scholarly journals Examination of Fluid-Structure Interaction in Stent Grafts and its Hemodynamic Implications

2018 ◽  
Author(s):  
Eric M. Looyenga ◽  
Stephen P. Gent
Keyword(s):  
Risk Factors ◽  
Shear Stress ◽  
Arterial Wall ◽  
The United States ◽  
Plaque Formation ◽  
Peripheral Arteries ◽  
Stent Grafts ◽  
Structure Interaction ◽  
Aneurysm Formation ◽  
Abdominal Aortic

Every year in the United States, 4,500 deaths occur from abdominal aortic aneurysm (AAA) rupture. Aneurysms develop when the arterial wall weakens. Many risk factors can contribute to aneurysm formation, including age, sex, ethnicity, smoking and hypertension [1]. AAAs are the most common form of aneurysm because the aorta experiences the highest wall shear stress (WSS) of any vessels in the human body. These aneurysms are 5–6% prevalent in men and 1–2% in women, both over 65 years of age [2]. In the aorta, high WSS causes plaque formation, but in peripheral arteries where the flow rate is lower, atherosclerosis can also trigger aneurysm formation.

Abstract 286: Loss of Smad3 Exacerbates Abdominal Aortic Aneurysm Formation With Enhanced Inflammation in an Experimental Mouse Model

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Xiaohua Dai ◽  
Anandita Arora ◽  
Jianbin Shen ◽  
Hong Jiang ◽  
Li Li
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Calcium Chloride ◽  
The United States ◽  
Protective Role ◽  
Elastic Fibers ◽  
Aneurysm Formation ◽  
Abdominal Aortic ◽  
The Media ◽  
Chloride Treatment

Introduction Abdominal aortic aneurysm (AAA) is a complex vascular disease that causes more than 10,000 deaths each year in the United States. Extensive studies have been performed in search of pharmaceutical treatment but surgical repair still remains the most effective treatment. TGF-β signaling is an important mechanism in the pathogenesis of aneurysms; however, there is debate as to whether its role is protective or destructive. Smad3 is a major intracellular mediator of the canonical pathway of TGF-β signaling. Hypothesis We hypothesize that Smad3-mediated TGF-β signal pathway plays important roles in the pathogenesis of AAA. Methods To test this hypothesis, we analyze the effects of loss of Smad3 on aneurysm formation in the calcium chloride induced AAA model using Smad3 knockout mice. Results Three weeks after calcium chloride treatment, the abdominal aorta displayed increased dilation, forming aneurysms. Histology and immunohistochemistry analyses show increased cell proliferation and enhanced inflammatory cell infiltration in the media and adventitia of the vessel wall. This was accompanied by elastic fibers degradation, increased MMPs expression and reduced expression of smooth muscle markers. Further analysis showed that the expression and nuclear localization of Smad2 and Smad4 was significantly increased. Conclusions These results demonstrate that Smad3-mediated TGF-β signaling plays a protective role in the pathogenesis of AAA and Smad2/Smad4 upregulation is not sufficient to compensate for the loss of Smad3 in this experimental model.

A New 3D Reconstruction Method for Human Coronary Bifurcations for Shear Stress Computations

2012 ◽  
Author(s):  
Frank Gijsen ◽  
Hans Schuurbiers ◽  
Michiel Schaap ◽  
Anton van der Steen ◽  
Jolanda Wentzel
Keyword(s):  
Shear Stress ◽  
Coronary Arteries ◽  
Arterial Wall ◽  
Plaque Formation ◽  
Atherosclerotic Plaques ◽  
Reconstruction Method ◽  
Human Coronary Artery ◽  
Multislice Computer Tomography ◽  
Stress Influences ◽  
The Impact

Atherosclerosis is characterized by lipid accumulation in the arterial wall, followed by an inflammatory response. Plaque formation is generally observed near bifurcations in coronary arteries. The composition of atherosclerotic plaques depends on the location, and it was hypothesized that blood flow induced shear stress influences plaque composition2. To study the impact of shear stress on atherosclerotic disease in human coronary arteries, we developed a technique that enables us to generate 3D lumen reconstruction based on multislice computer tomography (MSCT) and intravascular ultrasound (IVUS).We describe two approaches to generate 3D reconstructions of human coronary artery bifurcations and apply them to coronary segments with bifurcations. We will evaluate the effect on shear stress distribution and its relationship to wall thickness.

