Viscoelasticity Of Arterial Wall Research Articles

Impact of disturbed flow and arterial stiffening on mechanotransduction in endothelial cells.

Disturbed flow promotes progression of atherosclerosis at particular regions of arteries where the recent studies show the arterial wall becomes stiffer. Objective of this study is to show how mechanotransduction in subcellular organelles of endothelial cells (ECs) will alter with changes in blood flow profiles applied on ECs surface and mechanical properties of arterial wall where ECs are attached to. We will examine the exposure of ECs to atherogenic flow profiles (disturbed flow) and non-atherogenic flow profiles (purely forward flow), while stiffness and viscoelasticity of arterial wall will change. A multicomponent model of endothelial cell monolayer was applied to quantify the response of subcellular organelles to the changes in their microenvironment. Our results show that arterial stiffening alters mechanotransduction in intra/inter-cellular organelles of ECs by slight increase in the transmitted stresses, particularly over central stress fibers (SFs). We also observed that degradation of glycocalyx and exposure to non-atherogenic flow profiles result in significantly higher stresses in subcellular organelles, while degradation of glycocalyx and exposure to atherogenic flow profiles result in dramatically lower stresses in the organelles. Moreover, we show that increasing the arterial wall viscoelasticity leads to slight increase in the stresses transmitted to subcellular organelles. FAs are particularly influenced with the changes in the arterial wall properties and viscoelasticity. Our study suggests that changes in viscoelasticity of arterial wall and degradation state of glycocalyx have to be considered along with arterial stiffening in designing more efficient treatment strategies for atherosclerosis. Our study provides insight into significant role of mechanotransduction in the localization of atherosclerosis by quantifying the role of ECs mechanosensors and suggests that mechanotransduction may play a key role in design of more efficient and precision therapeutics to slow down or block the progression of atherosclerosis.

Internal pressure dependence on viscoelasticity of arterial wall by ultrasonic measurement

Previously, we proposed an ultrasonic measurement method of arterial wall elasticity for the early detection of arteriosclerosis. Since vascular wall elasticity depends on blood pressure, in this study, the elasticity and viscosity were estimated using the hysteresis loop determined between the incremental strain in the wall and internal pressure by altering the internal pressure in the phantom and in vivo experiments. Consequently, both the estimated elasticity and viscosity increased with the internal pressure. Moreover, the slope of each hysteresis loop was larger than that of the approximated curve for the lowest blood pressures of the hysteresis loops with different internal pressures, as the blood pressure changed in the order of several hertz within a single heartbeat. Hence, we conclude that measuring both the blood pressure and the elastic and viscous moduli would be beneficial in comprehensively investigating more vessel wall properties that change with the progression of arteriosclerosis.

Viscoelasticity inversion for arterial shear wave elastography

Arterial stiffness, an important biomarker of many cardiovascular diseases, is strongly influenced by the wall modulus. In shear wave elastography, the arterial wall is excited by acoustic radiation force, and the resulting wave propagation characteristics are used to infer arterial stiffness. In earlier ASA meeting, we presented a forward model that returns arterial wall motion for a given geometry, material properties of the waveguide, and input acoustic radiation force. In this work, we propose an inversion approach developed on this forward model to estimate arterial viscoelasticity, which is also considered an important biomarker. Recently, the phase-velocity dispersion is utilized to estimate the arterial wall elastic modulus. However, this approach fails to estimate the viscoelastic modulus since the dispersion curve is not strongly influenced by the arterial wall viscoelasticity. Conversely, the spatiotemporal representation of the wall velocity is sensitive to both moduli. Therefore, in the inverse model, we minimize the mismatch between the measured and simulated particle velocities to invert for the parameters of viscoelasticity, e.g., modulus and damping coefficient for the Voigt model, modulus, and exponent for the Spring-pot model. This talk would contain the details of the underlying formulations and numerical examples illustrating the effectiveness of the proposed approach.

