Identification of in vivo material and geometric parameters of a human aorta: toward patient-specific modeling of abdominal aortic aneurysm

2010 ◽  
Vol 10 (5) ◽  
pp. 689-699 ◽  
Author(s):  
Shahrokh Zeinali-Davarani ◽  
L. Guy Raguin ◽  
David A. Vorp ◽  
Seungik Baek
Author(s):  
S. Zeinali-Davarani ◽  
A. Sheidaei ◽  
S. Baek

There has been a clear need for better understanding of the progression of abdominal aortic aneurysm (AAA) and obtaining reliable prediction of the AAA rupture. Finite element analysis (FEA) using non-axisymmetric models of AAAs provides better estimation of stress distribution in the aneurysmal wall with complex shapes [1]. However, FEA alone does not provide a mathematical description for the evolution of an AAA through growth and remodeling (G&R). A computational framework for modeling stress-mediated growth and structural remodeling of the arterial wall under physiological and pathological conditions has been suggested using a constrained mixture assumption [2]. Stress-mediated enlargement of intracranial aneurysms has been investigated using idealized axisymmetric geometries [3,4]. The kinetics of stress-mediated turnover of collagen fiber families and degradation of elastin were found to have particular importance in the G&R of aneurysmal wall.


2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Eduardo Soudah ◽  
E. Y. K. Ng ◽  
T. H. Loong ◽  
Maurizio Bordone ◽  
Uei Pua ◽  
...  

The objective of this study is to find a correlation between the abdominal aortic aneurysm (AAA) geometric parameters, wall stress shear (WSS), abdominal flow patterns, intraluminal thrombus (ILT), and AAA arterial wall rupture using computational fluid dynamics (CFD). Real AAA 3D models were created by three-dimensional (3D) reconstruction of in vivo acquired computed tomography (CT) images from 5 patients. Based on 3D AAA models, high quality volume meshes were created using an optimal tetrahedral aspect ratio for the whole domain. In order to quantify the WSS and the recirculation inside the AAA, a 3D CFD using finite elements analysis was used. The CFD computation was performed assuming that the arterial wall is rigid and the blood is considered a homogeneous Newtonian fluid with a density of 1050 kg/m3and a kinematic viscosity of4×10-3Pa·s. Parallelization procedures were used in order to increase the performance of the CFD calculations. A relation between AAA geometric parameters (asymmetry index (β), saccular index (γ), deformation diameter ratio (χ), and tortuosity index (ε)) and hemodynamic loads was observed, and it could be used as a potential predictor of AAA arterial wall rupture and potential ILT formation.


Author(s):  
Samarth S. Raut ◽  
Anirban Jana ◽  
Satish C. Muluk ◽  
Mark Doyle ◽  
Robert W. Biederman ◽  
...  

Abdominal Aortic Aneurysm (AAA) is a localized permanent dilatation occurring in abdominal region of the aorta. Nearly 8% of the population above 65 years old is diagnosed with this disease [1], which has been shown to be associated with smoking history, heredity, and male gender. As it is asymptomatic, vascular surgeons may opt for surgical intervention or follow a wait-and-watch strategy if their assessment of the risk of rupture is low. During surgical intervention grafts are placed inside the aorta. Design of such intravascular devices as well as monitoring the progression of the disease by means of scientific approach may benefit from information on the strains that occur in the aneurysmatic region at different instances due to cyclic internal pressurization during cardiac cycle.


2011 ◽  
Vol 5 (2) ◽  
Author(s):  
Polina A. Segalova ◽  
Guanglei Xiong ◽  
K. T. Rao ◽  
Christopher K. Zarins ◽  
Charles A. Taylor

2010 ◽  
Vol 39 (1) ◽  
pp. 42-48 ◽  
Author(s):  
E. Georgakarakos ◽  
C.V. Ioannou ◽  
Y. Kamarianakis ◽  
Y. Papaharilaou ◽  
T. Kostas ◽  
...  

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Dawn A Savio ◽  
Anita R Halpern ◽  
Yuchuan Wu ◽  
Wei Li ◽  
Joseph Sypek ◽  
...  

Abdominal aortic aneurysm (AAA) is an inflammatory disorder characterized by local connective tissue degradation, macrophage recruitment and infiltration leading to aortic dilation and rupture. Aneurysms of the abdominal aorta represent a significant cardiovascular risk for which inflammation plays an integral role in the defined pathology. Genetic ablation of metalloprotease-12 (MMP-12) eliminates metalloelastase activity and attenuates aneurysm formation in apoE−/− mice. In the current study, a selective MMP-12 inhibitor, WAY-644 was evaluated in the well-established murine model of ANGII-induced aneurysm formation. This inhibitor displays activity for murine MMP-12, IC50 = 6.3 nM by FRET analysis, with low crossreactivity for other MMPs (exception MMP-8), and has established in vivo efficacy in inflammation models. Coadministration of WAY-644 to hyperlipidemic apoE−/− mice during ANGII infusion (1.44 mg/kg) for 28d alters the severity of AngII-induced AAAs as measured by changes in abdominal aortic wet weights and typical AAA classification. As expected, plasma MMP-12 protease activity measured by FRET analysis was inhibited. RNA profiling of abdominal aortic aneurysm tissue characterizes ANGII-induced AAA expansion driven by macrophage infiltration, destructive MMP production and attenuation by MMP-12 inhibition. The transcription of a subset of proinflammatory genes activated with ANGII treatment was repressed by the inhibitor. These genes include quantitative markers of macrophage accumulation in the vessel wall, CD68, MCP1/CCL2, CCR2, MMP-12, and Csf1. Associated reductions in gene markers for inflammation and oxidative stress, ie., heme oxidase (HO), nitric oxide synthase (nos2), Ikbkb, and Stat3 also correlate with MMP-12 antagonism. These changes occur in the absence of lipid changes (TC or TG), or quantitative changes in aortic arch lesions in the ANGII-infused animals. The findings support a mechanism whereby MMP-12 metalloelastase inactivation reduces macrophage recruitment to aneurysmal lesion sites, to lessen activated-macrophage expression of proinflammatory cytokines that figure prominently in vascular wall destruction and the pathogenesis of AAAs.


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