scholarly journals Design and Analysis of Balloon-expandable Stainless Steel Coronary Stent

2018 ◽  
Vol 6 (3) ◽  
Author(s):  
Xiaolin Pan ◽  
Gengqiang Shi ◽  
Yuan Li ◽  
Shanshan Wu ◽  
Long Chen

<p>This thesis uses “Volume Control” ballon-stent model, and according to results of deformation of a stent and vascular during implantation, we obtain the stress contours of the stent during implantation. The results conclude by ANSYS simulation show that during the implantation process, expansion of balloon body will make the narrow part of the blood wall fragment tough. After placement of the stent, due to blood flow in vessel makes that the inner wall of blood vessels has uneven distribution of shear stress; And, in the vicinity of the stent structure, it has a lower <sup>[7]</sup><sup> </sup>shear stress to vessel wall. During the expansion of the stent, the maximum principal stress concentrate on the connection between coronary stent itself and stiffeners.</p>

Water ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 535
Author(s):  
Shuaiqi Liu ◽  
Fengshan Ma ◽  
Haijun Zhao ◽  
Jie Guo ◽  
Xueliang Duan ◽  
...  

Water inrush caused by hydrosplitting is an extremely common disaster in the engineering of underground tunnels. In this study, the propagation of fluid-driven fractures based on an improved discrete element fluid-solid coupling method was modeled. First, the interactions between hydrosplitting fractures (HFs) and preexisting weak planes (WPs) with different angles were simulated considering water pressure in the initial fracture. Second, the influence of the in situ stress ratio and the property of WPs were analyzed, and corresponding critical pressure values of different interactions were calculated. Lastly, the maximum principal stress and maximum shear stress variation inside the pieces were reproduced. The following conclusions can be drawn: (1) Five different types of interaction modes between HFs and natural WPs were obtained, prone to crossing the WPs under inclination of 90°. (2) The initiation pressure value decreased with an increased in situ stress ratio, and the confining stress status had an effect on the internal principal stress. (3) During HFs stretching in WPs with a high elastic modulus, the value of the maximum principal stress was low and rose slowly, and the maximum shear stress value was smaller. Through comprehensive analysis, the diversity of the principal stress curves is fundamentally determined by the interaction mode between HFs and WPs, which are influenced by the variants mentioned in the paper. The analysis provides a better guideline for understanding the failure mechanism of water gushing out of deep buried tunnel construction and cracking seepage of high head tunnels.


2016 ◽  
Vol 83 (5) ◽  
Author(s):  
Chenglin Liu ◽  
Shijie He ◽  
Xiaojun Li ◽  
Bo Huo ◽  
Baohua Ji

It has been recognized that cells are able to actively sense and respond to the mechanical signals through an orchestration of many subcellular processes, such as cytoskeleton remodeling, nucleus reorientation, and polarization. However, the underlying mechanisms that regulate these behaviors are largely elusive; in particular, the quantitative understanding of these mechanical responses is lacking. In this study, combining experimental measurement and theoretical modeling, we studied the effects of rigidity and pattern geometry of substrate on collective cell behaviors. We showed that the mechanical force took pivotal roles in regulating the alignment and polarization of cells and subcellular structures. The cell, cytoskeleton, and nucleus preferred to align and polarize along the direction of maximum principal stress in cell monolayer, and the driving force is the in-plane maximum shear stress. The higher the maximum shear stress, the more the cells and their subcellular structures preferred to align and polarize along the direction of maximum principal stress. In addition, we proved that in response to the change of in-plane shear stresses, the actin cytoskeleton is more sensitive than the nucleus. This work provides important insights into the mechanisms of cellular and subcellular responses to mechanical signals. And it also suggests that the mechanical force does matter in cell behaviors, and quantitative studies through mechanical modeling are indispensable in biomedical and tissue engineering applications.


2020 ◽  
Author(s):  
Carolina Giorgetti ◽  
Marie Violay

&lt;p&gt;Despite natural faults are variably oriented to the Earth's surface and to the local stress field, the mechanics of fault reactivation and slip under variable loading paths (sensu Sibson, 1993) is still poorly understood.&amp;#160;Nonetheless, different loading paths commonly occur in natural faults, from load-strengthening when the increase in shear stress is coupled with an increase in normal stress (e.g., reverse faults in absence of the fluid pressure increase) to load-weakening when the increase in shear stress is coupled with a decrease in normal stress (e.g., normal faults). According to the Mohr-Coulomb theory, the reactivation of pre-existing faults is only influenced by the fault orientation to the stress field, the fault friction, and the principal stresses magnitude. Therefore, the stress path the fault experienced is often neglected when evaluating the potential for reactivation. Yet, in natural faults characterized by thick, incohesive fault zone and highly fractured damage zone, the loading path could not be ruled out. Here we propose a laboratory approach aimed at reproducing the typical tectonic loading paths for reverse and normal faults. We performed triaxial saw-cut experiments, simulating the reactivation of well-oriented (i.e., 30&amp;#176; to the maximum principal stress) and misoriented (i.e., 50&amp;#176; to the maximum principal stress), normal and reverse gouge-bearing faults under dry and water-saturated conditions. We find that load-strengthening versus load-weakening path results in clearly different hydro-mechanical behavior. Particularly, prior to reactivation, reverse faults undergo &lt;em&gt;compaction&lt;/em&gt; even at differential stresses well below the value required for reactivation. Contrarily, normal faults experience &lt;em&gt;dilation&lt;/em&gt;, most of which occurs only near the differential stress values required for reactivation. Moreover, when reactivating at comparable normal stress, normal faults (load-weakening path) are more prone to slip seismically than reverse fault (load-strengthening path). Indeed, the higher mean stress that normal fault experienced before reactivation compacts more efficiently the gouge layer, thus increasing the fault stiffness and favoring seismic slip. This contrasting fault zone compaction and dilation prior to reactivation may occur in different natural tectonic settings, affecting the fault hydro-mechanical behavior. Thus, to take into account the loading path the fault experienced is fundamental in evaluating both natural and induced fault reactivation and the related seismic risk assessment.&lt;/p&gt;


