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Endothelial cell density as a function of distance from impingement after 48-h exposure to low flow (Re 5 125, open squares) and high flow (Re 5 250, closed diamonds). Static control for each experiment is represented at far left with a matching shape. 

Endothelial cell density as a function of distance from impingement after 48-h exposure to low flow (Re 5 125, open squares) and high flow (Re 5 250, closed diamonds). Static control for each experiment is represented at far left with a matching shape. 

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Little is known about endothelial responses to the impinging flow hemodynamics that occur at arterial bifurcation apices, where intracranial aneurysms usually form. Such hemodynamic environments are characterized by high wall shear stress (WSS >40 dynes/cm(2)) and high wall shear stress gradients (WSSG >300 dynes/cm(3)). In this study, confluent bo...

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... cells subjected to impinging flow exhibited a spatially varying density. At the impinge- ment, cells were sparse and large, whereas they were crowded downstream in both branches of the impingement chamber. Cell quantitation verified this impression, as seen in Fig. 6, where cell density (number of cells/mm 2 ) after 48 h of flow exposure to low flow (Re = 125) or high flow (Re = 250) is plotted as a function of distance from the stagnation point. Three independent experiments under each condition produced very similar plots. A consistent pattern was observed in which both high-and low-flow experi- ments showed the same trend: decreased cell density (compared to the static control) forming a trough at the stagnation point in Region I, and increased cell density forming a peak in Region II. In Region III, density returned to a relatively constant level that was lower than the peak but higher than the trough. However, since culture age and passage number were different among experiments and can affect the cell density, there was some variability among six experi- ments that were performed in terms of absolute density and exact peak location. Nonetheless, the density dis- tribution pattern was always the ...

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... At the peak site especially Peak 1, the WSS, dynamic pressure, vorticity and strain rate are the maximal, whereas the total pressure remains very high. High shear stress will damage the vascular wall endothelial cells and predispose the artery to destructive aneurysmal remodeling [29][30][31] . After arterial destructive damage at the peak site, concomitant high pressure at this site will cause the arterial wall to expand outward to form an aneurysm. ...
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Currently, the relationship of bifurcation morphology and aneurysm presence at the major cerebral bifurcations is not clear. This study was to investigate cerebral arterial bifurcation morphology and accompanied hemodynamic stresses associated with cerebral aneurysm presence at major cerebral arterial bifurcations. Cerebral angiographic data of major cerebral artery bifurcations of 554 anterior cerebral arteries, 582 internal carotid arteries, 793 middle cerebral arteries and 195 basilar arteries were used for measurement of arterial diameter, lateral and bifurcation angles and aneurysm deviation. Hemodynamic stresses were analyzed using computational fluid dynamic simulation. Significantly (P < 0.001) more aneurysms deviated toward the smaller branch and the smaller lateral angle than towards the larger branch and larger lateral angle at all four major bifurcations. At the flow direct impinging center, the total pressure was the greatest while the dynamic pressure, wall shear stress (WSS), vorticity and strain rate were the least. Peak 1 and Peak 2 were located on the branch forming a smaller and larger angle with the parent artery, respectively. The dynamic pressure (175.4 ± 18.6 vs. 89.9 ± 7.6 Pa), WSS (28.9 ± 7.4 vs. 15.7 ± 5.3 Pa), vorticity (9874.6 ± 973.4 vs. 7237.8 ± 372.7 1/S), strain rate (9873.1 ± 625.6 vs. 7648.3 ± 472.5 1/S) and distance (1.9 ± 0.8 vs. 1.3 ± 0.3 mm) between the peak site and direct flow impinging center were significantly greater at Peak 1 than at Peak 2 (P < 0.05 or P < 0.01). Moreover, aneurysms deviation and Peak 1 were always on the same side. In conclusion, the branch forming a smaller angle with the parent artery is associated with abnormally enhanced hemodynamic stresses to initiate an aneurysm at the bifurcation apex.
