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      Endoleak Assessment Using Computational Fluid Dynamics and Image Processing Methods in Stented Abdominal Aortic Aneurysm Models

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          Abstract

          Endovascular aortic aneurysm repair (EVAR) is a predominant surgical procedure to reduce the risk of aneurysm rupture in abdominal aortic aneurysm (AAA) patients. Endoleak formation, which eventually requires additional surgical reoperation, is a major EVAR complication. Understanding the etiology and evolution of endoleak from the hemodynamic perspective is crucial to advancing the current posttreatments for AAA patients who underwent EVAR. Therefore, a comprehensive flow assessment was performed to investigate the relationship between endoleak and its surrounding pathological flow fields through computational fluid dynamics and image processing. Six patient-specific models were reconstructed, and the associated hemodynamics in these models was quantified three-dimensionally to calculate wall stress. To provide a high degree of clinical relevance, the mechanical stress distribution calculated from the models was compared with the endoleak positions identified from the computed tomography images of patients through a series of imaging processing methods. An endoleak possibly forms in a location with high local wall stress. An improved stent graft (SG) structure is conceived accordingly by increasing the mechanical strength of the SG at peak wall stress locations. The presented analytical paradigm, as well as numerical analysis using patient-specific models, may be extended to other common human cardiovascular surgeries.

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          Most cited references33

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          Decreased vascular smooth muscle cell density in medial degeneration of human abdominal aortic aneurysms.

          Abdominal aortic aneurysms (AAAs) are characterized by structural deterioration of the aortic wall leading to progressive aortic dilatation and eventual rupture. The histopathological changes in AAAs are particularly evident within the elastic media, which is normally dominated by vascular smooth muscle cells (SMCs). To determine whether a decrease in vascular SMCs contributes to medial degeneration, we measured SMC density in 21 normal and pathological human abdominal aortic tissue specimens using immunohistochemistry for alpha-SMC actin and direct cell counts (medial SMCs per high-power field (HPF)). Medial SMC density was not significantly different between normal aorta (n = 5; 199.5 +/- 14.9 SMCs/HPF) and atherosclerotic occlusive disease (n = 6; 176.4 +/- 13.9 SMCs/HPF), but it was reduced by 74% in AAA (n = 10; 50.9 +/- 6.1 SMCs/HPF; P < 0.01 versus normal aorta). Light and electron microscopy revealed no evidence of overt cellular necrosis, but SMCs in AAAs exhibited ultrastructural changes consistent with apoptosis. Using in situ end-labeling (ISEL) of fragmented DNA to detect apoptotic cells, up to 30% of aortic wall cells were ISEL positive in AAAs. By double-labeling techniques, many of these cells were alpha-actin-positive SMCs distributed throughout the degenerative media. In contrast, ISEL-positive cells were observed only within the intimal plaque in atherosclerotic occlusive disease. The amount of p53 protein detected by immunoblotting was increased nearly fourfold in AAA compared with normal aorta and atherosclerotic occlusive disease (P < 0.01), and immunoreactive p53 was localized to lymphocytes and residual SMCs in the aneurysm wall. Using reverse transcription polymerase chain reaction assays a substantial amount of p53 mRNA expression was observed in AAAs. These results demonstrate that medial SMC density is significantly decreased in human AAA tissues associated with evidence of SMC apoptosis and increased production of p53, a potential mediator of cell cycle arrest and programmed cell death. Given the role that SMCs normally play in maintaining medial architecture and in arterial wall matrix remodeling, the induction of SMC apoptosis likely makes an important contribution to the evolution of aneurysm degeneration.
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            Current concepts in the pathogenesis of abdominal aortic aneurysm.

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              Fluid-structure interaction within realistic three-dimensional models of the aneurysmatic aorta as a guidance to assess the risk of rupture of the aneurysm.

              Abdominal aortic aneurysm (AAA) disease is a degenerating process whose ultimate event is the rupture of the vessel wall. Rupture occurs when the stresses acting on the wall rise above the strength of the AAA wall tissue. The complex mechanical interaction between blood flow and wall dynamics in a three dimensional custom model of a patient AAA was studied by means of computational coupled fluid-structure interaction analysis. Real 3D AAA geometry is obtained from CT scans image processing. The results provide a quantitative local evaluation of the stresses due to local structural and fluid dynamic conditions. The method accounts for the complex geometry of the aneurysm, the presence of a thrombus and the interaction between solid and fluid. A proven clinical efficacy may promote the method as a tool to determine factual aneurysm risk of rupture and aid the surgeon to refer elective surgery patients.
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                Author and article information

                Journal
                Comput Math Methods Med
                Comput Math Methods Med
                CMMM
                Computational and Mathematical Methods in Medicine
                Hindawi Publishing Corporation
                1748-670X
                1748-6718
                2016
                31 August 2016
                : 2016
                : 9567294
                Affiliations
                1Department of Radiology, Taipei City Hospital, Zhongxing Branch, Taipei 103, Taiwan
                2National Yang-Ming University, Taipei 112, Taiwan
                3Department of Mechanical Engineering, National Cheng Kung University, Tainan 701, Taiwan
                Author notes

                Academic Editor: Xiaopeng Zhao

                Author information
                http://orcid.org/0000-0002-4112-892X
                Article
                10.1155/2016/9567294
                5021907
                42d916ea-05ad-4244-a419-035130aa78c8
                Copyright © 2016 Yueh-Hsun Lu et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 1 April 2016
                : 2 July 2016
                : 9 August 2016
                Funding
                Funded by: Ministry of Science and Technology of Taiwan
                Award ID: MOST 105-2628-E-006-006-MY3
                Award ID: 104-2221-E-006-169
                Categories
                Research Article

                Applied mathematics
                Applied mathematics

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