Mechanism of sac expansion without evident endoleak analyzed with X ray phase-contrast tomography
Objective: Synchrotron radiation-based X ray phase-contrast tomography (XPCT) was used in this study to evaluate abdominal aorta specimens from patients with sac expansion without evidence of an endoleak (endotension) following endovascular aortic repair (EVAR) for an abdominal aortic aneurysm (AAA)...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Takateru Yamamoto, MD [verfasserIn] Takuro Tsukube, MD, PhD [verfasserIn] Yuko Wada, MD, PhD [verfasserIn] Masato Hoshino, PhD [verfasserIn] Naoto Yagi, PhD [verfasserIn] Kazunori Nakagawa, PhD [verfasserIn] Yutaka Nakashima, MD, PhD [verfasserIn] Kenji Okada, MD, PhD [verfasserIn] Tatsuichiro Seto, MD, PhD [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2023 |
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| Schlagwörter: |
Stent graft-induced aortopathy |
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| Übergeordnetes Werk: |
In: JVS - Vascular Science - Elsevier, 2021, 4(2023), Seite 100123- |
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| Übergeordnetes Werk: |
volume:4 ; year:2023 ; pages:100123- |
| Links: |
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| DOI / URN: |
10.1016/j.jvssci.2023.100123 |
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| Katalog-ID: |
DOAJ097968978 |
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| 520 | |a Objective: Synchrotron radiation-based X ray phase-contrast tomography (XPCT) was used in this study to evaluate abdominal aorta specimens from patients with sac expansion without evidence of an endoleak (endotension) following endovascular aortic repair (EVAR) for an abdominal aortic aneurysm (AAA). The aim of this study was to analyze the morphologic structure of the aortic wall in patients with this condition and to establish the cause of the endotension. Methods: Human aortic specimens of the abdominal aorta were obtained during open repair, fixed with formalin, and analyzed among three groups. Group A was specimens from open abdominal aortic aneurysm repairs (n = 7). Group E was specimens from sac expansion without an evident endoleak after EVAR (n = 7). Group N was specimens from non-aneurysmal “normal” cadaveric abdominal aortas (n = 5). Using XPCT (effective voxel size, 12.5 μm; density resolution, 1 mg/cm3), we measured the density of the tunica media (TM) in six regions of each sample. Then, any changes to the elastic lamina and the vasa vasorum were analyzed pathologically. The specimens were immunohistochemically examined with anti-CD31 and vascular endothelial growth factor antibodies. Results: The time from EVAR to open aortic repair was 64.2 ± 7.2 months. There were significant differences in the thickness of the TM among three groups: 0.98 ± 0.03 mm in Group N; 0.31 ± 0.01 mm in Group A; and 0.15 ± 0.03 mm in Group E (P < .005). There were significant differences in the TM density among the groups: 1.087 ± 0.004 g/cm3 in Group N; 1.070 ± 0.001 g/cm3 in Group A; and 1.062 ± 0.007 g/cm3 in Group E (P < .005). Differences in the thickness and density of the TM correlated with the thickness of the elastic lamina; in Group N, uniform high-density elastic fibers were observed in the TM. By contrast, a thinning of the elastic lamina in the TM was observed in Group A. A marked thinness and loss of elastic fibers was observed in Group E. CD31 immunostaining revealed that the vasa vasorum was localized in the adventitia and inside the outer third of the TM in Group N, and in the middle of the TM in Group A. In Group E, the vasa vasorum advanced up to the intima with vascular endothelial growth factor-positive cells in the intimal section. Conclusions: XPCT could be used to demonstrate the densitometric property of the aortic aneurysmal wall after EVAR. We confirmed that the deformation process that occurs in the sac expansion