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Although unphysiological wall shear stress (WSS) has become the consensus hemodynamic mechanism for coronary atherosclerosis, the complex biomechanical stimulus affecting atherosclerosis evolution is still undetermined. This has motivated the interest on the contraction/expansion action exerted by WSS on the endothelium, obtained through the WSS topological skeleton analysis. This study tests the ability of this WSS feature, alone or combined with WSS magnitude, to predict coronary wall thickness (WT) longitudinal changes. Nine coronary arteries of hypercholesterolemic minipigs underwent imaging with local WT measurement at three time points: baseline (T1), after 5.6 ± 0.9 (T2), and 7.6 ± 2.5 (T3) months. Individualized computational hemodynamic simulations were performed at T1 and T2. The variability of the WSS contraction/expansion action along the cardiac cycle was quantified using the WSS topological shear variation index (TSVI). Alone or combined, high TSVI and low WSS significantly co-localized with high WT at the same time points and were significant predictors of thickening at later time points. TSVI and WSS magnitude values in a physiological range appeared to play an atheroprotective role. Both the variability of the WSS contraction/expansion action and WSS magnitude, accounting for different hemodynamic effects on the endothelium, (1) are linked to WT changes and (2) concur to identify WSS features leading to coronary atherosclerosis.

Cardiovascular pathologies such as intracranial aneurysms (IAs) and atherosclerosis preferentially localize to bifurcations and curvatures where hemodynamics are complex. While extensive knowledge about low wall shear stress (WSS) has been generated in the past, due to its strong relevance to atherogenesis, high WSS (typically >3 Pa) has emerged as a key regulator of vascular biology and pathology as well, receiving renewed interests. As reviewed here, chronic high WSS not only stimulates adaptive outward remodeling, but also contributes to saccular IA formation (at bifurcation apices or outer curves) and atherosclerotic plaque destabilization (in stenosed vessels). Recent advances in understanding IA pathogenesis have shed new light on the role of high WSS in pathological vascular remodeling. In complex geometries, high WSS can couple with significant spatial WSS gradient (WSSG). A combination of high WSS and positive WSSG has been shown to trigger aneurysm initiation. Since endothelial cells (ECs) are sensors of WSS, we have begun to elucidate EC responses to high WSS alone and in combination with WSSG. Understanding such responses will provide insight into not only aneurysm formation, but also plaque destabilization and other vascular pathologies and potentially lead to improved strategies for disease management and novel targets for pharmacological intervention.

Abdominal aortic aneurysms (AAA) can lead to catastrophic events such as dissection or rupture, and are an expression of general aortic disease. Low wall shear stress (WSS), high oscillatory shear index (OSI), and high relative residence time (RRT) have been correlated against increased uptake of inflammatory markers in the vessel wall and may improve risk stratification of AAA. We sought to obtain a comprehensive view of WSS, OSI, and RRT in the whole aorta for patients with AAA and age-matched elderly controls and young normal controls. 4D Flow cardiovascular magnetic resonance images of the whole aorta were acquired in 18 AAA patients (70.8 ± 3.4 years), 22 age-matched controls (71.4 ± 3.4 years), and 23 young subjects (23.3 ± 3.1 years), all males. Three-dimensional segmentations of the whole aorta were created for all timeframes using a semi-automatic approach. The aorta was divided into five segments: ascending aorta, arch, descending aorta, suprarenal and infrarenal abdominal aorta. For each segment, average values of peak WSS, OSI, and RRT were computed. Student’s t-tests were used to compare values between the three cohorts (AAA patients vs elderly controls, and elderly controls vs young controls) where the data were normally distributed, and the non-parametric Wilcoxon rank sum tests were used otherwise. AAA patients had lower peak WSS in the descending aorta as well as in the abdominal aorta compared to elderly controls (p ≤ 0.001), similar OSI, but higher RRT in the descending and abdominal aorta (p ≤ 0.001). Elderly controls had lower peak WSS compared to young controls throughout the aorta (p < 0.001), higher OSI in all segments except for the infrarenal aorta (p < 0.001), and higher RRT throughout the aorta, except the infrarenal aorta (p < 0.001). This study provides novel insights into WSS, OSI, and RRT in patients with AAA in relation to normal ageing, highlighting how AAA patients have markedly abnormal hemodynamic stresses not only in the infrarenal, but in the entire aorta. Moreover, we identified RRT as a marker for abnormal AAA hemodynamics. Further investigations are needed to explore if RRT or other measures of hemodynamics stresses best predict AAA growth and/or rupture.