... Hemodynamics at apices of arterial bifurcations are also subjected to disturbed flow. At these regions, blood flow impinges at the apex and locally accelerates downstream, forming a region at the center of the impingement that experiences flow stagnation characterized by a low SS and high SSG [71]. ECs in vitro can be studied under these circumstances by use of a radial impinging flow chamber, in which an incoming fluid impinges on the opposite wall of the chamber and flows radially outward. ...
Article
In the native vasculature, flowing blood produces a frictional force on vessel walls that directly effects endothelial cell phenotype and function. In the arterial system, the vasculature's local geometry directly influences variations in flow profiles and shear stress magnitudes. Straight arterial sections with pulsatile shear stress have been shown to promote an athero-protective endothelial phenotype. Conversely, areas with a more complex geometry, such as arterial bifurcations and branch points with disturbed flow patterns and a lower, oscillatory shear stress, typically lead to endothelial dysfunction and the pathogenesis of cardiovascular diseases. Many studies have investigated the regulation of endothelial responses to various shear stress environments. Importantly, the accurate in vitro simulation of in vivo hemodynamics is critical to the deeper understanding of mechano-transduction through the proper use and design of flow chamber devices. In this review, we describe several flow chamber apparatuses and their fluid mechanics design parameters, including parallel plate flow chambers, cone-and plate devices, and microfluidic devices. In addition, chamber-specific design criteria and relevant equations are defined in detail for the accurate simulation of shear stress environments to study endothelial cell responses
... Taken together, our study of the biomechanical responses of the brain of a rat resulting from a torso-only blast exposure highlights the potential structural effects, which in turn may lead to functional deficits, of the indirect mechanism on the brain vasculature. Extensive evidence from both in vivo and in vitro studies supports the notion that increases in hemodynamic stresses, such as in our predictions of elevated wall shear stresses, can alter the endothelial cells at the walls of the blood vessels (Lehoux et al., 2006;Szymanski et al., 2008;Aoki et al., 2011;Lu and Kassab, 2011;Chalouhi et al., 2012). Based on different rodent models, previous experimental studies have also reported varying degrees of acute (24 h) and chronic (6 weeks following blast exposure) vascular pathologies associated with whole-body exposure, including impairment of the vasodilation mechanisms (Rodriguez et al., 2018), permeability of the blood-brain barrier (Kuriakose et al., 2018(Kuriakose et al., , 2019Heyburn et al., 2019), and structural alterations in the smooth muscle layers of the cerebral arteries (Gama Sosa et al., 2013Sosa et al., , 2014Sosa et al., , 2019. ...
Article
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The interaction of explosion-induced blast waves with the torso is suspected to contribute to brain injury. In this indirect mechanism, the wave-torso interaction is assumed to generate a blood surge, which ultimately reaches and damages the brain. However, this hypothesis has not been comprehensively and systematically investigated, and the potential role, if any, of the indirect mechanism in causing brain injury remains unclear. In this interdisciplinary study, we performed experiments and developed mathematical models to address this knowledge gap. First, we conducted blast-wave exposures of Sprague-Dawley rats in a shock tube at incident overpressures of 70 and 130 kPa, where we measured carotid-artery and brain pressures while limiting exposure to the torso. Then, we developed three-dimensional (3-D) fluid-structure interaction (FSI) models of the neck and cerebral vasculature and, using the measured carotid-artery pressures, performed simulations to predict mass flow rates and wall shear stresses in the cerebral vasculature. Finally, we developed a 3-D finite element (FE) model of the brain and used the FSI-computed vasculature pressures to drive the FE model to quantify the blast-exposure effects in the brain tissue. The measurements from the torso-only exposure experiments revealed marginal increases in the peak carotid-artery overpressures (from 13.1 to 28.9 kPa). Yet, relative to the blast-free, normotensive condition, the FSI simulations for the blast exposures predicted increases in the peak mass flow rate of up to 255% at the base of the brain and increases in the wall shear stress of up to 289% on the cerebral vasculature. In contrast, our simulations suggest that the effect of the indirect mechanism on the brain-tissue-strain response is negligible (<1%). In summary, our analyses show that the indirect mechanism causes a sudden and abundant stream of blood to rapidly propagate from the torso through the neck to the cerebral vasculature. This blood surge causes a considerable increase in the wall shear stresses in the brain vasculature network, which may lead to functional and structural effects on the cerebral veins and arteries, ultimately leading to vascular pathology. In contrast, our findings do not support the notion of strain-induced brain-tissue damage due to the indirect mechanism.
