A Thick-Walled Fluid–Solid-Growth Model of Abdominal Aortic Aneurysm Evolution: Application to a Patient-Specific Geometry

2015 ◽  
Vol 137 (3) ◽  
Author(s):  
Andrii Grytsan ◽  
Paul N. Watton ◽  
Gerhard A. Holzapfel
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Vascular Disease ◽  
Arterial Wall ◽  
Cylindrical Tube ◽  
Patient Specific ◽  
Constant Density ◽  
Disease Evolution ◽  
Elastin Degradation ◽  
Abdominal Aortic

We propose a novel thick-walled fluid–solid-growth (FSG) computational framework for modeling vascular disease evolution. The arterial wall is modeled as a thick-walled nonlinearly elastic cylindrical tube consisting of two layers corresponding to the media-intima and adventitia, where each layer is treated as a fiber-reinforced material with the fibers corresponding to the collagenous component. Blood is modeled as a Newtonian fluid with constant density and viscosity; no slip and no-flux conditions are applied at the arterial wall. Disease progression is simulated by growth and remodeling (G&R) of the load bearing constituents of the wall. Adaptions of the natural reference configurations and mass densities of constituents are driven by deviations of mechanical stimuli from homeostatic levels. We apply the novel framework to model abdominal aortic aneurysm (AAA) evolution. Elastin degradation is initially prescribed to create a perturbation to the geometry which results in a local decrease in wall shear stress (WSS). Subsequent degradation of elastin is driven by low WSS and an aneurysm evolves as the elastin degrades and the collagen adapts. The influence of transmural G&R of constituents on the aneurysm development is analyzed. We observe that elastin and collagen strains evolve to be transmurally heterogeneous and this may facilitate the development of tortuosity. This multiphysics framework provides the basis for exploring the influence of transmural metabolic activity on the progression of vascular disease.

Detection of Lumen, Thrombus and Outer Wall Boundaries of an Abdominal Aortic Aneurysm From 2D Medical Images Using Level Set Methods

2008 ◽  
Author(s):  
Georgios Kossioris ◽  
Yannis Papaharilaou ◽  
Christos Zohios
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Arterial Wall ◽  
Aortic Wall ◽  
Level Set Methods ◽  
Outer Wall ◽  
Surrounding Tissue ◽  
Patient Specific ◽  
Rupture Risk ◽  
Abdominal Aortic

Abdominal aortic aneurysm (AAA) is a localized dilatation of the aortic wall. Accurate geometric characterization is critical for a reliable patient specific estimate of AAA rupture risk. However, current imaging modalities do not provide sufficient contrast between thrombus, arterial wall and surrounding tissue thus making the task of segmenting these structures very challenging.

scholarly journals A Methodology for the Derivation of Unloaded Abdominal Aortic Aneurysm Geometry With Experimental Validation

2016 ◽  
Vol 138 (10) ◽  
Author(s):  
Santanu Chandra ◽  
Vimalatharmaiyah Gnanaruban ◽  
Fabian Riveros ◽  
Jose F. Rodriguez ◽  
Ender A. Finol
Keyword(s):  
Finite Element ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Stress Component ◽  
Wall Stress ◽  
Patient Specific ◽  
Element Analysis ◽  
Nodal Surface ◽  
Abdominal Aortic ◽  
Peak Wall Stress

In this work, we present a novel method for the derivation of the unloaded geometry of an abdominal aortic aneurysm (AAA) from a pressurized geometry in turn obtained by 3D reconstruction of computed tomography (CT) images. The approach was experimentally validated with an aneurysm phantom loaded with gauge pressures of 80, 120, and 140 mm Hg. The unloaded phantom geometries estimated from these pressurized states were compared to the actual unloaded phantom geometry, resulting in mean nodal surface distances of up to 3.9% of the maximum aneurysm diameter. An in-silico verification was also performed using a patient-specific AAA mesh, resulting in maximum nodal surface distances of 8 μm after running the algorithm for eight iterations. The methodology was then applied to 12 patient-specific AAA for which their corresponding unloaded geometries were generated in 5–8 iterations. The wall mechanics resulting from finite element analysis of the pressurized (CT image-based) and unloaded geometries were compared to quantify the relative importance of using an unloaded geometry for AAA biomechanics. The pressurized AAA models underestimate peak wall stress (quantified by the first principal stress component) on average by 15% compared to the unloaded AAA models. The validation and application of the method, readily compatible with any finite element solver, underscores the importance of generating the unloaded AAA volume mesh prior to using wall stress as a biomechanical marker for rupture risk assessment.

scholarly journals A Novel Patient-Specific Human Cardiovascular System Phantom (HCSP) for Reconstructions of Pulsatile Blood Hemodynamic Inside Abdominal Aortic Aneurysm