Steel frame infilled with composite plate shear wall (SF-CPSW) is an effective structure for lateral-load resisting. In the structural design, the vertical loads are primarily carried by the boundary SF, while the horizontal loads are expected to be totally carried by CPSW. CPSW incorporates the steel web and the concrete encasements. For the CPSW bays, the boundary SF also inevitably withstands the lateral-loads due to the coordinated deformations between boundary SF and CPSW. The available researches, however, have not given a certain shear force assignment between the boundary SF and CPSW. Furthermore, their interactions under the cyclic lateral-loading are unclear. This paper conducted a study on the load-resisting mechanism of SF-CPSW by a structural model test and finite element analyses. The deformation pattern, failure mode, internal forces, and interactions of structural members were investigated. The effects of steel web and concrete thicknesses, cross-sections of boundary SF, and axial compression ratio on the lateral-load resistance of SF-CPSW were assessed. The results indicated that the interactions of CPSW and boundary SF caused significant normal stresses at the corners of CPSW, reducing the shear strength of steel web. However, the concrete encasements and boundary SF compensate it and mutually improved the stiffness and ductility. According to the analysis results, the formulas of the lateral stiffness and strengths of SF-CPSW were proposed for its seismic design.

Nuclear power plants use reinforced concrete shear walls with flanges for lateral load-resisting systems. The present study investigated the shear-friction strength of reinforced concrete walls with flanges by testing eight wall specimens under cyclic lateral loading. The test parameters were the flange length, flange configuration, wall thickness, interface roughness, and load direction. The test results showed that vertical reinforcing bars in the flanges, as well as the web, increased the shear-friction strength of the walls. However, due to the premature punching failure at the web-flange joint, the contribution of the thin flange was limited. Further, the shear-friction strength of the symmetric flanged wall was identical, regardless of the load direction: the shear-friction strength of the flanged wall was determined by the total vertical reinforcing bars placed in the web and flange. The tested shear-friction strengths, including previous test results, were compared with the predictions of current design methods. Including the flange contribution in the current design methods improved the prediction of test results compared to the case neglecting the flange contribution. Keywords: cyclic loading; flanged wall; shear-friction strength; shear wall.

Spatial variation of the haemodynamic stresses acting on the arterial wall is commonly assumed to explain the focal development of atherosclerosis. Disturbed flow in particular is thought to play a key role. However, widely-used metrics developed to quantify its extent are unable to distinguish between uniaxial and multidirectional flows. We analysed pulsatile flow fields obtained in idealised and anatomically-realistic arterial geometries using computational fluid dynamics techniques, and in particular investigated the multidirectionality of the flow fields, capturing this aspect of near-wall blood flow with a new metric – the transverse wall shear stress (transWSS) – calculated as the time-average of wall shear stress components perpendicular to the mean flow direction. In the idealised branching geometry, multidirectional flow was observed downstream of the branch ostium, a region of flow stagnation, and to the sides of the ostium. The distribution of the transWSS was different from the pattern of traditional haemodynamic metrics and more dependent on the velocity waveform imposed at the branch outlet. In rabbit aortas, transWSS patterns were again different from patterns of traditional metrics. The near-branch pattern varied between intercostal ostia, as is the case for lesion distribution; for some branches there were striking resemblances to the age-dependent patterns of disease seen in rabbit and human aortas. The new metric may lead to improved understanding of atherogenesis.

Direct numerical simulations of the turbulence of a Herschel–Bulkley (HB) fluid in a rough channel are performed at a shear Reynolds number $Re_{\\tau } \\approx 300$ and a Bingham number ${Bn} \\approx 0.9$. For the type of rough surface used in this study, the results indicate that Townsend's wall similarity hypothesis also holds for HB fluids. However, there are notable differences compared with the effect of roughness on Newtonian fluids. More specifically, the effect of roughness appears to be slightly stronger for HB fluids, in the sense that the bulk Reynolds number, based on the viscosity at the wall, is reduced further due to the increase in viscosity in the troughs of the roughness surface induced by the low shear. At the same time, for the simulated rough surface, the contribution of form drag to the total pressure drop is reduced from 1/4 to about 1/5 due to the persistence of viscous shear in the boundary layer, reducing its shielding effect. As for the friction factor, due to the nonlinearity of the HB constitutive relation, its use with the wall shear rate from the mean wall shear stress underpredicts the minimum viscosity at the wall by up to 18 %. This inevitably leads to uncertainties in the prediction of the friction factor. Finally, it is observed that the rough surface is unable to break the peculiar near-wall flow structure of HB fluids, which consists of long persistent low-speed streaks occupying the entire domain. This means that the small-scale energy is significantly reduced for HB fluids, even in rough channels, with the energy more concentrated in the lower wavenumber range, implying an increase in the slope of the power spectrum to $-7/2$ in the inertial range, as shown by Mitishita et al. (J. Non-Newtonian Fluid Mech., vol. 293, 2021, 104570).

