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Identification of rupture locations in patient-specific abdominal aortic aneurysms using experimental and computational techniques.

ABSTRACT: In the event of abdominal aortic aneurysm (AAA) rupture, the outcome is often death. This paper aims to experimentally identify the rupture locations of in vitro AAA models and validate these rupture sites using finite element analysis (FEA). Silicone rubber AAA models were manufactured using two different materials (Sylgard 160 and Sylgard 170, Dow Corning) and imaged using computed tomography (CT). Experimental models were inflated until rupture with high speed photography used to capture the site of rupture. 3D reconstructions from CT scans and subsequent FEA of these models enabled the wall stress and wall thickness to be determined for each of the geometries. Experimental models ruptured at regions of inflection, not at regions of maximum diameter. Rupture pressures (mean+/-SD) for the Sylgard 160 and Sylgard 170 models were 650.6+/-195.1mmHg and 410.7+/-159.9mmHg, respectively. Computational models accurately predicted the locations of rupture. Peak wall stress for the Sylgard 160 and Sylgard 170 models was 2.15+/-0.26MPa at an internal pressure of 650mmHg and 1.69+/-0.38MPa at an internal pressure of 410mmHg, respectively. Mean wall thickness of all models was 2.19+/-0.40mm, with a mean wall thickness at the location of rupture of 1.85+/-0.33 and 1.71+/-0.29mm for the Sylgard 160 and Sylgard 170 materials, respectively. Rupture occurred at the location of peak stress in 80% (16/20) of cases and at high stress regions but not peak stress in 10% (2/20) of cases. 10% (2/20) of models had defects in the AAA wall which moved the rupture location away from regions of elevated stress. The results presented may further contribute to the understanding of AAA biomechanics and ultimately AAA rupture prediction.

SUBMITTER: Doyle BJ

PROVIDER: S-EPMC2857518 | biostudies-literature | 2010 May

REPOSITORIES: biostudies-literature

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Identification of rupture locations in patient-specific abdominal aortic aneurysms using experimental and computational techniques.

Doyle Barry J BJ Cloonan Aidan J AJ Walsh Michael T MT Vorp David A DA McGloughlin Timothy M TM

Journal of biomechanics 20100212 7

In the event of abdominal aortic aneurysm (AAA) rupture, the outcome is often death. This paper aims to experimentally identify the rupture locations of in vitro AAA models and validate these rupture sites using finite element analysis (FEA). Silicone rubber AAA models were manufactured using two different materials (Sylgard 160 and Sylgard 170, Dow Corning) and imaged using computed tomography (CT). Experimental models were inflated until rupture with high speed photography used to capture the ...[more]

PMID: 20152982

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Project description:Background Abdominal aortic aneurysms (AAA) are characterized by vascular inflammation and remodeling that can lead to aortic rupture resulting in significant mortality. Pannexin-1 channels on endothelial cells (ECs) can modulate ATP secretion to regulate the pathogenesis of AAA formation. Our hypothesis focused on potential of spironolactone to inhibit EC-mediated ATP release for the mitigation of AAA formation. Methods A topical elastase AAA model was used initially in C57BL/6 (wild-type; WT) male mice. Mice were administered either a vehicle control (saline) or spironolactone and analyzed on day 14. In a second chronic AAA model, mice were subjected to elastase and β-aminopropionitrile (BAPN) treatment with/without administration of spironolactone to pre-formed aneurysms starting on day 14 and analyzed on day 28. Aortic diameter was evaluated by video micrometry and aortic tissue was analyzed for cytokine expression and histology. ATP measurement and matrix metalloproteinase (MMP2) activity was evaluated in aortic tissue on days 14 or -28. In vitro studies were performed to evaluate the crosstalk between aortic ECs with macrophages or smooth muscle cells. Results In the elastase AAA model, spironolactone treatment displayed a significant decrease in aortic diameter compared to elastase-treated controls on day 14. A significant increase in smooth muscle α-actin expression as well as decrease in elastic fiber disruption and immune cell (macrophages and neutrophils) infiltration was observed in mice treated with spironolactone compared to saline-treated controls. Spironolactone treatment also significantly mitigated pro-inflammatory cytokine expression, MMP2 activity and ATP content in aortic tissue compared to controls. Moreover, in the chronic AAA model, spironolactone treatment of pre-formed aneurysms significantly attenuated vascular inflammation and remodeling to attenuate the progression of AAAs compared to controls. Mechanistically, in vitro data demonstrated that spironolactone treatment attenuates extracellular ATP release from endothelial cells to mitigate macrophage activation (IL-1β and HMGB1 expression) and smooth muscle cell-dependent vascular remodeling (MMP2 activity). Conclusion These results demonstrate that spironolactone can mitigate aortic inflammation and remodeling to attenuate AAA formation as well as decrease growth of pre-formed aneurysms via inhibition of EC-dependent ATP release. Therefore, this study implicates a therapeutic application of spironolactone in the treatment of AAAs.

Dataset Information

Identification of rupture locations in patient-specific abdominal aortic aneurysms using experimental and computational techniques.

Publications

Identification of rupture locations in patient-specific abdominal aortic aneurysms using experimental and computational techniques.

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