than the rigid wall. Moreover, at the peak systole of the cardiac cycle (0.38 s), the maximum percentage of arterial wall deformation was found to be 1.9%. On the other hand, for the stenotic carotid artery, the maximum percentage of arterial wall deformation was found to be 0.46%. A comparison between FSI results and those obtained by rigid wall arteries is carried out. Findings indicate slight differences in results for large-diameter arteries such as the carotid artery. Accordingly, the rigid wall assumption is plausible in flow modeling for relatively large diameters such as the carotid artery. Additionally, the FSI approach is essential in flow modeling in small diameters.

Morphologic and Morphometric Evaluation of the Carotid Artery Wall: A Cadaver-Based Light and Scanning Electron Microscopic Study

Introduction: A variety of changes occur on the elastic artery wall with age. Ultrastructural studies made in this area are mostly animal based. We aimed to evaluate wall changes and three-dimensional organization of the elastic lamellae with aging in humans. Material and Methods: Common carotid arteries were obtained from 17 human cadavers which were grouped as G1 (n = 6), 30–39 years; G2 (n = 5), 40–49 years; and G3 (n = 6), >50 years of age. Samples were evaluated under light and scanning electron microscopes. Results: Examination of G1 revealed intimal thickening and foamy cell infiltration. G2 and G3 had plaques bulging into the lumen and interlamellar space was widened. The lamellae were more straight. There was a positive correlation between intimal thickness and age. Elastic fiber content decreased with aging. Scanning electron microscopic analysis confirmed the findings. G1 and G2 had a smooth surfaced internal elastic lamina with uniform fenestrations whereas G3 contained numerous irregular fenestrae. Discussion and Conclusion: With this study, we showed some other wall structure changes beside plaque formation by aging. Which layer is affected the most was not clear at previous clinical studies because using ultrasonography (USG) cannot address the layer. Microscopic evaluation of this study revealed that when a wall thickening is detected by USG, it is due to intimal thickening. The specific vessel layer structural changes are important for proper treatment.

Influence of cross-sectional velocity profile on flow characteristics of arterial wall modeled as elastic and viscoelastic material.

In the present work, blood flow behavior in a single artery and in arterial network is studied using time domain based one-dimensional wave propagation model retaining the nonlinear convective force. 1-D Navier-Stokes equation is used to model the flow behavior of the blood, using three unknown parameters: flow rate (q), cross-sectional area of artery (A) and pressure (p) based formulation. Three different approximate velocity profile functions across the cross-section namely modified flat, parabolic and the one proposed by Bessems are used to calculate the nonlinear convective force and the frictional force. Two different constitutive models, linear elastic model and standard linear solid model (Zener model) are used to model the arterial wall mechanical behavior. The system of partial differential equations is discretized using finite element and Crank Nicolson methods in space and time domains, respectively. Based on the formulation, an in house finite element code is developed to simulate flow behavior in both a single artery as well as in arterial network consisting of 20 small and large size arteries. Simulations are performed by enforcing a flow rate at the inlet and Windkessel model at the outlet. The results for elastic arterial wall model are found to be in good agreement with the results available in the literature. The flow rate/pressure predictions using different velocity profile functions are found to be nearly the same, however the Bessems velocity profile predicts more closer to 3D results compared to modified flat and parabolic profiles. Whereas, significant difference is found in the results predicted using elastic and viscoelastic artery wall models.

Effect of stenosis and dilatation on the hemodynamic parameters associated with left coronary artery

Background and Objective: The main objective of the work is to examine the curvature effects of stenosis/dilatation region pertaining to left coronary artery. The hemodymamic features during the cardiac cycle is thoroughly examined.Methods: A numerical fluid structure interaction model incorporating multi- layered elastic artery wall, non-Newtonian blood viscosity and pulsating boundary conditions is developed. The composite arterial wall consists of a thin layer tunica intima, atheroma and a thick wall. Higher stiffness of atheroma is captured by using higher Young’s modulus. The CFD and FSI models are validated with available experimental and analytical data. Computations are done with five different non-Newtonian models and arterial wall with various elasticity levels. The local and time averaged WSS, velocity contours downstream of stenosis, wall pressure and pressure drop during various phases of cardiac cycle are provided in detail.Results: The influence of non-Newtonian effects of blood viscosity is found to be significant especially at stenosis regions. The flexible wall caused wall deformation and the associated flow and pressure wave propagation affecting WSS and pressure drop compared to the rigid wall. Flow recirculation is noticed at stenosis downstream locations and its strength increases with increased severity of the stenosis. A stenosis is characterised by a sudden drop in wall pressure and a slower two stage recovery during peak velocity periods of the cardiac cycle.Conclusions: The pressure drop, local WSS at stenosis centre, and radial velocity increase are significantly higher for stenosis cases and the effect is severe during peak diastole. The variation in hemodynamic parameters is found to be less significant for dilatation. Significantly lower WSS is noticed for the recirculation regions downstream of stenosis which can enhance the tendency for monocytes to attach to the endothelium. The radius of curvature of the stenosis is found to be the most sensitive parameter affecting the hemodynamic characteristics rather than the detailed geometry of the stenosis. The main effect of variation of artery wall stiffness is noted at recirculation regions present downstream of stenosis. The results from the study may be useful for predicting wall shear stress signatures associated with stenosis/dilatation changes and the management of specific cases.

