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Paper has a porous structure, and fluid imbibition in a paper channel is possible passively through the hydrophilic surfaces by capillary action, so it can be an appropriate substrate in the field of microfluidics. To realize the fluid behavior in a paper-based microchannel, there is a need to obtain a model for fluid flow. In this study, the capillary-driven flow in a porous structure was simulated, and the effect of geometrical and physical parameters on the wetted length and average fluid pressure was investigated. Geometric parameters are pores’ shape and size, channel dimensions, and porosity, while the investigated physical parameters were the contact angle, surface tension coefficient, and viscosity. According to the results, geometric parameters influenced the capillary pressure through the capillary surface and channel resistance variation, and physical parameters directly impacted the capillary pressure. Considering the wetted length results, the fluid imbibition velocity was fast at the beginning of the simulation and reached a constant value over time due to the increase in the flow resistance. The pressure drop was observed in the liquid phase suggesting the fluid flow from the higher pressure to the lower. The wetted-length equation was obtained based on geometrical and physical parameters. Finally, the proposed equation can be used to design and predict the liquid imbibition in porous channels.

Myocardial infarction is one of the leading causes of death in the developed countries. A majority of myocardial infarctions are caused by the rupture of coronary artery plaques. In order to achieve a better understanding of the effect of the extension of the lipid core into the artery wall on the change of flow field and its effect on plaque vulnerability, we have studied the hemodynamic parameters by utilizing a finite element method and taking into account the fluid-structure interaction (FSI). Four groups of stenosis models with different sizes of lipid core were used in the study. The fully developed pulsatile velocity profile of the right coronary artery was used as the inlet boundary condition, and the pressure pulse was applied as the outlet boundary condition. The non-Newtonian Carreau model was used to simulate the non-Newtonian behavior of blood. Results indicate that the extension of the lipid core into the artery wall influences the flow field; subsequently, creates favorable conditions for additional development of the lipid core which can lead to a higher risk of plaque rupture.

Since the effect of magnetic fields on blood flow is not fully understood or studied comprehensively, this paper, for the first time, addresses the effect of uniform magnetic fields with different intensities on the pulsatile non-Newtonian blood flow in an elastic artery with axially symmetrical single and double stenoses using the commercial software COMSOL Multiphysics 5.1. The results are suggestive that an increase in the percent stenosis increases the pressure drop, which is more dramatic in double stenosis. Moreover, for a given percent stenosis, increasing the Hartmann (Ha) number, in addition to increasing the pressure drop, increases the amount by which the pressure drop is raised. The shear stress results revealed that increasing the magnetic field intensity results in the reduction of the vortex region formed in the back of the stenosis, reducing the area prone to disease, which can resolve pathological issues. The impact of the magnetic field was found to be decreased by increasing the percent stenosis. It was also observed that the percentage difference between the maximum wall shear stresses for various percent stenoses is reduced by increasing the Ha number for both single and double stenoses.

Clinical evidence has shown that hemodynamics plays an important role in vascular diseases that hemodynamic parameters are highly dependent on the elasticity of the artery wall. Since so far, no study has not been done about turbulent and non-Newtonian blood flow in carotid artery under a magnetic field, in this study we use computational fluid dynamics and fluid–structure interaction (FSI) models to study the hemodynamics of a patient-specific carotid artery. The comparative and cumulative effects of turbulence modeling, arterial wall elasticity, and magnetic field intensities are investigated by quantifying their effects on different variables of interest. These variables include blood pressure, time-averaged wall shear stress, relative residence time (RRT), and oscillating shear index (OSI), which are important in the onset and development of atherosclerosis. The results showed that the effects of turbulence are significant for predictions of OSI, while for other variables the turbulent simulation results were comparable to laminar simulations. The effects of wall elasticity were significant for all variables, such that FSI modeling will be essential for an accurate computational framework. The effects of magnetic fields were also found to be relatively significant. By increasing Hartman number from zero to five, the maximum shear stress was reduced by about 10%. Other effects of increased intensity of magnetic field included reduction in the average amount of RRT, sharp decrease in the OSI > 0 region, and transfer of maximum OSI from distal part of carotid sinus to the proximal part.

Atherosclerosis develops due to different hemodynamic factors, among which time-averaged Wall shear stress (mean WSS) and Oscillatory shear index (OSI) are two of the most important. These two factors not only depend on flow geometry, but are also influenced by rheological characteristics of blood. Since analytical solutions are limited to simple problems and since experimental tests are costly and time consuming, CFD solutions been prominently and effectively used to solve such problems. We conducted a numerical study via ADINA 8.8 software on the non-Newtonian pulsatile flow of blood through an elastic blood artery with single and consecutive stenosis. The studied stenosis cross sectional area was 70 % that of the unstenosed artery. The single stenosis results were compared with the consecutive stenosis results. The five non-Newtonian flow models, the Carreau model, the Carreau-Yasuda model, the modified Casson model, the power-law model, and the generalized power-law model, were used to model the non-Newtonian blood flow. The obtained results showed that increasing the number of stenoses would lead to reduced length of the oscillatory area after the first stenosis, thus forming another oscillatory area with a larger length after the second stenosis. Thus, a consecutive stenosis would develop a larger disease prone area. Upon examining the mean WSS and OSI, we found that, as compared with the other models, the modified Casson model and the power-law model produced predictions for the most extent of damage to endothelial cells and the most disease prone areas, respectively.