3Pa5-10 Examination of change in arterial wall viscoelasticity by internal pressure in ultrasonic measurement

3Pa5-10 Examination of change in arterial wall viscoelasticity by internal pressure in ultrasonic measurement

波動で測る血管の粘弾性 ――超音波による血管壁・血液の性状評価――

波動で測る血管の粘弾性 ――超音波による血管壁・血液の性状評価――

Development and characterization of viscoelastic polydimethylsiloxane phantoms for simulating arterial wall motion

Arterial wall viscoelasticity is likely to be a good diagnostic indicator of vascular disease, but only a few studies on the assessment of wall viscosity have been performed. Artery phantoms are manufactured using polydimethylsiloxane (PDMS) to simulate the viscoelastic characteristics of the artery wall, which depends on the wall tissue composition and progression of atherosclerosis. The viscoelastic property of PDMS is controlled by adjusting the mixture ratio of resin, curing agent, and pure silicone oil. The pressure and diameter waveforms of the artery phantom were measured to estimate the wall viscoelasticity. Elasticity is assessed using the diameter distention over the pulse pressure, and the viscosity is evaluated using the energy dissipation ratio of the pressure-diameter curve and the phase lag between the first harmonics of pressure and diameter waveforms (DP1).PDMS phantoms with resin-to-curing-agent ratios of 20:1 and 25:1 show viscoelastic characteristics similar to those of young and old human carotid arteries, respectively. Adding pure silicone oil further softens the silicone elastomer while decreasing its viscosity. The phantoms with 10:1:5 and 10:1:8 mixture ratios (resin: curing agent: silicone oil) show elasticity similar to that of the 20:1:0 and 25:1:0 ratios, respectively, albeit with a noticeable decrease in viscosity. An abrupt decrease in the phase lag (DP1) was found near the interface of the arterial phantom with different mixture ratios (20:1:0 and 10:1:5), while the change in diameter distension was negligible. DP1 may be a new index to differentiate wall tissues with similar elastic properties but different viscous behavior. The pressure diameter curve and DP1 of the phantom simulating the atherosclerosis wall can be compared with patient data and applied to clinical evaluation of plaque viscoelasticity.Computational analysis of arterial wall motion was performed using a standard linear viscoelastic model. The model parameters were determined from the measured pressure-diameter relationship, and the arterial wall motions of phantoms with different viscoelastic properties were successfully simulated. The computational model may provide a useful insight into the changes of arterial viscoelasticity caused by pathogenic wall degeneration.

Three-Element Fractional-Order Viscoelastic Arterial Windkessel Model.

Arterial hemodynamic assessment has always been essential for clinical Cardiovascular System (CVS) diagnosis. Using Windkessel (WK) lumped parametric model as non-invasive measurement tool provides the potential of achieving a very convenient, computational inexpensive and accurate prediction of the arterial parameters. Many versions of WK models have been proposed and extensively studied, over the last century. In general, they can be classified into two categories: elastic and viscoelastic models. Recently, several studies have discussed the potential of describing the arterial wall viscoelasticity using fractional order models, reducing the number of parameters and exposing a natural response. Hence, a key missing item in the arterial Windkessel modeling is a fractional-order analog component that can provide a reliable, realistic and reduced representation of the fractional viscoelasticity behavior. In this paper, we present, for the first time, a three-element fractional-order viscoelastic Windkessel model. The proposed model incorporates a fractional-order capacitor that substitutes the ideal capacitor of standard three-elements WK model. The latter non-ideal element combines both resistive and capacitive properties which displays viscoelastic behavior of the arterial vessel. The contribution of both properties is controlled by the fractional differentiation order α enabling an accurate and reliable physiological description.

An effective fractal-tree closure model for simulating blood flow in large arterial networks.