... 20,33 In regions of high ESSG, endothelial cells may be stretched or compressed according to the magnitude and direction of the shear stress differential, affecting expression and function of cell-cell junction proteins such as connexin43 and PECAM-1. [17][18][19]34 High ESSG modulates endothelial function in concert with and independent of ESS, 17,35 and has been associated in vitro and in vivo with endothelial disorientation 16,36 loss of normal actin fibre development and cell architecture, 36 increased cell turnover, 16,19,37 permeability, 16,18,38 downstream cell migration, 39,40 apoptosis and metalloproteinase-mediated extracellular matrix degradation, 17,19 and inflammatory cell infiltration. 21 Similarly, high OSI also modulates endothelial vasodilation, 24 While we have demonstrated independent associations between rupture and high ESSG and also between erosion and high ESSG, ESS, and OSI, our results do not demonstrate causality. ...
Article
Aims To investigate local haemodynamics in the setting of acute coronary plaque rupture and erosion. Methods and results Intracoronary optical coherence tomography performed in 37 patients with acute coronary syndromes caused by plaque rupture (n = 19) or plaque erosion (n = 18) was used for three-dimensional reconstruction and computational fluid dynamics simulation. Endothelial shear stress (ESS), spatial ESS gradient (ESSG), and oscillatory shear index (OSI) were compared between plaque rupture and erosion through mixed-effects logistic regression. Lipid, calcium, macrophages, layered plaque, and cholesterol crystals were also analysed. By multivariable analysis, only high ESSG [odds ratio (OR) 5.29, 95% confidence interval (CI) 2.57–10.89, P < 0.001], lipid (OR 12.98, 95% CI 6.57–25.67, P < 0.001), and layered plaque (OR 3.17, 95% CI 1.82–5.50, P < 0.001) were independently associated with plaque rupture. High ESSG (OR 13.28, 95% CI 6.88–25.64, P < 0.001), ESS (OR 2.70, 95% CI 1.34–5.42, P = 0.005), and OSI (OR 2.18, 95% CI 1.33–3.54, P = 0.002) independently associated with plaque erosion. ESSG was higher at rupture sites than erosion sites [median (interquartile range): 5.78 (2.47–21.15) vs. 2.62 (1.44–6.18) Pa/mm, P = 0.009], OSI was higher at erosion sites than rupture sites [1.04 × 10−2 (2.3 × 10−3–4.74 × 10−2) vs. 1.29 × 10−3 (9.39 × 10−5–3.0 × 10−2), P < 0.001], but ESS was similar (P = 0.29). Conclusions High ESSG is independently associated with plaque rupture while high ESSG, ESS, and OSI associate with plaque erosion. While ESSG is higher at rupture sites than erosion sites, OSI is higher at erosion sites and ESS was similar. These results suggest that ESSG and OSI may play critical roles in acute plaque rupture and erosion, respectively.
... The shapes and orientations of ECs have been related to local SSs, and EC layers are elongated in the direction of flow under certain levels of SS [12][13][14][15]. Szymanski et al. observed cell migration toward areas of high SS [16]. ...