after EVAR without evidence of an endoleak could be explained by hypoxia in the aortic wall. : Clinical Relevance: The pathophysiology of the sac expansion without evidence of an endoleak (endotension) following EVAR remains an enigma. Several theories have been proposed regarding the cause of endotension, including the presence of blood flow below the sensitivity limits of current imaging modalities, pressure transmission through a thrombus or endograft fabric, and the presence of microleak or ultrafiltration. We demonstrated the marked thinning of the elastic lamella and neovascularization in the TM and the intima and proposed that the insertion of a stent graft into an aortic aneurysm may worsen the hypoxic conditions of the aneurysmal wall. | ||
| 650 | 4 | |a Endovascular aortic repair | |
| 650 | 4 | |a Sac expansion | |
| 650 | 4 | |a Stent graft-induced aortopathy | |
| 650 | 4 | |a Synchrotron radiation-based X-ray phase-contrast tomography | |
| 650 | 4 | |a Tissue density | |
| 653 | 0 | |a Diseases of the circulatory (Cardiovascular) system | |
| 700 | 0 | |a Takuro Tsukube, MD, PhD |e verfasserin |4 aut | |
| 700 | 0 | |a Yuko Wada, MD, PhD |e verfasserin |4 aut | |
| 700 | 0 | |a Masato Hoshino, PhD |e verfasserin |4 aut | |
| 700 | 0 | |a Naoto Yagi, PhD |e verfasserin |4 aut | |
| 700 | 0 | |a Kazunori Nakagawa, PhD |e verfasserin |4 aut | |
| 700 | 0 | |a Yutaka Nakashima, MD, PhD |e verfasserin |4 aut | |
| 700 | 0 | |a Kenji Okada, MD, PhD |e verfasserin |4 aut | |
| 700 | 0 | |a Tatsuichiro Seto, MD, PhD |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i In |t JVS - Vascular Science |d Elsevier, 2021 |g 4(2023), Seite 100123- |w (DE-627)1755580096 |x 26663503 |7 nnns |
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10.1016/j.jvssci.2023.100123 doi (DE-627)DOAJ097968978 (DE-599)DOAJb727ca92199546b4902aaad51b00d2b1 DE-627 ger DE-627 rakwb eng RC666-701 Takateru Yamamoto, MD verfasserin aut Mechanism of sac expansion without evident endoleak analyzed with X ray phase-contrast tomography 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective: Synchrotron radiation-based X ray phase-contrast tomography (XPCT) was used in this study to evaluate abdominal aorta specimens from patients with sac expansion without evidence of an endoleak (endotension) following endovascular aortic repair (EVAR) for an abdominal aortic aneurysm (AAA). The aim of this study was to analyze the morphologic structure of the aortic wall in patients with this condition and to establish the cause of the endotension. Methods: Human aortic specimens of the abdominal aorta were obtained during open repair, fixed with formalin, and analyzed among three groups. Group A was specimens from open abdominal aortic aneurysm repairs (n = 7). Group E was specimens from sac expansion without an evident endoleak after EVAR (n = 7). Group N was specimens from non-aneurysmal “normal” cadaveric abdominal aortas (n = 5). Using XPCT (effective voxel size, 12.5 μm; density resolution, 1 mg/cm3), we measured the density of the tunica media (TM) in six regions of each sample. Then, any changes to the elastic lamina and the vasa vasorum were analyzed pathologically. The specimens were immunohistochemically examined with anti-CD31 and vascular endothelial growth factor antibodies. Results: The time from EVAR to open aortic repair was 64.2 ± 7.2 months. There were significant differences in the thickness of the TM among three groups: 0.98 ± 0.03 mm in Group N; 0.31 ± 0.01 mm in Group A; and 0.15 ± 0.03 mm in Group E (P < .005). There were significant differences in the TM density among the groups: 1.087 ± 0.004 g/cm3 in Group N; 1.070 ± 0.001 g/cm3 in Group A; and 1.062 ± 0.007 g/cm3 in Group E (P < .005). Differences in the thickness and density of the TM correlated with the thickness of the elastic lamina; in Group N, uniform high-density elastic fibers were observed in the TM. By