Numerical Studies of Blood Flow in Left Coronary Model

Introduction: Artery blockage is the most prevailing cause of Coronary Artery Disease (CAD). The presence of blockage inside the artery breaks the continuity of blood supply to the other part of the body and therefore causes for heart attack. Objective: Two different three-dimensional models namely; normal and 50% plaque are used for the numerical studies. Five inlet velocities 0.10, 0.20, 0.50, 0.70 and 0.80 m/s are considered corresponding to different blood flow conditions to study the effect of velocity on the human heart. Methods: Finite Volume Method (FVM) based Computational Fluid Dynamics (CFD) technique is executed for the numerical simulation of blood flow. Hemodynamic factors are computed and compared for the two geometrical models (Normal Vs. Blockage model). Results: Blood hemodynamic factor i.e. Area Average Wall Shear Stress (AAWSS) ranges from 4.1-33.6 Pa at the façade of the Left Anterior Descending (LAD) part of the Left Coronary Artery (LCA) for the constricted artery. Conclusion: The predominantly low WSS index is analogous to the normal artery affirms the existence of plaque. From the medical point of view, this can prove as an excellent factor for early diagnosis of CAD. Therefore, a hindrance can be created in the increasing frequency of Myocardial Infarction (MI). In future research we will adopt the unsteady flow with both rigid and elastic arterial wall.

Comment on "Radial and longitudinal motion of the arterial wall: Their relation to pulsatile pressure and flow in the artery".

Most researchers derived the arterial pressure-wave equation by taking the axial blood flow as the major mechanism and assumed the flow motion was governed by the Navier-Stokes equation. However, only realistic hemodynamic theory can help to develop method for future healthcare. Here, we pointed out a different rigorous hemodynamic model that explained many physiological facts. Our previous work started directly from Newton's law by deriving the radial and the axial momentum equations of the elastic arterial wall system and of the enclosed blood system, with the contact forces between the two systems being counted explicitly. Our model has some important applications in future healthcare, such as providing a basis for studying the collective behavior of the cardiovascular system and developing quantitative methods for disease prevention and diagnosis.

OP.1C.04] STRUCTURAL AND FUNCTIONAL ARTERIAL ABNORMALITIES IN FIBROMUSCULAR DYSPLASIA ARE IN THE CONTINUUM OF HYPERTENSION

Objective: Fibromuscular dysplasia (FMD) is a non-atherosclerotic non-inflammatory arterial disease, which occurs mostly in middle-aged women and affects medium-sized arteries. We previously showed abnormalities within common carotid artery (CCA) wall, with the presence of triple signal (TS) at ultrasound suggesting the presence of supplementary layers. We aimed at coupling TS presence with microconstituents of the vessel wall, derived from fitting of the pressure-diameter curve. Design and method: We included 50 non-smoking patients with multifocal FMD, 50 essential hypertensive (EH) patients and 50 healthy subjects (HS) matched for age, sex, ethnicity and BP (EH and FD). TS score from the right and left CCA ranging from 2 (normal) to 14 (most advanced) were assessed from 15-MHz echotracking system coupled with aplanation tonometry. Microconstituents of the CCA were derived from inverse-problem resolution using non-linear least-squares method. The strain-energy function included 14 parameters representing geometry (opening-angle, reference radius, in vivo axial stretch), perivascular tethering, and wall material coefficients (elastic modulus, fiber orientation). Results: FMD, EH and HS were well matched. TS was significantly and positively associated with age, hypercholesterolemia, aortic stiffness and carotid intima media thickness (IMT). In multivariate analysis, age, hypercholesterolemia and IMT were significantly associated with TS, explaining 9.5% of its variance. TS was more frequent in FMD than HS (49% vs 16%, p Conclusions: We confirmed that FMD is associated with higher frequency of TS, but with overlap with matched EH and HS. The strong association between TS and carotid remodeling, independently of age and BP, suggests that it corresponds to the muscular transition of an elastic artery wall in parallel with the hypertrophic process (Sarkola T et al. Atherosclerosis 2010). The association of TS with circular collagen stiffness suggests that TS has subtle but measurable mechanical consequences.