... Previous in vitro studies investigated EC distribution under flow environment using several types of flow chamber. In these results, flow stimuli, especially WSS induced by viscous fluid, has been considered as one of the factors for cell migration, elongation, and orientation [12][13][14]16,22,23]. Though our chamber system uses identical flow domain, CFD results (Fig. 3) indicates that even one wire can reconstruct inner flow environment by its deployment. ...
Article
Background: Blood vessels are constantly exposed to flow-induced stresses, and endothelial cells (ECs) respond to these stresses in various ways. Objective: In order to facilitate endothelialization after endovascular implantation, cell behaviors around a metallic wire using a flow circulation system are observed. Methods: A parallel flow chamber was designed to reproduce constant shear stresses (SSs) on cell surfaces and to examine the effects of a straight bare metal wire on cell monolayers. Cells were then exposed to flow for 24 h under SS conditions of 1, 2, and 3 Pa. Subsequently, cell distributions were observed on the plate of the flow chamber and on the surface of the bare metal wire. Flow fields inside the flow chamber were analyzed using computational fluid dynamics under each SS condition. Results: After 24 h, ECs on the bottom plate were concentrated toward the area of flow reattachment. The matching of higher cell density and CFD result suggests that flow-induced stimuli have an influence on EC distributions. Conclusion: Typical cell concentration occurs on dish plate along the vortexes, which produces large changes in SSs on cell layer.
... The direct consequence of a pressure gradient orthogonal to the surface, where the surface is an endothelial cellular layer, is relatively unexplored in the literature. However, accelerated cellular deposition or growth on an endothelial layer at or near the rejoining stagnation zone of vortex flow has been observed clinically [27][28][29]. Fig. 2 provides a representation (after the clinical trials reported in 27-29) of cellular growth distribution proximal to a rejoining stagnation point (for steady unidirectional flow). ...
... The impact on cellular structure of these different orthogonal pressure influences would be expected to be different. Stagnation points have been associated with both cellular growth [27,28] and also with cell distortion, depletion, apoptosis, lifting and plaque deposition [29][30][31][32][33][34][35]. Initial clinical trial indications are, however, that for very steady (non-oscillating) flow, in a very narrow region at the zero-velocity stagnation point, endothelial cell density is reduced [29]. ...
... Stagnation points have been associated with both cellular growth [27,28] and also with cell distortion, depletion, apoptosis, lifting and plaque deposition [29][30][31][32][33][34][35]. Initial clinical trial indications are, however, that for very steady (non-oscillating) flow, in a very narrow region at the zero-velocity stagnation point, endothelial cell density is reduced [29]. However, immediately proximal to this region of cellular excavation is a region of increased cell density. ...
Article
This paper hypothesizes, based on fluid dynamics principles, that in multiple sclerosis (MS) non-laminar, vortex blood flow occurs in the superior vena cava (SVC) and brachiocephalic veins (BVs), particularly at junctions with their tributary veins. The physics-based analysis demonstrates that the morphology and physical attributes of the major thoracic veins, and their tributary confluent veins, together with the attributes of the flowing blood, predict transition from laminar to non-laminar flow, primarily vortex flow, at select vein curvatures and junctions. Non-laminar, vortex flow results in the development of immobile stenotic valves and intraluminal flow obstructions, particularly in the internal jugular veins (IJVs) and in the azygos vein (AV) at their confluences with the SVC or BVs. Clinical trials’ observations of vascular flow show that regions of low and reversing flow are associated with endothelial malformation. The physics-based analysis predicts the growth of intraluminal flaps and septa at segments of vein curvature and flow confluences. The analysis demonstrates positive correlations between predicted and clinically observed elongation of valve leaflets and between the predicted and observed prevalence of immobile valves at various venous flow confluences. The analysis predicts the formation of sclerotic plaques at venous junctions and curvatures, in locations that are analogous to plaques in atherosclerosis. The analysis predicts that increasing venous compliance increases the laminarity of venous flow and reduces the prevalence and severity of vein malformations and plaques, a potentially significant clinical result. An over-arching observation is that the correlations between predicted phenomena and clinically observed phenomena are sufficiently positive that the physics-based approach represents a new means for understanding the relationships between venous flow in MS and clinically observed venous malformations.