contrast, a thinning of the elastic lamina in the TM was observed in Group A. A marked thinness and loss of elastic fibers was observed in Group E. CD31 immunostaining revealed that the vasa vasorum was localized in the adventitia and inside the outer third of the TM in Group N, and in the middle of the TM in Group A. In Group E, the vasa vasorum advanced up to the intima with vascular endothelial growth factor-positive cells in the intimal section. Conclusions: XPCT could be used to demonstrate the densitometric property of the aortic aneurysmal wall after EVAR. We confirmed that the deformation process that occurs in the sac expansion after EVAR without evidence of an endoleak could be explained by hypoxia in the aortic wall. : Clinical Relevance: The pathophysiology of the sac expansion without evidence of an endoleak (endotension) following EVAR remains an enigma. Several theories have been proposed regarding the cause of endotension, including the presence of blood flow below the sensitivity limits of current imaging modalities, pressure transmission through a thrombus or endograft fabric, and the presence of microleak or ultrafiltration. We demonstrated the marked thinning of the elastic lamella and neovascularization in the TM and the intima and proposed that the insertion of a stent graft into an aortic aneurysm may worsen the hypoxic conditions of the aneurysmal wall. Endovascular aortic repair Sac expansion Stent graft-induced aortopathy Synchrotron radiation-based X-ray phase-contrast tomography Tissue density Diseases of the circulatory (Cardiovascular) system Takuro Tsukube, MD, PhD verfasserin aut Yuko Wada, MD, PhD verfasserin aut Masato Hoshino, PhD verfasserin aut Naoto Yagi, PhD verfasserin aut Kazunori Nakagawa, PhD verfasserin aut Yutaka Nakashima, MD, PhD verfasserin aut Kenji Okada, MD, PhD verfasserin aut Tatsuichiro Seto, MD, PhD verfasserin aut In JVS - Vascular Science Elsevier, 2021 4(2023), Seite 100123- (DE-627)1755580096 26663503 nnns volume:4 year:2023 pages:100123- https://doi.org/10.1016/j.jvssci.2023.100123 kostenfrei https://doaj.org/article/b727ca92199546b4902aaad51b00d2b1 kostenfrei http://www.sciencedirect.com/science/article/pii/S2666350323000275 kostenfrei https://doaj.org/toc/2666-3503 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 4 2023 100123- |
| spelling |
10.1016/j.jvssci.2023.100123 doi (DE-627)DOAJ097968978 (DE-599)DOAJb727ca92199546b4902aaad51b00d2b1 DE-627 ger DE-627 rakwb eng RC666-701 Takateru Yamamoto, MD verfasserin aut Mechanism of sac expansion without evident endoleak analyzed with X ray phase-contrast tomography 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective: Synchrotron radiation-based X ray phase-contrast tomography (XPCT) was used in this study to evaluate abdominal aorta specimens from patients with sac expansion without evidence of an endoleak (endotension) following endovascular aortic repair (EVAR) for an abdominal aortic aneurysm (AAA). The aim of this study was to analyze the morphologic structure of the aortic wall in patients with this condition and to establish the cause of the endotension. Methods: Human aortic specimens of the abdominal aorta were obtained during open repair, fixed with formalin, and analyzed among three groups. Group A was specimens from open abdominal aortic aneurysm repairs (n = 7). Group E was specimens from sac expansion without an evident endoleak after EVAR (n = 7). Group N was specimens from non-aneurysmal “normal” cadaveric abdominal aortas (n = 5). Using XPCT (effective voxel size, 12.5 μm; density resolution, 1 mg/cm3), we measured the density of the tunica media (TM) in six regions of each sample. Then, any changes to the elastic lamina and the vasa vasorum were analyzed pathologically. The specimens were immunohistochemically examined with anti-CD31 and vascular endothelial growth factor antibodies. Results: The time from EVAR to open aortic