IEEE Access ◽  
2018 ◽  
Vol 6 ◽  
pp. 61896-61903 ◽  
Author(s):  
Andrzej Polanczyk ◽  
Michal Podgorski ◽  
Maciej Polanczyk ◽  
Aleksandra Piechota-Polanczyk ◽  
Christoph Neumayer ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Cardiovascular System ◽  
Patient Specific ◽  
Abdominal Aortic ◽  
Human Cardiovascular System

scholarly journals A preclinical ultrasound method for the assessment of vascular disease progression in murine models

Ultrasound ◽  
2018 ◽  
Vol 27 (2) ◽  
pp. 85-93
Author(s):  
Justyna Janus ◽  
Baris Kanber ◽  
Wadhah Mahbuba ◽  
Charlotte Beynon ◽  
Kumar V Ramnarine ◽  
...  
Keyword(s):  
Image Processing ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Vascular Disease ◽  
Mouse Models ◽  
Murine Models ◽  
Analysis Method ◽  
Manual Analysis ◽  
Abdominal Aortic ◽  
Automatic Image Processing

Introduction The efficacy of preclinical ultrasound at providing a quantitative assessment of mouse models of vascular disease is relatively unknown. In this study, preclinical ultrasound was used in combination with a semi-automatic image processing method to track arterial distension alterations in mouse models of abdominal aortic aneurysm and atherosclerosis. Methods Longitudinal B-mode ultrasound images of the abdominal aorta were acquired using a preclinical ultrasound scanner. Arterial distension was assessed using a semi-automatic image processing algorithm to track vessel wall motion over the cardiac cycle. A standard, manual analysis method was applied for comparison. Results Mean arterial distension was significantly lower in abdominal aortic aneurysm mice between day 0 and day 7 post-onset of disease (p < 0.01) and between day 0 and day 14 (p < 0.001), while no difference was observed in sham control mice. Manual analysis detected a significant decrease (p < 0.05) between day 0 and day 14 only. Atherosclerotic mice showed alterations in arterial distension relating to genetic modification and diet. Arterial distension was significantly lower (p < 0.05) in Ldlr−/− (++/−−) mice fed high-fat western diet when compared with both wild type (++/++) mice and Ldlr−/− (++/−−) mice fed chow diet. The manual method did not detect a significant difference between these groups. Conclusions Arterial distension can be used as an early marker for the detection of arterial disease in murine models. The semi-automatic analysis method provided increased sensitivity to differences between experimental groups when compared to the manual analysis method.

scholarly journals IKK Epsilon Deficiency Attenuates Angiotensin II-Induced Abdominal Aortic Aneurysm Formation in Mice by Inhibiting Inflammation, Oxidative Stress, and Apoptosis

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Hao Chai ◽  
ZhongHao Tao ◽  
YongChao Qi ◽  
HaoYu Qi ◽  
Wen Chen ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Angiotensin Ii ◽  
Aortic Aneurysm ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Ang Ii ◽  
Elastin Degradation ◽  
Maximal Diameter ◽  
Abdominal Aortic ◽  
Primary Mouse

Abdominal aortic aneurysm (AAA) is a vascular disorder that is considered a chronic inflammatory disease. However, the precise molecular mechanisms involved in AAA have not been fully elucidated. Recently, significant progress has been made in understanding the function and mechanism of action of inhibitor of kappa B kinase epsilon (IKKε) in inflammatory and metabolic diseases. The angiotensin II- (Ang II-) induced or pharmacological inhibitors were established to test the effects of IKKε on AAA in vivo. After mice were continuously stimulated with Ang II for 28 days, morphologically, we found that knockout of IKKε reduced AAA formation and drastically reduced maximal diameter and severity. We also observed a decrease in elastin degradation and medial destruction, which were independent of systolic blood pressure or plasma cholesterol concentrations. Western blot analyses and immunohistochemical staining were carried out to measure IKKε expression in AAA tissues and cell lines. AAA phenotype of mice was measured by ultrasound and biochemical indexes. In zymography, immunohistology staining, immunofluorescence staining, and reactive oxygen species (ROS) analysis, TUNEL assay was used to examine the effects of IKKε on AAA progression in AAA mice. IKKε deficiency significantly inhibited inflammatory macrophage infiltration, matrix metalloproteinase (MMP) activity, ROS production, and vascular smooth muscle cell (VSMC) apoptosis. We used primary mouse aortic VSMC isolated from apolipoprotein E (Apoe) −/− and Apoe−/−IKKε−/− mice. Mechanistically, IKKε deficiency blunted the activation of the ERK1/2 pathway. The IKKε inhibitor, amlexanox, has the same impact in AAA. Our results demonstrate a critical role of IKKε in AAA formation induced by Ang II in Apoe−/− mice. Targeting IKKε may constitute a novel therapeutic strategy to prevent AAA progression.

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