... primarily produce a small disturbed flow region that limits biochemical assays requiring larger cell numbers (e.g., immunoprecipitation). While capillary tubes [22] can be used to simulate impinging flow (such as at artery bifurcations), imaging is challenging within these 3D devices. Therefore new recirculating flow devices are needed that create larger disturbed flow areas, produce shear stress gradients, and facilitate both imaging and biochemical assays. ...
... MRI imaging of human carotid atherosclerotic lesions [31] reported shear stresses ranging from 137 dynes/cm 2 at the obstruction apex to below 10 dynes/cm 2 distal to the lesion, which is similar to maximum (DFG-High) and minimum Interestingly, ECs exposed to atheroprotective shear stress levels within the disturbed flow device did not exhibit a completely atheroprotective phenotype. NO should increase in atheroprotective flow [41][42][43] while EC proliferation, permeability, and inflammation should decrease or remain low [22]. However, for NO level in particular, ECs in the DFG-High and DFG-2Pa regions were statistically similar to cells in the recirculating and low shear stress regions. ...
... In vivo lesions may experience a ~120 dynes/cm 2 shear stress drop across approximately 3.5 mm, compared to an average 36 dynes/cm 2 shear stress drop in this device across 1 mm. Previous work examining gradients did so at much higher shear stress [21,22,70]; much of the existing literature focuses on extremely high shear stress found in cranial arteries. As some authors indicate, however, there is a need to study gradient effects on EC at lower shear stresses [71]. ...
Article
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Atherosclerosis develops at arterial sites where endothelial cells (ECs) are exposed to low time-averaged shear stress, in particular in regions of recirculating disturbed flow. To understand how hemodynamics contributes to EC dysfunction in atheroma development, an in vitro parallel plate flow chamber gasket was modified with protruding baffles to produce large recirculating flow regions. Computational fluid dynamics predicted that more than 60% of the flow surface area was below the 12 dynes/cm2 atheroprotective threshold. Bovine aortic endothelial cells (BAECs) were then seeded in the parallel plate flow chamber with either the standard laminar or the new disturbed flow gasket and exposed to flow for 36 hours. Cell morphology, nitric oxide, proliferation, permeability, and monocyte adhesion were assessed by phase contrast and confocal microscopy. BAEC exposed to 20 dynes/cm2 shear stress in the laminar flow device aligned and elongated in the flow direction while increasing nitric oxide, decreasing permeability, and maintaining low proliferation and monocyte adhesion. As expected, BAEC in the recirculating flow and low shear stress disturbed flow device regions did not elongate or align, produced less nitric oxide, and showed higher proliferation, permeability, and monocyte adhesion than cells in the laminar flow device. Surprisingly, cells in disturbed flow device regions exposed to atheroprotective shear stress did not consistently align or decrease permeability, and these cells demonstrated low nitric oxide levels. These results suggest that atheroprotective signaling may be inhibited by neighboring cells exposed to recirculating flow, highlighting the complex relationship between hemodynamics and atheroma.
... Endothelial injury and vascular wall inflammation may contribute to the formation of IA, and the bifurcation of an artery is a common location where IA occurs (3). The aneurysm-promoting environment is characterized by a high wall shear stress (WSS) and a high positive wall shear stress gradient (WSSG) (4). ...
... Flow data. According to previous studies (4,13,18,19), three regions were set to define different conditions of hemodynamics in the modified T chamber. Region I: A stagnation point and a low to normal WSS compared with the baseline level in straight vessels. ...
... As previously reported by Szymanski et al (4), bovine aortic ECs around the stagnation point maintain a polygonal shape; however, cell density is reduced. Conversely, cells in adjacent regions exposed to very high WSS and WSSG are elongated, aligned parallel to the flow and cell density is increased. ...