ATHEROMATOSIS OF ARTERIAL INTIMA AS A RESULT OF THE BIOLOGICAL FUNCTION OF ENDOECOLOGY, BIOLOGICAL REACTION OF INFLAMMATION AND UTILIZATION OF NON-LIGAND PALMITIC VERY LOW DENSITY-LOW DENSITY LIPOPROTEINS

Phylogenetically late intima of elastic arteries has no proteins for transportation of non-ligand oxidized low density lipoproteins (LDL) adsorbed on the matrix to resident macrophages. Phylogenetically early cells realize the reaction of extracellular digestion by secreting the proteolytic enzymes metalloproteases in the matrix. They hydrolyze matrix proteoglycans, adsorbed and non-ligand LDL, absorb detritis, and terminate hydrolysis of the most hydrophobic polyenic cholesterol esters (poly-CE) in lysosomes. Smooth muscle cells migrate from arterial media, change their phenotype from contractile to synthetic and produce in situ de novo matrix proteoglycans. Elastic arterial wall consists of three layers: a) endothelial monolayer, b) intima + media (smooth muscle cells) and b) adventitia. It seems reasonable to define functional differences between phylogenetically early resident macrophages and phylogenetically late monocytes-macrophages. They may be associated with scavenger receptors, CD36 translocase activity, production of acid hydrolases for poly-CE or realization of the biological reaction of extracellular digestion. We suppose that atheromatous masses are formed in the matrix of arterial intima but not in lysosomes when the ability of monocytes-macrophages to provide endocytosis of non-ligand LDL from the matrix is limited. If atheromatosis is a syndrome caused by intracellular deficiency of essential polyenic fatty acids (PFA), intimal atheromatosis is associated with partial utilization of excess PFA in the matrix of elastic arteria. At late stages of phylogenesis the intima formed from smooth muscle cells of the media.

A maximum dissipation thermodynamic multi-scale model for the dynamic response of the arterial elastin–water system

The mechanical response of the elastin–water system in an artery wall is viscoelastic. Elastin in vivo must operate in the rubbery region, i.e., above the glass transition, that depends on moisture content. A dynamic multi-scale time-dependent evolution equation is presented for the mechanical response of the elastin–water system that captures the effect of moisture content on the glass transition of the elastin. To define non-equilibrium evolution processes, the construction requires only a hyperelastic strain energy density function describing the long-term behavior and the thermodynamic relaxation modulus that describes the relaxation speed of non-equilibrium processes. The thermodynamic relaxation modulus also relates spatial scales, the molecular scale including moisture bonding to the bulk material scale. The model reproduces published experimental data on the elastin glass transition behavior with respect to load frequency and to ambient relative humidity but is not merely empirical in the sense of being a fit to such data because it predicts dynamic responses such as non-physiological creep and physiological rate-dependent stress–stretch relations. The new viscoelastic model predicts the influence of moisture content and the glass transition of the elastin on the time-dependent response of the circumferential stretch and the change in radius of a hydrated arterial cylindrical elastin lamella under cyclic radial pressure loads in the hemodynamic range. Such an elastin cylinder approximates the behavior of the elastin substructure in an elastic artery wall.

Elastic artery wall in hyper-tensive patients with different patterns of left ventricle remodeling

Elastic artery wall in hyper-tensive patients with different patterns of left ventricle remodeling

Treatment of lower extremity vascular disease: the Diamondback 360°™ Orbital Atherectomy System