repair was 64.2 ± 7.2 months. There were significant differences in the thickness of the TM among three groups: 0.98 ± 0.03 mm in Group N; 0.31 ± 0.01 mm in Group A; and 0.15 ± 0.03 mm in Group E (P < .005). There were significant differences in the TM density among the groups: 1.087 ± 0.004 g/cm3 in Group N; 1.070 ± 0.001 g/cm3 in Group A; and 1.062 ± 0.007 g/cm3 in Group E (P < .005). Differences in the thickness and density of the TM correlated with the thickness of the elastic lamina; in Group N, uniform high-density elastic fibers were observed in the TM. By contrast, a thinning of the elastic lamina in the TM was observed in Group A. A marked thinness and loss of elastic fibers was observed in Group E. CD31 immunostaining revealed that the vasa vasorum was localized in the adventitia and inside the outer third of the TM in Group N, and in the middle of the TM in Group A. In Group E, the vasa vasorum advanced up to the intima with vascular endothelial growth factor-positive cells in the intimal section. Conclusions: XPCT could be used to demonstrate the densitometric property of the aortic aneurysmal wall after EVAR. We confirmed that the deformation process that occurs in the sac expansion after EVAR without evidence of an endoleak could be explained by hypoxia in the aortic wall. : Clinical Relevance: The pathophysiology of the sac expansion without evidence of an endoleak (endotension) following EVAR remains an enigma. Several theories have been proposed regarding the cause of endotension, including the presence of blood flow below the sensitivity limits of current imaging modalities, pressure transmission through a thrombus or endograft fabric, and the presence of microleak or ultrafiltration. We demonstrated the marked thinning of the elastic lamella and neovascularization in the TM and the intima and proposed that the insertion of a stent graft into an aortic aneurysm may worsen the hypoxic conditions of the aneurysmal wall. Endovascular aortic repair Sac expansion Stent graft-induced aortopathy Synchrotron radiation-based X-ray phase-contrast tomography Tissue density Diseases of the circulatory (Cardiovascular) system Takuro Tsukube, MD, PhD verfasserin aut Yuko Wada, MD, PhD verfasserin aut Masato Hoshino, PhD verfasserin aut Naoto Yagi, PhD verfasserin aut Kazunori Nakagawa, PhD verfasserin aut Yutaka Nakashima, MD, PhD verfasserin aut Kenji Okada, MD, PhD verfasserin aut Tatsuichiro Seto, MD, PhD verfasserin aut In JVS - Vascular Science Elsevier, 2021 4(2023), Seite 100123- (DE-627)1755580096 26663503 nnns volume:4 year:2023 pages:100123- https://doi.org/10.1016/j.jvssci.2023.100123 kostenfrei https://doaj.org/article/b727ca92199546b4902aaad51b00d2b1 kostenfrei http://www.sciencedirect.com/science/article/pii/S2666350323000275 kostenfrei https://doaj.org/toc/2666-3503 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 4 2023 100123- |
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10.1016/j.jvssci.2023.100123 doi (DE-627)DOAJ097968978 (DE-599)DOAJb727ca92199546b4902aaad51b00d2b1 DE-627 ger DE-627 rakwb eng RC666-701 Takateru Yamamoto, MD verfasserin aut Mechanism of sac expansion without evident endoleak analyzed with X ray phase-contrast tomography 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective: Synchrotron radiation-based X ray phase-contrast tomography (XPCT) was used in this study to evaluate abdominal aorta specimens from patients with sac expansion without evidence of an endoleak (endotension) following endovascular aortic repair (EVAR) for an abdominal aortic aneurysm (AAA). The aim of this study was to analyze the morphologic structure of the aortic wall in patients with this condition and to establish the cause of the endotension. Methods: Human aortic specimens of the abdominal aorta were obtained during open repair, fixed with formalin, and analyzed among three groups. Group A was specimens from open abdominal