Article
At present, the mechanisms underlying intracranial aneurysm (IA) development remain unclear; however, hemodynamics is considered a crucial factor in the induction of IA. To elucidate the association between hemodynamics and endothelial cell (EC) functions, a modified T chamber system was designed to simulate the adjustable hemodynamic conditions of an artery bifurcation. Normal human umbilical vein ECs (HUVECs) and HUVECs with P120 catenin (P120ctn) knockdown were cultured on coverslips and placed in the chamber. A flow rate of 250 or 500 ml/min impinged on the cell layer. Subsequently, the expression levels of P120ctn and other proteins, and EC morphological alterations, were examined. In normal HUVECs, after 3 h under a flow rate of 500 ml/min, the expression levels of P120ctn, vascular endothelial (VE)‑Cadherin, Kaiso and α‑catenin were decreased, whereas matrix metalloproteinase‑2 (MMP‑2) was increased. In HUVECs with P120ctn knockdown, the period during which ECs adhered to the coverslip was reduced to 1 h under a flow rate of 500 ml/min. In addition, the expression levels of VE‑Cadherin, Kaiso and α‑catenin in ECs were decreased, whereas those of MMP‑2 were increased after 1 h; more prominent alterations were detected under a 500 ml/min flow rate compared with a 250 ml/min flow rate. Adherens junctions (AJs) are critical to the maintenance of normal morphology and EC functioning in the vascular wall, and P120ctn is an important regulator of AJs. Loss of P120ctn may be induced by hemodynamic alterations. In response to changes in hemodynamic conditions, a loss of P120ctn may aggravate AJs between ECs, thus inducing inflammation in the vascular wall. Clinically, hemodynamic alterations may result in a loss of P120ctn and endothelial injury; therefore, P120ctn may have a critical role in inducing intracranial aneurysms.
... variations, but also to discriminate between positive and negative spatial WSS gradients (WSSGs) was previously documented. 5,6,24 Positive spatial WSSG occurs when WSS is increasing with direction of flow, such as in flow acceleration, whereas negative WSSG is seen in cases of decelerating flow. Destructive cellular and extracellular responses to high WSS have been shown to be triggered by positive WSSG and mitigated by negative WSSG. ...
... Destructive cellular and extracellular responses to high WSS have been shown to be triggered by positive WSSG and mitigated by negative WSSG. 5,6,24 Positive WSSG also leads to endothelial misalignment and turnover, with high proliferation and apoptosis, 6 whereas negative WSSG leads to an opposite, protective effect. Surgically created de novo branching points showed that changes in arterial morphology resulted in altered WSS patterns, and triggered arterial remodeling resembling early-stage intracranial aneurysms in areas of flow acceleration and positive WSSG, including a decrease in the overall thickness of the media and intima, loss of the internal elastic lamina, and disrupted endothelium. ...
... 25 Although the mechanism for aneurysm initiation is not completely understood, consensus is building regarding the disruptive role of local high WSS and high positive WSSG in the pathological process of aneurysm origination. 5,6,17,24 Studies in animals subjected to unilateral or bilateral common carotid artery ligation have shown that, without other known predisposing factors, flow increase alone at cerebral bifurcations can lead to EC remodeling consistent with aneurysm initiation. 10,18 We hypothesized that WSSG direction and magnitude are dependent on bifurcation geometry, and we sought to explore the effect of individual daughter branch angulations, mother vessel geometry, and flow rate on spatial shear gradient direction in order to link known aneurysmogenic shear conditions to observed aneurysm colocation in wider bifurcations. ...