Atherosclerotic disease affecting the arteries of the lower extremities becomes symptomatic with the onset of pain either at rest or with ambulation. The disease, commonly referred to as peripheral arterial disease (PAD), affects nearly 30 million individuals in Europe and North America alone. The predominant factor responsible for the impaired functional capacity and quality of life in the presence of lower-extremity PAD is inadequate blood flow due to atherosclerotic plaque build-up within the arteries. Without successful lifestyle risk modifications or judicious pharmacotherapy, individuals with lower-extremity PAD may develop disabling complications that require endovascular treatment, bypass surgery or amputation of the affected extremity. The Diamondback 360°™ Orbital Atherectomy System is a promising new methodology for treating symptomatic PAD within the major and branch arteries of the leg. The device differs from other atherectomy technologies by its unique orbiting action to remove plaque and the ability to increase lumen diameter by increasing the orbital speed. Applying the principles of centrifugal force, an eccentrically mounted diamond-coated crown rotates at high speed to sand away plaque as the crown is slowly advanced through the narrowed or occluded section of artery. As crown rotation increases, centrifugal force presses the crown against the stenotic lesion to effect plaque removal, while the less diseased, more elastic arterial wall flexes away from the crown, minimizing the risk of vessel trauma. The increasing crown orbit creates a larger lumen and minimizes procedure time and the need for catheter upsizing. This device profile presents an overview of the prevalence and symptoms of PAD, describes the Diamondback 360 Orbital Atherectomy System components and mechanism of action, and closes with a case study review and perspective regarding how lower-extremity PAD will be treated in the next 5 years.

A viscoelastic model of arterial wall motion in pulsatile flow: implications for Doppler ultrasound clutter assessment

The existing computational model studies of pulsatile blood flow in arteries have assumed either rigid wall characteristics or elastic arterial wall behavior with wall movement limited to the radial direction. Recent in vivo studies have identified significant viscoelastic wall properties and longitudinal wall displacements over the cardiac cycle. Determining the nature of these movements is important for predicting the effects of ultrasound clutter in Doppler ultrasound measurements. It is also important for developing an improved understanding of the physiology of vessel wall motion. We present an analytically-based computational model based on the Womersley equations for pulsatile blood flow within elastic and viscoelastic arteries. By comparison with published in vivo data of the human common carotid artery as well as uncertainty and sensitivity analyses, it is found that the predicted waveforms are in reasonable quantitative agreement. Either a pressure, pressure gradient or volumetric flow rate waveform over a single cardiac cycle is used as an input. Outputs include the pressure, pressure gradient, radial and longitudinal fluid velocities and arterial wall displacements, volumetric flow rate and average longitudinal velocity. It is concluded that longitudinal wall displacements comparable to the radial displacements can be present and should be considered when studying the effects of tissue movement on Doppler ultrasound clutter.

Ambulatory arterial stiffness index (AASI) does not predict baroreflex sensitivity or the pressor response to mental stress in normotensive humans

Ambulatory arterial stiffness index (AASI) is a novel measure of arterial stiffness, which independently predicts cardiovascular mortality, even in nomortensive subjects. Baroreflex sensitivity (BRS) is integral to BP regulation, and varies among healthy persons. Baroreceptors sense arterial pressure indirectly from the degree of stretch of the elastic arterial walls. A reduced ability of baroreflex buffering in elderly, hypertensives, and patients with carotid denervation results in an elevated pressor response to mental stress (MS). We hypothesized that there might be a correlation between BRS and AASI in healthy subjects, and individuals with higher BRS would have a lower pressor response to MS. We measured 24-hour ambulatory BP, BRS (modified Oxford), HR, and intra-arterial pressure (AP) during MS in 53 healthy, normotensive, non-obese individuals (32 women, 21 men, mean age ± SE: 28 ± 1). AASI was defined as 1 minus the regression slope plotted from diastolic over systolic BP using all of the ambulatory BP readings. Although all measures were widely variable among subjects, there was no relationship between AASI, BRS, or pressor response to MS. We conclude that in the absence of aging, cardiovascular, or autonomic disease, the novel stiffness index (AASI) and baroreflex control of heart rate are unable to account for the complex pressor response to MS. Support: K23 RR17520, HL 46493, DFG grant He 4605/1-1.

Coupled vibration analysis of large arterial vessels

A coupled vibration model, which takes into account the elastic arterial wall, the interior blood, and exterior tissue, is presented. The arterial wall is considered as a cylindrical elastic shell and is modeled with the thick shell theory due to the large thickness-to-radius ratios. Both the blood and the tissue are considered as ideal fluids and are modeled with acoustic wave theory. A newly developed method, the wave propagation approach, is extended for the coupled vibration of arterial walls. The theoretic model is evaluated against those available in the literature. The experiments were carried out on a silicone rubber tube in a water tank with an ultrasound stimulated system. This system uses the radiation force of ultrasound to vibrate the tube at low frequency and records the resulting response by a laser vibrometer. Both the excitation and measurement are remote and noncontact. The measured fundamental frequency is in good agreement with the theoretical prediction.

