A simulation framework for estimating wall stress distribution of abdominal aortic aneurysm

Author(s):  
Jing Qin ◽  
Jing Zhang ◽  
Chee-Kong Chui ◽  
Wei-Min Huang ◽  
Tao Yang ◽  
...  
2000 ◽  
Vol 31 (4) ◽  
pp. 760-769 ◽  
Author(s):  
M.L. Raghavan ◽  
David A. Vorp ◽  
Michael P. Federle ◽  
Michel S. Makaroun ◽  
Marshall W. Webster

2001 ◽  
Vol 15 (3) ◽  
pp. 355-366 ◽  
Author(s):  
Mano J. Thubrikar ◽  
Jihad Al-Soudi ◽  
Francis Robicsek

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

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Uwe Raaz ◽  
Alexander M Zöllner ◽  
Ryuji Toh ◽  
Futoshi Nakagami ◽  
Isabel N Schellinger ◽  
...  

Stiffening of the aortic wall is a phenomenon consistently observed in abdominal aortic aneurysm (AAA). However, its role in AAA pathophysiology is largely undefined. Using an established murine elastase-induced AAA model, we demonstrate that segmental aortic stiffening (SAS) precedes aneurysm growth. Finite elements analysis (FEA)-based wall stress calculations reveal that early stiffening of the aneurysm-prone aortic segment leads to axial (longitudinal) stress generated by cyclic (systolic) tethering of adjacent, more compliant wall segments. Interventional stiffening of AAA-adjacent segments (via external application of surgical adhesive) significantly reduces aneurysm growth. These changes correlate with reduced segmental stiffness of the AAA-prone aorta (due to equalized stiffness in adjacent aortic segments), reduced axial wall stress, decreased production of reactive oxygen species (ROS), attenuated elastin breakdown, and decreased expression of inflammatory cytokines and macrophage infiltration, as well as attenuated apoptosis within the aortic wall. Cyclic pressurization of stiffened aortic segments ex vivo increases the expression of genes related to inflammation and extracellular matrix (ECM) remodeling. Finally, human ultrasound studies reveal that aging, a significant AAA risk factor, is accompanied by segmental infrarenal aortic stiffening. The present study introduces the novel concept of segmental aortic stiffening (SAS) as an early pathomechanism generating aortic wall stress and thereby triggering AAA growth. Therefore monitoring SAS by ultrasound might help to better identify patients at risk for AAA disease and better predict the susceptibility of small AAA to further growth. Moreover our results suggest that interventional mechanical stiffening of the AAA-adjacent aorta may be further tested as a novel treatment option to limit early AAA growth.


2016 ◽  
Vol 138 (10) ◽  
Author(s):  
Santanu Chandra ◽  
Vimalatharmaiyah Gnanaruban ◽  
Fabian Riveros ◽  
Jose F. Rodriguez ◽  
Ender A. Finol

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.


2012 ◽  
Vol 12 (01) ◽  
pp. 1250005 ◽  
Author(s):  
MAMADOU TOUNGARA ◽  
GREGORY CHAGNON ◽  
CHRISTIAN GEINDREAU

Recently, hyperelastic mechanical models were proposed to well capture the aneurismal arterial wall anisotropic and nonlinear features experimentally observed. These models were formulated assuming the material incompressibility. However in numerical analysis, a nearly incompressible approach, i.e., a mixed formulation pressure-displacement, is usually adopted to perform finite element stress analysis of abdominal aortic aneurysm (AAA). Therefore, volume variations of the material are controlled through the volumetric energy which depends on the initial bulk modulus κ. In this paper, an analytical analysis of the influence of κ on the mechanical response of two invariant-based anisotropic models is first performed in the case of an equibiaxial tensile test. This analysis shows that for the strongly nonlinear anisotropic model, even in a restricted range of deformations, large values of κ are necessary to ensure the incompressibility condition, in order to estimate the wall stress with a reasonable precision. Finite element simulations on idealized AAA geometries are then performed. Results from these simulations show that the maximum stress in the AAA wall is underestimated in previous works, committed errors vary from 26% to 58% depending on the geometrical model complexity. In addition to affect the magnitude of the maximum stress in the aneurysm, we found that too small value of κ may also affect the location of this stress.


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