This article investigates the pulsatile and turbulent blood flows in flexible artery with single and double stenoses. The changes in pressure drop, mean wall shear stress (WSS), radial displacement of the artery, and oscillating shear index are investigated. Similar to experimental data, the results of the present study show that a laminar flow occurs for stenosis of up to 70%, and for 80% stenosis the flow is turbulent. The mean WSS analysis shows that assuming the flow is laminar causes more errors than assuming the walls are solid. The comparison of the results for single stenosis with those for double stenosis reveals that the dilation in the arterial walls in double stenoses is much more common than in single stenosis. Therefore, the maximum mean WSS in double stenoses is less than that in single stenosis. The results also indicate that the axial pressure drop in double stenoses is higher than that in single stenosis.

Research on the development and incidence of cardiovascular diseases has revealed the importance of vascular wall shear stress. In this paper, the vascular wall shear stress was numerically simulated in an elastic vessel with simple and consecutive Stenosis during a pulsatile laminar non-Newtonian blood flow using ADINA 8.8. The cross-sectional area of the studied stenosis was 70% of the unstenosed vascular cross-sectional area. The results of the simple stenosis were compared with those of the double stenosis. Five non-Newtonian models of Carreau, Carreau-Yasuda, Casson, Power Law, and Generalized Power Law were employed to simulate the non-Newtonian properties of blood. The axial velocity values at the maximum flow rate showed that in both simple and consecutive Stenosis, the highest and lowest axial velocities occur in the Generalized Power Law and Power Law models, respectively. Wall shear stress profiles at the maximum flow rate showed that the Power Law model underestimates the stress values compared to other non-Newtonian models and the Newtonian model. In general, results showed that the Power Law model is not suitable for simulating the non-Newtonian behavior of blood.

Growth of stenosis is mainly due to the high concentration of plasma lipoprotein such as low density lipoprotein (LDL) near the art ery walls. Accurate prediction of LDL concentration especially near the stenosis and where the shear stress is low, can help to predict the plaque growth. In this paper, a novel model is introduced to predict the LDL concentration near a plaque. This model is based on variable diffusion coefficient of LDL due to the non-Newtonian behavior of the blood flow in low shear stress regions such as flow around plaques. The new model for diffusion coefficient consists of two parts: the stationary and the shear- induced particle diffusivity due to rotation of red blood cells. The results show that the new model predicts the LDL concentration well and unlike the constant diffusion coefficient which is used by others, produces more physical and meaningful results.

To study the effects of increase in the degree of stenosis severity and subsequent complexity of hemodynamic patterns on hemodynamic parameters, experimental investigations and numerical simulations were performed. The correlations between the large negative Stress Phase Angle (SPA), the low mean Wall Shear Stress (WSS) and high Oscillatory Shear Index (OSI) were investigated at the distal shoulder and post-stenotic regions as the outcomes of elevated stenosis severity. Models included non-Newtonian fluid flow in stenotic arteries with 30-80% symmetrical stenoses. To study the interactions between pulsatile WSS and pulsatile wall circumferential stress (WCS) acting on endothelial cells, SPA as the phase difference between WSS and WCS waves was used. Moreover, the distribution of SPA on the lumen axis was compared to the distributions of the mean WSS and OSI that have been regarded until now as the determinants of atherosclerosis-prone regions. Results indicate that an increase in stenosis severity, not only affects the mean WSS, mean WCS and pulse amplitudes, but also influences the phase difference between them. The SPA is large negative on the distal shoulder and post-stenotic areas where atherosclerotic plaque develops. The increasing stenosis severity and the subsequent increasing complexity of hemodynamic patterns affect the correlation between any of the low mean WSS and high OSI with large negative SPA, such that it not only leads to create and develop some regions where the correlation between any of the low mean WSS and high OSI with large negative SPA is well but also leads to create and develop other regions where such correlations fail.

Low-density lipoprotein (LDL), which is recognized as bad cholesterol, typically has been regarded as a main cause of atherosclerosis. LDL infiltration across arterial wall and subsequent formation of Ox-LDL could lead to atherogenesis. In the present study, combined effects of non-Newtonian fluid behavior and fluid–structure interaction (FSI) on LDL mass transfer inside an artery and through its multilayer arterial wall are examined numerically. Navier–Stokes equations for the blood flow inside the lumen and modified Darcy’s model for the power-law fluid through the porous arterial wall are coupled with the equations of mass transfer to describe LDL distributions in various segments of the artery. In addition, the arterial wall is considered as a heterogeneous permeable elastic medium. Thus, elastodynamics equation is invoked to examine effects of different wall elasticity on LDL distribution in the artery. Findings suggest that non-Newtonian behavior of filtrated plasma within the wall enhances LDL accumulation meaningfully. Moreover, results demonstrate that at high blood pressure and due to the wall elasticity, endothelium pores expand, which cause significant variations on endothelium physiological properties in a way that lead to higher LDL accumulation. Additionally, results describe that under hypertension, by increasing angular strain, endothelial junctions especially at leaky sites expand more dramatic for the high elastic model, which in turn causes higher LDL accumulation across the intima layer and elevates atherogenesis risk.