The Effect of Wall Distensibility on Flow in a Two-Dimensional End-to-Side Anastomosis

The development of intimal hyperplasia at the distal anastomosis is the major cause of long-term bypass graft failure. To evaluate the suspected role of hemodynamic factors in the pathogenesis of distal intimal hyperplasia, an understanding of anastomotic flow patterns is essential. Due to the complexity of arterial flow, model studies typically make simplifying assumptions, such as treating the artery and graft walls as rigid. In the present study this restriction is relaxed to consider the effects of vessel wall distensibility on anastomotic flow patterns. Flow was simulated in an idealized 2-D distensible end-to-side anastomosis model, using parameters appropriate for the distal circulation and assuming a purely elastic artery wall. A novel numerical approach was developed in which the wall velocities are solved simultaneously with the fluid and pressure fields, while the wall displacements are treated via an iterative update. Both the rigid and distensible cases indicated the presence of elevated temporal variations and low average magnitudes of wall shear stress at sites known to be susceptible to the development of intimal hyperplasia. At these same sites, large spatial gradients of wall shear stress were also noted. Comparison between distensible-walled and corresponding rigid-walled simulations showed moderate changes in wall shear stress at isolated locations, primarily the bed, toe and heel. For example, in the case of a distensible geometry and a physiologic pressure waveform, the heel experienced a 38 percent increase in cycle-averaged shear stress, with a corresponding 15 percent reduction in shear stress variability, both relative to the corresponding values in the rigid-walled case.(ABSTRACT TRUNCATED AT 250 WORDS)

Anatomic barriers influence the distribution of in vivo gene transfer into the arterial wall. Modeling with microscopic tracer particles and verification with a recombinant adenoviral vector.

We evaluated the extent to which anatomic barriers to vector penetration might influence the distribution of successful in vivo gene transfer into the normal arterial wall. A double-balloon catheter technique with infusion pressures of 100 to 400 mm Hg was used to infuse microscopic tracer particles of the size range of liposomes and viral vectors into normal elastic arteries of sheep. Localization of the tracer particles in tissue sections by light, fluorescence, and electron microscopy suggested that vector-sized particles were delivered to the intima by direct infusion and to the adventitia via the arterial vasa vasorum. Particles were virtually absent from the arterial media. To test the predictions made from the particle studies, we repeated the infusion protocol with high-titer adenoviral vectors. Gene transfer occurred at high levels in the intima and along the adventitial vasa vasorum but again was virtually absent within the media. The ability of medial smooth muscle cells to be transduced was established in separate experiments with a high-pressure (5 atm) porous balloon infusion catheter. We conclude that (1) the anatomy of the normal elastic arterial wall imposes significant limitations on the penetration of particles in the size range of most gene-transfer vectors and (2) the distribution of in vivo gene transfer with adenoviral vectors is correctly predicted by the distribution of inert tracer particles. These findings have important implications for the design of arterial gene-transfer and gene-therapy protocols.

Numerical analysis of intramural stresses and blood flow in arterial bifurcation models

The study deals with the calculation of the stresses in elastic arterial walls and with the analysis of the interaction of local blood flow and vessel wall motion. While the stress study is primarily carried out in a basic end-to-side bypass anastomosis model incorporating different material properties of the graft and the artery, the flow study is performed in a compliant carotid artery bifurcation model. The displacement and stress analysis uses geometrically non-linear shell theory. The flow analysis applies the time-dependent, three-dimensional, incompressible, Navier-Stokes equations for non-Newtonian inelastic fluids In an iteratively coupled approach the equations of the fluid motion and the transient shell equations are numerically solved using the finite element method.

The importance of viscoelasticity in arterial blood flow models

The assumption of negligible viscoelastic response in arterial walls has been routinely made in the analysis of cardiovascular fluid dynamics, however, with incomplete justification. The present study was designed to explore this justification in depth. In a commonly used one-dimensional blood flow model, the viscoelastic properties of the thoracic aorta are mathematically modelled as an area pressure shift in the State Equation. From experimentally measured proximal pressure and velocity waveforms, distal waveforms are computed by the periodic method of characteristics for different levels of viscoelasticity and compared with those waveforms obtained from the same model having purely elastic arterial walls. The results indicate that viscoelasticities encountered physiologically do not discernibly affect the development of the pressure and velocity waveforms. Further, for stiffer vessel walls, the viscous wall component is even less important. It is concluded that for most practical purposes in single large artery models, the arterial walls may be considered to be purely elastic. The corresponding justification for multiple artery models or for smaller arteries has not been examined.