Author(s):  
Diego Gallo ◽  
Raffaele Ponzini ◽  
Filippo Consolo ◽  
Diana Massai ◽  
Luca Antiga ◽  
...  

The initiation and progression of vessel wall pathologies have been linked to disturbances of blood flow and altered wall shear stress. The development of computational techniques in fluid dynamics, together with the increasing performances of hardware and software allow to routinely solve problems on a virtual environment, helping to understand the role of biomechanics factors in the healthy and diseased cardiovascular system and to reveal the interplay of biology and local fluid dynamics nearly intractable in the past, opening to detailed investigation of parameters affecting disease progression. One of the major difficulties encountered when wishing to model accurately the cardiovascular system is that the flow dynamics of the blood in a specific vascular district is strictly related to the global systemic dynamics. The multiscale modelling approach for the description of blood flow into vessels consists in coupling a detailed model of the district of interest in the framework of a synthetic description of the surrounding areas of the vascular net [1]. In the present work, we aim at evaluating the effect of boundary conditions on wall shear stress (WSS) related vessel wall indexes and on bulk flow topology inside a carotid bifurcation. To do it, we coupled an image-based 3D model of carotid bifurcation (local computational domain), with a lumped parameters (0D) model (global domain) which allows for physiological mimicking of the haemodynamics at the boundaries of the 3D carotid bifurcation model here investigated. Two WSS based blood-vessel wall interaction descriptors, the Time Averaged WSS (TAWSS), and the Oscillating Shear Index (OSI) were considered. A specific Lagrangian-based “bulk” blood flow descriptor, the Helical Flow Index (HFI) [2], was calculated in order to get a “measure” of the helical structure in the blood flow. In a first analysis the effects of the coupled 0D models on the 3D model are evaluated. The results obtained from the multiscale simulation are compared with the results of simulations performed using the same 3D model, but imposing a flow rate at internal carotid (ICA) outlet section equal to the maximum (60%) and the minimum (50%) flow division obtained out from ICA in the multiscale model simulation (the presence of the coupled 0D model gives variable internal/external flow division ratio during the cardiac cycle), and a stress free condition on the external carotid (ECA).


2019 ◽  
Vol 47 (1) ◽  
pp. E2 ◽  
Author(s):  
Brittany Staarmann ◽  
Matthew Smith ◽  
Charles J. Prestigiacomo

Wall shear stress, the frictional force of blood flow tangential to an artery lumen, has been demonstrated in multiple studies to influence aneurysm formation and risk of rupture. In this article, the authors review the ways in which shear stress may influence aneurysm growth and rupture through changes in the vessel wall endothelial cells, smooth-muscle cells, and surrounding adventitia, and they discuss shear stress–induced pathways through which these changes occur.


2013 ◽  
Vol 135 (12) ◽  
Author(s):  
Mahmudul Hasan ◽  
David A. Rubenstein ◽  
Wei Yin

The goal of this study was to establish a computational fluid dynamics model to investigate the effect of cyclic motion (i.e., bending and stretching) on coronary blood flow. The three-dimensional (3D) geometry of a 50-mm section of the left anterior descending artery (normal or with a 60% stenosis) was constructed based on anatomical studies. To describe the bending motion of the blood vessel wall, arbitrary Lagrangian–Eularian methods were used. To simulate artery bending and blood pressure change induced stretching, the arterial wall was modeled as an anisotropic nonlinear elastic solid using the five-parameter Mooney–Rivlin hyperelastic model. Employing a laminar model, the flow field was solved using the continuity equations and Navier–Stokes equations. Blood was modeled as an incompressible Newtonian fluid. A fluid–structure interaction approach was used to couple the fluid domain and the solid domain iteratively, allowing force and total mesh displacement to be transferred between the two domains. The results demonstrated that even though the bending motion of the coronary artery could significantly affect blood cell trajectory, it had little effect on flow parameters, i.e., blood flow velocity, blood shear stress, and wall shear stress. The shape of the stenosis (asymmetric or symmetric) hardly affected flow parameters either. However, wall normal stresses (axial, circumferential, and radial stress) can be greatly affected by the blood vessel wall motion. The axial wall stress was significantly higher than the circumferential and radial stresses, as well as wall shear stress. Therefore, investigation on effects of wall stress on blood vessel wall cellular functions may help us better understand the mechanism of mechanical stress induced cardiovascular disease.


