Reproducibility of Thrombus Volume Quantification and Aortic Wall Stress in Abdominal Aortic Aneurysm

2021 ◽  
Vol 30 ◽  
pp. S203-S204
Author(s):  
T. Singh
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Wall Stress ◽  
Abdominal Aortic

Abstract 297: Segmental Aortic Stiffening is a Mechanism Driving Early Abdominal Aortic Aneurysm Pathogenesis

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Uwe Raaz ◽  
Alexander M Zöllner ◽  
Ryuji Toh ◽  
Futoshi Nakagami ◽  
Isabel N Schellinger ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Ex Vivo ◽  
Wall Stress ◽  
Finite Elements Analysis ◽  
External Application ◽  
Abdominal Aortic ◽  
Aneurysm Growth ◽  
Aortic Stiffening

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.

scholarly journals Analysis of aortic wall stress and rupture risk in patients with abdominal aortic aneurysm with a gender perspective

2011 ◽  
Vol 54 (2) ◽  
pp. 295-299 ◽  
Author(s):  
Emma Larsson ◽  
Fausto Labruto ◽  
T. Christian Gasser ◽  
Jesper Swedenborg ◽  
Rebecka Hultgren
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Wall Stress ◽  
Rupture Risk ◽  
Gender Perspective ◽  
Abdominal Aortic

scholarly journals Segmental Aortic Stiffening Contributes to Experimental Abdominal Aortic Aneurysm Development

Circulation ◽  
2015 ◽  
Vol 131 (20) ◽  
pp. 1783-1795 ◽  
Author(s):  
Uwe Raaz ◽  
Alexander M. Zöllner ◽  
Isabel N. Schellinger ◽  
Ryuji Toh ◽  
Futoshi Nakagami ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Molecular Mechanisms ◽  
Aortic Wall ◽  
Ex Vivo ◽  
Wall Stress ◽  
External Application ◽  
Abdominal Aortic ◽  
Aneurysm Growth ◽  
Aortic Stiffening

Background— Stiffening of the aortic wall is a phenomenon consistently observed in age and in abdominal aortic aneurysm (AAA). However, its role in AAA pathophysiology is largely undefined. Methods and Results— Using an established murine elastase-induced AAA model, we demonstrate that segmental aortic stiffening precedes aneurysm growth. Finite-element analysis reveals that early stiffening of the aneurysm-prone aortic segment leads to axial (longitudinal) wall stress generated by cyclic (systolic) tethering of adjacent, more compliant wall segments. Interventional stiffening of AAA-adjacent aortic segments (via external application of surgical adhesive) significantly reduces aneurysm growth. These changes correlate with the reduced segmental stiffness of the AAA-prone aorta (attributable to equalized stiffness in adjacent segments), reduced axial wall stress, decreased production of reactive oxygen species, attenuated elastin breakdown, and decreased expression of inflammatory cytokines and macrophage infiltration, and attenuated apoptosis within the aortic wall, as well. Cyclic pressurization of segmentally stiffened aortic segments ex vivo increases the expression of genes related to inflammation and extracellular matrix remodeling. Finally, human ultrasound studies reveal that aging, a significant AAA risk factor, is accompanied by segmental infrarenal aortic stiffening. Conclusions— The present study introduces the novel concept of segmental aortic stiffening as an early pathomechanism generating aortic wall stress and triggering aneurysmal growth, thereby delineating potential underlying molecular mechanisms and therapeutic targets. In addition, monitoring segmental aortic stiffening may aid the identification of patients at risk for AAA.

Wall Stress Studies of Abdominal Aortic Aneurysm in a Clinical Model

2001 ◽  
Vol 15 (3) ◽  
pp. 355-366 ◽  
Author(s):  
Mano J. Thubrikar ◽  
Jihad Al-Soudi ◽  
Francis Robicsek
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Wall Stress ◽  
Clinical Model ◽  
Stress Studies ◽  
Abdominal Aortic

scholarly journals The Role of Geometric Parameters in the Prediction of Abdominal Aortic Aneurysm Wall Stress

2010 ◽  
Vol 39 (1) ◽  
pp. 42-48 ◽  
Author(s):  
E. Georgakarakos ◽  
C.V. Ioannou ◽  
Y. Kamarianakis ◽  
Y. Papaharilaou ◽  
T. Kostas ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Wall Stress ◽  
Geometric Parameters ◽  
Aneurysm Wall ◽  
Abdominal Aortic ◽  
Abdominal Aortic Aneurysm Wall

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 The relationship between aortic wall distensibility and rupture of infrarenal abdominal aortic aneurysm

2003 ◽  
Vol 37 (1) ◽  
pp. 112-117 ◽  
Author(s):  
Katie A. Wilson ◽  
Amanda J. Lee ◽  
Amanda J. Lee ◽  
Peter R. Hoskins ◽  
F.Gerry R. Fowkes ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Infrarenal Abdominal Aortic Aneurysm ◽  
Abdominal Aortic ◽  
The Relationship ◽  
Wall Distensibility

Abstract 667: The Role of Aortic Wall-Nuclear Factor- kappa B (NF-kB) Signaling in Formation of Dissecting Aortic Aneurysms

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Talha Ijaz ◽  
Hong Sun ◽  
Adrian Recinos ◽  
Ronald G Tilton ◽  
Allan R Brasier
Keyword(s):  
Flow Cytometry ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Aortic Rupture ◽  
Aortic Aneurysms ◽  
Tunel Staining ◽  
Abdominal Aortic ◽  
Significant Difference

Introduction: Abdominal aortic aneurysm is a devastating disease since it can lead to aortic rupture and instantaneous death. We previously demonstrated that IL-6 secreted from the aortic wall is necessary for the development of abdominal aortic aneurysm and dissection (AAD). Since IL-6 is a NF-kB/RelA dependant gene, we investigated the role of aortic wall- NF-kB/RelA signaling in the development of AAD. Methods and Results: To test the role of aortic wall-RelA, we utilized Cre-Lox technology to delete RelA from aortic cells. Tamoxifen-inducible, Col1a2-promoter driven Cre mice (Col1a2-Cre) were crossed with mT/mG Cre-reporter mice to determine which aortic cells undergo genetic recombination after Cre activation. Flow cytometry analysis of the aortic wall indicated that 88% of the genetically recombined cells were SMCs and 8% were fibroblasts. Next, RelA floxed (RelA f/f) mice, generated in our lab, were crossed with Col1a2-Cre mice. RelA f/f Cre+ and RelA f/f Cre- were stimulated with tamoxifen for 10 days to generate aortic-RelA deficient (Ao-RelA-/-) or wild-type (Ao-RelA+/+) transgenics. Flow cytometry, qRT-PCR, and immunohistochemistry analysis suggested a depletion of aortic-RelA greater than 60%. To test the role of Ao-RelA in AAD, Ao-RelA -/- (n= 20) and Ao-RelA +/+ (n=14) mice were infused with angiotensin II for 7 days. Surprisingly, 20% of Ao-RelA-/- mice died from development of AAD and aortic rupture while no deaths were observed in Ao-RelA+/+ group. In addition, 40% of Ao-RelA-/- mice developed AAD compared to 14% of Ao-RelA+/+ mice. There was no significant difference in TUNEL staining or ERTR7+ fibroblast population between the two groups. Conclusion: Our studies suggest that aortic wall-RelA may be necessary for protection from AAD.

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