Hemodynamics in Human Abdominal Aortic Aneurysms During Rest and Simulated Exercise

2007 ◽  
Author(s):  
Andrea S. Les ◽  
Christopher P. Cheng ◽  
Mary T. Draney Blomme ◽  
C. Alberto Figueroa ◽  
John F. LaDisa ◽  
...  
Keyword(s):  
United States ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Surgical Repair ◽  
Abdominal Aortic Aneurysms ◽  
The United States ◽  
Aortic Aneurysms ◽  
High Particle ◽  
Abdominal Aortic ◽  
Natural Progression

Abdominal Aortic Aneurysms (AAAs) — the localized enlargement of the abdominal aorta — represent the 13th leading cause of death in the United States. The natural progression of small (3–5 cm) AAAs is 2–6% growth per year until rupture or surgical repair [1]. As AAAs enlarge, adverse hemodynamic conditions (including regions of low mean wall shear stress and high particle residence time) are exacerbated under normal resting conditions.

scholarly journals A Literature Review of the Numerical Analysis of Abdominal Aortic Aneurysms Treated with Endovascular Stent Grafts

2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
David Roy ◽  
Claude Kauffmann ◽  
Sébastien Delorme ◽  
Sophie Lerouge ◽  
Guy Cloutier ◽  
...  
Keyword(s):  
Numerical Analysis ◽  
Medical Images ◽  
Fluid Structure Interaction ◽  
Abdominal Aortic Aneurysms ◽  
Aortic Aneurysms ◽  
Initial Stresses ◽  
Stent Grafts ◽  
Fluid Structure ◽  
Structure Interaction ◽  
Abdominal Aortic

The purpose of this paper is to present the basic principles and relevant advances in the computational modeling of abdominal aortic aneurysms and endovascular aneurysm repair, providing the community with up-to-date state of the art in terms of numerical analysis and biomechanics. Frameworks describing the mechanical behavior of the aortic wall already exist. However, intraluminal thrombus nonhomogeneous structure and porosity still need to be well characterized. Also, although the morphology and mechanical properties of calcifications have been investigated, their effects on wall stresses remain controversial. Computational fluid dynamics usually assumes a rigid artery wall, whereas fluid-structure interaction accounts for artery compliance but is still challenging since arteries and blood have similar densities. We discuss alternatives to fluid-structure interaction based on dynamic medical images that address patient-specific hemodynamics and geometries. We describe initial stresses, elastic boundary conditions, and statistical strength for rupture risk assessment. Special emphasis is accorded to workflow development, from the conversion of medical images into finite element models, to the simulation of catheter-aorta interactions and stent-graft deployment. Our purpose is also to elaborate the key ingredients leading to virtual stenting and endovascular repair planning that could improve the procedure and stent-grafts.

scholarly journals Disruption of P2X4 purinoceptor and suppression of the inflammation associated with cerebral aneurysm formation

2019 ◽  
pp. 1-13 ◽  
Author(s):  
Miyuki Fukuda ◽  
Shunichi Fukuda ◽  
Joji Ando ◽  
Kimiko Yamamoto ◽  
Naohiro Yonemoto ◽  
...  
Keyword(s):  
Shear Stress ◽  
Cerebral Aneurysm ◽  
Arterial Wall ◽  
Quantitative Polymerase Chain Reaction ◽  
Cerebral Aneurysms ◽  
Artery Ligation ◽  
Hemodynamic Stress ◽  
Aneurysm Formation ◽  
Aneurysm Development ◽  
Cox 2