The aim of the present work is to address the closure problem for hemodynamic simulations by developing a flexible and effective model that accurately distributes flow in the downstream vasculature and can stably provide a physiological pressure outflow boundary condition. To achieve this goal, we model blood flow in the sub-pixel vasculature by using a non-linear 1D model in self-similar networks of compliant arteries that mimic the structure and hierarchy of vessels in the meso-vascular regime (radii [Formula: see text]). We introduce a variable vessel length-to-radius ratio for small arteries and arterioles, while also addressing non-Newtonian blood rheology and arterial wall viscoelasticity effects in small arteries and arterioles. This methodology aims to overcome substantial cut-off radius sensitivities, typically arising in structured tree and linearized impedance models. The proposed model is not sensitive to outflow boundary conditions applied at the end points of the fractal network, and thus does not require calibration of resistance/capacitance parameters typically required for outflow conditions. The proposed model convergences to a periodic state in two cardiac cycles even when started from zero-flow initial conditions. The resulting fractal-trees typically consist of thousands to millions of arteries, posing the need for efficient parallel algorithms. To this end, we have scaled up a Discontinuous Galerkin solver that utilizes the MPI/OpenMP hybrid programming paradigm to thousands of computer cores, and can simulate blood flow in networks of millions of arterial segments at the rate of one cycle per 5min. The proposed model has been extensively tested on a large and complex cranial network with 50 parent, patient-specific arteries and 21 outlets to which fractal trees where attached, resulting to a network of up to 4,392,484 vessels in total, and a detailed network of the arm with 276 parent arteries and 103 outlets (a total of 702,188 vessels after attaching the fractal trees), returning physiological flow and pressure wave predictions without requiring any parameter estimation or calibration procedures. We present a novel methodology to overcome substantial cut-off radius sensitivities.

Correction of change in propagation time delay of pulse wave during flow-mediated dilation in ultrasonic measurement of arterial wall viscoelasticity

It is considered that the endothelial dysfunction occurs in the initial step of atherosclerosis. Although assessments of the endothelial function and viscoelastic properties of the intima-media region are important for the diagnosis of early-stage atherosclerosis, regional viscoelasticity has not yet been measured in vivo. Our group has developed an ultrasonic method for measuring the transient change in viscoelasticity during flow-mediated dilation (FMD). However, in this method, the stress (blood pressure) and strain of the intima-media region of the radial artery are measured in different arms, and the change in pulse wave velocity (PWV) due to FMD has not yet been considered. In the present study, we measured blood pressure waveforms using two pressure sensors, which were placed along the same radial artery for the ultrasonic measurement, to obtain blood pressure waveforms and estimate the PWV between the two sensors. Using the measured PWV, the pulse wave propagation time from the pressure sensor to the position of the ultrasound probe was corrected, and viscoelasticity was estimated from the corrected stress–strain relationship. In the basic experiment, we applied the proposed method to a silicone tube phantom and evaluated the accuracy of the estimation of viscoelasticity by comparing the ultrasonic measurement to the results of the tensile test. In the in vivo measurements, the change in the propagation time delay of the pulse wave was also corrected using the two pressure sensors and the stress–strain relationship of the radial arterial wall was then obtained to estimate viscoelasticity. Furthermore, a decrease in elasticity owing to FMD after recirculation was clearly observed, and the unstable temporal variation in viscosity was significantly reduced. These results demonstrated the improvement in the accuracy of the measurement of viscoelasticity by the proposed method.

Effect of viscoelasticity of arterial wall on pulse wave: a comparative study on ovine

Effect of viscoelasticity of arterial wall on pulse wave: a comparative study on ovine

血管粘弾性インデックスの変化を指標とした機械的侵害刺激に対する疼痛の定量的評価

血管粘弾性インデックスの変化を指標とした機械的侵害刺激に対する疼痛の定量的評価

Viscoelastic Characteristics of In Vitro Vital and Devitalized Rat Aorta and Human Arterial Prostheses