The turbulent pulsatile blood flow through stenosed arteries considering the elastic property of the wall is investigated numerically. During the numerical model validation both standardk-εmodel and RNGK-εmodel are used. Compared with the RNGK-εmodel, the standardK-εmodel shows better agreement with previous experimental results and is better able to show the reverse flow region. Also, compared with experimental data, the results show that, up to 70% stenosis, the flow is laminar and for 80% stenosis the flow becomes turbulent. Assuming laminar or turbulent flow and also rigid or elastic walls, the results are compared with each other. The investigation of time-averaged shear stress and the oscillatory shear index for 80% stenosis show that assuming laminar flow will cause more error than assuming a rigid wall. The results also show that, in turbulent flow compared with laminar flow, the importance of assuming a flexible artery wall is more than assuming a rigid artery wall.

Blood non-Newtonian behavior on low-density lipoproteins (LDL) accumulation is analyzed numerically, while fluid-multilayered arteries are adopted for nonstenotic and 30%–60% symmetrical stenosed models. Present model considers non-Newtonian effects inside the lumen and within arterial layers simultaneously, which has not been examined in previous studies. Navier–Stokes equations are solved along with the mass transport convection–diffusion equations and Darcy’s model for species transport inside the luminal flow and across wall layers, respectively. Carreau model for the luminal flow and the modified Darcy equation for the power-law fluid within arterial layers are employed to model blood rheological characteristics, appropriately. Results indicate that in large arteries with relatively high Reynolds number Newtonian model estimates LDL concentration patterns well enough, however, this model seriously incompetent for regions with low WSS. Moreover, Newtonian model for plasma underestimates LDL concentration especially on luminal surface and across arterial wall. Therefore, applying non-Newtonian model seems essential for reaching to a more accurate estimation of LDL distribution in the artery. Finally, blood flow inside constricted arteries demonstrates that LDL concentration patterns along the stenoses inside the luminal flow and across arterial layers are strongly influenced as compared to the nonstenotic arteries. Additionally, among four stenosis severity grades, 40% stenosis is prone to more LDL accumulation along the post-stenotic regions.

Symmetrical 30-60% stenosis in a common carotid artery under unsteady flow condition for Newtonian and six non-Newtonian viscosity models are investigated numerically. Results show power-law model produces higher deviations, in terms of velocity and wall shear stress in comparison with other models while generalized power-law and modified-Casson models are more prone to Newtonian state. Comparing separation length of recirculation region at different critical points of cardiac cycle confirms the necessity of considering blood flow in unsteady mode. Increasing stenosis intensity causes flow patterns more disturbed downstream of the stenosis and WSS appear to develop remarkably at the stenosis throat.

Rupture of the abdominal aortic aneurysm (AAA) is the result of the relatively complex interaction of blood hemodynamics and material behavior of arterial walls. In the present study, the cumulative effects of physiological parameters such as the directional growth, arterial wall properties (isotropy and anisotropy), iliac bifurcation and arterial wall thickness on prediction of wall stress in fully coupled fluid-structure interaction (FSI) analysis of five idealized AAA models have been investigated. In particular, the numerical model considers the heterogeneity of arterial wall and the iliac bifurcation, which allows the study of the geometric asymmetry due to the growth of the aneurysm into different directions. Results demonstrate that the blood pulsatile nature is responsible for emerging a time-dependent recirculation zone inside the aneurysm, which directly affects the stress distribution in aneurismal wall. Therefore, aneurysm deviation from the arterial axis, especially, in the lateral direction increases the wall stress in a relatively nonlinear fashion. Among the models analyzed in this investigation, the anisotropic material model that considers the wall thickness variations, greatly affects the wall stress values, while the stress distributions are less affected as compared to the uniform wall thickness models. In this regard, it is confirmed that wall stress predictions are more influenced by the appropriate structural model than the geometrical considerations such as the level of asymmetry and its curvature, growth direction and its extent.

In this study, Lumen Surface Concentration (LSC) of Low Density Lipoprotein (LDL) particles in arteries with a permeable wall and up to 60% stenosis under steady state conditions, for Newtonian and non-Newtonian fluids, has been numerically investigated. The results show the Concentration Polarization (CP) phenomenon. Also, an increase in wall suction velocity (high blood pressure) and a reduction in Wall Shear Stress (WSS) are introduced as factors for an increase in LSC. Maximum LSC are observed for 40% stenosis.