2020 ◽  
Vol 14 ◽  
Author(s):  
Zhenzhou Li ◽  
Yongfeng Wang ◽  
Xinyin Wu ◽  
Xin Liu ◽  
Shanshan Huang ◽  
...  

Carotid plaque neovascularization is one of the major factors for the classification of vulnerable plaque, but the axial force effects of the pulsatile blood flow on the plaque with neovessel and intraplaque hemorrhage was unclear. Together with the severity of stenosis, the fibrous cap thickness, large lipid core, and the neovascularization followed by intraplaque hemorrhage (IPH) have been regarded as high-risk features of plaque rupture. In this work, the effects of these factors were evaluated on the progression and rupture of the carotid atherosclerotic plaques. Five geometries of carotid artery plaque were developed based on contrast-enhanced ultrasound (CEUS) images, which contain two types of neovessel and IPH, and geometry without neovessel and IPH. A one-way fluid-structure interaction model was applied to compute the maximum principal stress and strain in the plaque. For that hyper-elastic and non-linear material, Yeoh 3rd Order strain energy density function was used for components of the plaque. The simulation results indicated that the maximum principal stress of plaque in the carotid artery was higher when the degree of the luminal stenosis increased and the thickness of the fibrous cap decreased. The neovessels within the plaque could introduce a 2.5% increments of deformation in the plaque under the pulsatile blood flow pressure. The IPH also contributed to the increased risk of plaque rupture that a gain of stress was 8.983, 14.526, and 34.47 kPa for the plaque with 50, 65, and 75%, respectively, when comparing stress in the plaque with IPH distributed at the middle to the shoulder of the plaque. In conclusion, neovascularization in the plaque could reduce the stability of the plaque by increasing the stress within the plaque. Also, the risk of plaque rupture increased when large luminal stenosis, thin fibrous cap, and IPH were observed.


2012 ◽  
Vol 204-208 ◽  
pp. 2440-2443 ◽  
Author(s):  
Sheng Rui Su ◽  
Hu Jun He ◽  
Ying Zhang ◽  
Peng Li

Two-dimensional finite element model of Longmenshan area was built on the basis of depth study on geological structure conditions and of rock mechanical properties in Longmenshan area, tectonic stress field and variation process of Longmenshan fault belt were inversed after the earthquake. The results show that: (1)After the earthquake, the maximum principal stress appears in fault endpoint, partial inflection point, intersection of Longmenshan fault and Xianshuihe fault and intersection of Minjiang fault, Animaqing-lueyang fault and Longmenshan Fault. The maximum principal stress in area is overall NEE to SEE.(2)After earthquake, shear stress distribution is more uniform, and compared after earthquake to before earthquake, shearing stress of Longmenshan central fault and Qianshan fault reduces obviously, but shear stress of Houshan fault increases.


Author(s):  
Roland Gårdhagen ◽  
Jonas Lantz ◽  
Fredrik Carlsson ◽  
Matts Karlsson

A majority of all deaths in the developed world are related to atherosclerosis, i.e. obstruction of blood vessels caused by growth of the vessel wall. Hemodynamic phenomena, especially wall shear stress, are since several decades thought to influence the risk to develop atherosclerosis; hence simulation of blood flow, either in order to elucidate the relation between the hemodynamic and disease initiation or to study the flow pattern, is an area of intense research [1,2].


2012 ◽  
Vol 303 (9) ◽  
pp. H1096-H1106 ◽  
Author(s):  
Krishna Sriram ◽  
Beatriz Y. Salazar Vázquez ◽  
Amy G. Tsai ◽  
Pedro Cabrales ◽  
Marcos Intaglietta ◽  
...  

Here, we present an analytic model of arteriolar mechanics that accounts for key autoregulation mechanisms, including the myogenic response and the vasodilatory effects of nitric oxide (NO) in the vasculature. It couples the fluid mechanics of blood flow in arterioles with solid mechanics of the vessel wall and includes the effects of wall shear stress- and stretch-induced endothelial NO production. The model can be used to describe the regulation of blood flow and NO transport under small changes in hematocrit and to analyze the regulatory response of arterioles to small changes in hematocrit. Our analysis revealed that the experimentally observed paradoxical increase in cardiac output with small increases in hematocrit results from the combination of increased NO production and the effects of a strong myogenic response modulated by elevated levels of WSS. Our findings support the hypothesis that vascular resistance varies inversely with blood viscosity for small changes in hematocrit in a healthy circulation that responds to shear stress stimuli. They also suggest beneficial effects independent of changes in O2carrying capacity associated with the postsurgical transfusion of one or two units of blood.


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