OBJECTIVEThere are no effective therapeutic drugs for cerebral aneurysms, partly because the pathogenesis remains unresolved. Chronic inflammation of the cerebral arterial wall plays an important role in aneurysm formation, but it is not clear what triggers the inflammation. The authors have observed that vascular endothelial P2X4 purinoceptor is involved in flow-sensitive mechanisms that regulate vascular remodeling. They have thus hypothesized that shear stress–associated hemodynamic stress on the endothelium causes the inflammatory process in the cerebral aneurysm development.METHODSTo test their hypothesis, the authors examined the role of P2X4 in cerebral aneurysm development by using P2X4−/− mice and rats that were treated with a P2X4 inhibitor, paroxetine, and subjected to aneurysm-inducing surgery. Cerebral aneurysms were induced by unilateral carotid artery ligation and renovascular hypertension.RESULTSThe frequency of aneurysm induction evaluated by light microscopy was significantly lower in the P2X4−/− mice (p = 0.0488) and in the paroxetine-treated male (p = 0.0253) and female (p = 0.0204) rats compared to control mice and rats, respectively. In addition, application of paroxetine from 2 weeks after surgery led to a significant reduction in aneurysm size in the rats euthanized 3 weeks after aneurysm-inducing surgery (p = 0.0145), indicating that paroxetine suppressed enlargement of formed aneurysms. The mRNA and protein expression levels of known inflammatory contributors to aneurysm formation (monocyte chemoattractant protein–1 [MCP-1], interleukin-1β [IL-1β], tumor necrosis factor–α [TNFα], inducible nitric oxide synthase [iNOS], and cyclooxygenase-2 [COX-2]) were all significantly elevated in the rats that underwent the aneurysm-inducing surgery compared to the nonsurgical group, and the values in the surgical group were all significantly decreased by paroxetine administration according to quantitative polymerase chain reaction techniques and Western blotting. Although immunolabeling densities for COX-2, iNOS, and MCP-1 were not readily observed in the nonsurgical mouse groups, such densities were clearly seen in the arterial wall of P2X4+/+ mice after aneurysm-inducing surgery. In contrast, in the P2X4−/− mice after the surgery, immunolabeling of COX-2 and iNOS was not observed in the arterial wall, whereas that of MCP-1 was readily observed in the adventitia, but not the intima.CONCLUSIONSThese data suggest that P2X4 is required for the inflammation that contributes to both cerebral aneurysm formation and growth. Enhanced shear stress–associated hemodynamic stress on the vascular endothelium may trigger cerebral aneurysm development. Paroxetine may have potential for the clinical treatment of cerebral aneurysms, given that this agent exhibits efficacy as a clinical antidepressant.

Computational Modeling and Simulation of Atherosclerotic Plaque Growth

2002 ◽  
Author(s):  
L. E. Breeher ◽  
Saikrishna Marella ◽  
H. S. Udaykumar ◽  
K. B. Chandran
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Atherosclerotic Plaque ◽  
Arterial Wall ◽  
Flow Characteristics ◽  
Plaque Formation ◽  
Constant Shear Stress ◽  
Plaque Growth ◽  
Serious Disease ◽  
Computational Modeling And Simulation

Research has been conducted by the authors with the objective to produce a computational model that will clearly display the coupled nature of the hemodynamics/fluid mechanics of blood flow and atherosclerotic plaque growth in the human carotid artery. The motivation for this investigation is the serious nature of atherosclerosis. Atherosclerosis is an inflammatory disease, which occurs in medium and large size arteries. Among the many effects stemming from the disease are heart attack, stroke, ischemia, and peripheral vascular disease. In healthy arteries, the collagen and elastin allow the artery to expand and contract with blood flow. This function enables the artery to maintain constant wall shear stress [1]. Plaque existence in the arterial wall results in decreased ductility of the wall, which inhibits the wall from maintaining constant shear stress. Plaque formations along the arterial wall then protrude into the artery, disturbing the blood flow. Characteristics of the fluid flow in the artery are also altered due to the presence of a plaque. Areas of low shear stress and recirculation move downstream from the plaque. These disturbances act not only to further the plaque formation at the site, but also to make the wall around the plaque formation more prone to lesions that could lead to new plaque initiation. Complex characteristics of the blood flow give areas of an artery such as bends and bifurcations a predisposition for the disease, whereas plaques affect blood flow, creating flow patterns that promote new plaque initiation. This interdependency makes atherosclerosis a very serious disease and one which is of great importance in research.

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