The arterial wall viscoelasticity plays an essential role in the vascular responsiveness to vasoactive drugs or pathologies. The aim of this investigation was to derive and compare resonance curve (RC), natural frequency (f(0)), dynamic modulus of elasticity (E'), and coefficient of viscosity (beta) of (i) vital and devitalized preparations of rat thoracic and abdominal aorta, (ii) human arterial prostheses, and to study the histomorphology of vital and devitalized rat aorta. The method of low frequency forced oscillations was employed. RC of vital preparations showed a hardening type of elasticity whereas in devitalized preparations it was of softening type. E' increased nonlinearly, f(0) decreased and beta increased linearly with equivalent intraluminal pressure (p(eqi)). Distensibility of abdominal aorta was lower than thoracic aorta. Distensibility decreased with increasing p(eqi). E', f(0), and beta increased significantly after devitalization. It was suggested that postmortem viscoelastic characteristics should not be used directly to specify the vital arteries viscoelasticity. RC of human prostheses showed a softening type of elasticity. Arterial prostheses have low circumferential distensibility with E'-values higher than reported in the literature for human arteries. The method of forced oscillations could be employed for studying the arterial wall biomechanics and viscoelasticity of arterial prostheses.

Arterial wall mechanics as a function of heart rate: role of vascular smooth muscle

Vascular wall viscoelasticity can be evaluated using a first-order lumped model. This model consists of a spring with elastic constant E and a dashpot with viscous constant η. More importantly, this viscoelastic model can be fitted in-vivo measuring arterial pressure and diameter. The aim of this work is to analyze the influence of heart rate over E and η. In two anesthetized sheep, diameter in thoracic aorta and intravascular pressure has been registered. The right atrium was connected to a programmable stimulator through a pair of pace-maker wires to produce changes in stimulation heart rate (HR) from 80 to 160 bpm. Additionally, local activation of vascular smooth muscle was induced with phenylephrine. After converting pressure and diameter signals into stress and strain respectively, E y η were calculated in control state and during muscle activation. The elastic modulus E did not present significant changes with heart rate. The viscous modulus η decreased 49% with a two-fold acceleration in heart rate from 80 to 160 bpm. However, the product η HR remained stable. The viscous modulus η increased 39% with smooth muscle activation. No significant pressure changes were registered during the experiment. The contractile action of vascular smooth muscle could contribute to increasing arterial wall viscosity. The decrease of η when HR increased might be related to smooth muscle relaxation mediated by endothelium activity, which was stimulated by flow increase. We conclude that HR can modulate arterial wall viscoelasticity through endothelium-dependent mechanisms.

Measurement of Change in Wall Thickness of Cylindrical Shell Due to Cyclic Remote Actuation for Assessment of Viscoelasticity of Arterial Wall

To characterize tissues in atherosclerotic plaques, we have developed a method, the phased tracking method, for measuring the strain (change in wall thickness) and elasticity of the arterial wall. However, some types of tissue, such as lipids and blood clots, cannot be discriminated from each other based only on elasticity because of the small difference in their elasticity. For more precise tissue characterization, we are attempting to measure the regional viscoelasticity. To determine viscoelastic properties, elastic moduli at multiple frequencies were obtained by generating the change in internal pressure due to remote cyclic actuation. From basic experiments using a silicone rubber tube, it was found that the change in internal pressure at the ultrasonic beam position (for measurement of the elastic modulus) can be generated by remotely applied actuation. Furthermore, from the resultant minute changes in wall thickness of less than 10 µm measured by the phased tracking method, elastic moduli were obtained at multiple actuation frequencies.

Smooth muscle contraction and viscoelasticity of arterial wall.

Elasticity and viscosity, of fully relaxed and gradedly contracted arterial wall, were measured on spirally cut rabbit aortic strips suspended in Ringer's solution. Pre-extended contracted tissue submitted to additional stretch shows an instantaneous and a slow elongation. Only instantaneous elongation was observed on fully relaxed tissue. This behavior can be simulated by a mechanical model consisting of a spring in series with a dashpot, and a second spring in parallel with the first spring–dashpot component. The modulus of the first spring and the coefficient of viscosity both increase steadily with increasing contraction, while the modulus of the second spring decreases. The first spring–dashpot component is believed to represent the viscoelastic behavior of smooth muscle on its non-contractile network. The second spring probably represents the combined elastic properties of arterial elastin and collagen.