Although the hemodynamics of cerebral aneurysms have been extensively studied using patient-specific computational fluid dynamics techniques, no specific hemodynamic factors characteristic of cerebral aneurysm development have yet been identified. We believe that one problem with previous hemodynamic studies of cerebral aneurysms has been the manner in which control groups were created for comparison with experimental groups. The purpose of this study was to determine hemodynamic factors that correlated with the development of cerebral aneurysms. The control group was established in a manner that differed from those of previous works. This allowed us to demonstrate the effectiveness of our method. We artificially removed aneurysms in the middle cerebral artery bifurcations of nine patients and reconstructed the vessel geometries before the aneurysms had occurred. Pulsatile blood flow simulations were performed using the vessel geometries ipsilateral and contralateral to the sites of aneurysm removal, and hemodynamic metrics were calculated. Use of the ipsilateral and contralateral sides as the experimental and control sites, respectively, allowed us to evaluate statistically the hemodynamic metrics between the two corresponding sites/groups. The results showed that only the normalized transverse wall shear stress (NtransWSS) was significantly higher at the MCA bifurcation ipsilateral to the site of aneurysm removal than at the contralateral bifurcation (p = 0.01). There were no significant differences in the other hemodynamic metrics between the bilateral bifurcations. Our findings imply that multi-directional disturbed wall shear stress, which is detected by the NtransWSS metric, may be one hemodynamic risk factor for the development of cerebral aneurysms.

Coronary arteries have high curvatures, and hence, flow through them causes disturbed flow patterns, resulting in stenosis and atherosclerosis. This in turn decreases the myocardial flow perfusion, causing myocardial ischemia and infarction. Therefore, in order to understand the mechanisms of these phenomena caused by high curvatures and branching of coronary arteries, we have conducted elaborate hemodynamic analysis for both (i) idealized coronary arteries with geometrical parameters representing realistic curvatures and stenosis and (ii) patient-specific coronary arteries with stenoses. Firstly, in idealized coronary arteries with approximated realistic arterial geometry representative of their curvedness and stenosis, we have computed the hemodynamic parameters of pressure drop, wall shear stress (WSS) and wall pressure gradient (WPG), and their association with the geometrical parameters of curvedness and stenosis. Secondly, we have similarly determined the wall shear stress and wall pressure gradient distributions in four patient-specific curved stenotic right coronary arteries (RCAs), which were reconstructed from medical images of patients diagnosed with atherosclerosis and stenosis; our results show high WSS and WPG regions at the stenoses and inner wall of the arterial curves. This paper provides useful insights into the causative mechanisms of the high incidence of atherosclerosis in coronary arteries. It also provides guidelines for how simulation of blood flow in patient’s coronary arteries and determination of the hemodynamic parameters of WSS and WPG can provide a medical assessment of the risk of development of atherosclerosis and plaque formation, leading to myocardial ischemia and infarction. The novelty of our paper is in our showing how in actual coronary arteries (based on their CT imaging) curvilinearity and narrowing complications affect the computed WSS and WPG, associated with risk of atherosclerosis. This is very important for cardiologists to be able to properly take care of their patients and provide remedial measures before coronary complications lead to myocardial infarctions and necessitate stenting or coronary bypass surgery. We want to go one step further and provide clinical application of our research work. For that, we are offering to cardiologists worldwide to carry out hemodynamic analysis of the medically imaged coronary arteries of their patients and compute the values of the hemodynamic parameters of WSS and WPG, so as to provide them an assessment of the risk of atherosclerosis for their patients.

Wall Shear Stress (WSS) topological skeleton, composed by fixed points and the manifolds linking them, reflects the presence of blood flow features associated to adverse vascular response. However, the influence of WSS topological skeleton on vascular pathophysiology is still underexplored. This study aimed to identify direct associations between the WSS topological skeleton and markers of vascular disease from real-world clinical longitudinal data of long-term restenosis after carotid endarterectomy (CEA). Personalized computational hemodynamic simulations were performed on a cohort of 13 carotid models pre-CEA and at 1 month after CEA. At 60 months after CEA, intima-media thickness (IMT) was measured to detect long-term restenosis. The analysis of the WSS topological skeleton was carried out by applying a Eulerian method based on the WSS vector field divergence. To provide objective thresholds for WSS topological skeleton quantitative analysis, a computational hemodynamic dataset of 46 ostensibly healthy carotid bifurcation models was considered. CEA interventions did not completely restore physiological WSS topological skeleton features. Significant associations emerged between IMT at 60 months follow-up and the exposure to (1) high temporal variation of WSS contraction/expansion (R2 = 0.51, p < 0.05), and (2) high fixed point residence times, weighted by WSS contraction/expansion strength (R2 = 0.53, p < 0.05). These WSS topological skeleton features were statistically independent from the exposure to low WSS, a previously reported predictor of long-term restenosis, therefore representing different hemodynamic stimuli and potentially impacting differently the vascular response. This study confirms the direct association between WSS topological skeleton and markers of vascular disease, contributing to elucidate the mechanistic link between flow disturbances and clinical observations of vascular lesions.