Article
OBJECTIVE Endothelium adapts to wall shear stress (WSS) and is functionally sensitive to positive (aneurysmogenic) and negative (protective) spatial WSS gradients (WSSG) in regions of accelerating and decelerating flow, respectively. Positive WSSG causes endothelial migration, apoptosis, and aneurysmal extracellular remodeling. Given the association of wide branching angles with aneurysm presence, the authors evaluated the effect of bifurcation geometry on local apical hemodynamics. METHODS Computational fluid dynamics simulations were performed on parametric bifurcation models with increasing angles having: 1) symmetrical geometry (bifurcation angle 60°–180°), 2) asymmetrical geometry (daughter angles 30°/60° and 30°/90°), and 3) curved parent vessel (bifurcation angles 60°–120°), all at baseline and double flow rate. Time-dependent and time-averaged apical WSS and WSSG were analyzed. Results were validated on patient-derived models. RESULTS Narrow symmetrical bifurcations are characterized by protective negative apical WSSG, with a switch to aneurysmogenic WSSG occurring at angles ≥ 85°. Asymmetrical bifurcations develop positive WSSG on the more obtuse daughter branch. A curved parent vessel leads to positive apical WSSG on the side corresponding to the outer curve. All simulations revealed wider apical area coverage by higher WSS and positive WSSG magnitudes, with increased bifurcation angle and higher flow rate. Flow rate did not affect the angle threshold of 85°, past which positive WSSG occurs. In curved models, high flow displaced the impingement area away from the apex, in a dynamic fashion and in an angle-dependent manner. CONCLUSIONS Apical shear forces and spatial gradients are highly dependent on bifurcation and inflow vessel geometry. The development of aneurysmogenic positive WSSG as a function of angular geometry provides a mechanotransductive link for the association of wide bifurcations and aneurysm development. These results suggest therapeutic strategies aimed at altering underlying unfavorable geometry and deciphering the molecular endothelial response to shear gradients in a bid to disrupt the associated aneurysmal degeneration.
... Because degenerative vascular changes such as aneurysm and post-stenotic dilatation develop at lower blood pressures than those necessary to rupture healthy blood vessels, mechanical stress acting on the wall cannot be the only cause for aneurysm growth and rupture. Flow impingement at arterial bifurcation apices generate only a 2% local pressure increase at the stagnation point [7]. Hemodynamic stress on the vessel wall is an important factor in these pathologies, triggering and driving the biologic mechanisms responsible for aneurysm growth and rupture [8,9]. ...
... High WSS and wall shear stress gradient (WSSG) do not directly damage the VECs. Furthermore, VECs migrate from the impingement point, where WSS is low, to the adjacent area characterized by high WSS and high positive WSSG [7]. An equilibrium must exist in a healthy bifurcation between the production of new endothelial cells and downstream migration. ...
... They found a stagnation zone at the location of eventual aneurysm formation presenting low WSS and strong secondary flows. Szymanski et al. [7] confirmed a low WSS and high WSSG at the impingent zone of arterial bifurcation apices, where intracranial aneurysms usually form. The area around the impingent zone, however, experiences both high WSS and high WSSGs. ...
Article
The presence of high-frequency velocity fluctuations in aneurysms have been confirmed by in-vivo measurements and by several numerical simulation studies. Only a few studies have located and recorded wall vibrations in in-vitro experiments using physiological patient models. In this study, we investigated the wall fluctuations produced by a flowing perfusion fluid in a true-to-scale elastic model of a cerebral fusiform aneurysm using a laser Doppler vibrometer (LDV). The model was obtained from patient data. The experimental setup reproduced physiologically relevant conditions using a compliant perfusion system, physiological flow parameters, unsteady flow and a non-Newtonian fluid. Three geometrically identical models with different wall elasticities were used for measurements. The influence of five different flow rates was considered. Wall vibrations were predominantly found at frequencies in the range 40-60 Hz and 255-265 Hz. Their amplitude increased with increasing elasticity of the model, but the spectral peaks remained at about the same frequency. Varying the flow rate produced almost no changes in the frequency domain of the models. The frequency of the spectral peaks varied slightly between points at the lateral wall and at the bottom of the aneurysm. Indeed, embedding the model in a fluid during measurements produced higher and smoother amplitude fluctuations.