aortic aneurysm repairs (n = 7). Group E was specimens from sac expansion without an evident endoleak after EVAR (n = 7). Group N was specimens from non-aneurysmal “normal” cadaveric abdominal aortas (n = 5). Using XPCT (effective voxel size, 12.5 μm; density resolution, 1 mg/cm3), we measured the density of the tunica media (TM) in six regions of each sample. Then, any changes to the elastic lamina and the vasa vasorum were analyzed pathologically. The specimens were immunohistochemically examined with anti-CD31 and vascular endothelial growth factor antibodies. Results: The time from EVAR to open aortic repair was 64.2 ± 7.2 months. There were significant differences in the thickness of the TM among three groups: 0.98 ± 0.03 mm in Group N; 0.31 ± 0.01 mm in Group A; and 0.15 ± 0.03 mm in Group E (P < .005). There were significant differences in the TM density among the groups: 1.087 ± 0.004 g/cm3 in Group N; 1.070 ± 0.001 g/cm3 in Group A; and 1.062 ± 0.007 g/cm3 in Group E (P < .005). Differences in the thickness and density of the TM correlated with the thickness of the elastic lamina; in Group N, uniform high-density elastic fibers were observed in the TM. By contrast, a thinning of the elastic lamina in the TM was observed in Group A. A marked thinness and loss of elastic fibers was observed in Group E. CD31 immunostaining revealed that the vasa vasorum was localized in the adventitia and inside the outer third of the TM in Group N, and in the middle of the TM in Group A. In Group E, the vasa vasorum advanced up to the intima with vascular endothelial growth factor-positive cells in the intimal section. Conclusions: XPCT could be used to demonstrate the densitometric property of the aortic aneurysmal wall after EVAR. We confirmed that the deformation process that occurs in the sac expansion after EVAR without evidence of an endoleak could be explained by hypoxia in the aortic wall. : Clinical Relevance: The pathophysiology of the sac expansion without evidence of an endoleak (endotension) following EVAR remains an enigma. Several theories have been proposed regarding the cause of endotension, including the presence of blood flow below the sensitivity limits of current imaging modalities, pressure transmission through a thrombus or endograft fabric, and the presence of microleak or ultrafiltration. We demonstrated the marked thinning of the elastic lamella and neovascularization in the TM and the intima and proposed that the insertion of a stent graft into an aortic aneurysm may worsen the hypoxic conditions of the aneurysmal wall. Endovascular aortic repair Sac expansion Stent graft-induced aortopathy Synchrotron radiation-based X-ray phase-contrast tomography Tissue density Diseases of the circulatory (Cardiovascular) system Takuro Tsukube, MD, PhD verfasserin aut Yuko Wada, MD, PhD verfasserin aut Masato Hoshino, PhD verfasserin aut Naoto Yagi, PhD verfasserin aut Kazunori Nakagawa, PhD verfasserin aut Yutaka Nakashima, MD, PhD verfasserin aut Kenji Okada, MD, PhD verfasserin aut Tatsuichiro Seto, MD, PhD verfasserin aut In JVS - Vascular Science Elsevier, 2021 4(2023), Seite 100123- (DE-627)1755580096 26663503 nnns volume:4 year:2023 pages:100123- https://doi.org/10.1016/j.jvssci.2023.100123 kostenfrei https://doaj.org/article/b727ca92199546b4902aaad51b00d2b1 kostenfrei http://www.sciencedirect.com/science/article/pii/S2666350323000275 kostenfrei https://doaj.org/toc/2666-3503 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 4 2023 100123- |
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10.1016/j.jvssci.2023.100123 doi (DE-627)DOAJ097968978 (DE-599)DOAJb727ca92199546b4902aaad51b00d2b1 DE-627 ger DE-627 rakwb eng RC666-701 Takateru Yamamoto, MD verfasserin aut Mechanism of sac expansion without evident endoleak analyzed with X ray phase-contrast tomography 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective: Synchrotron radiation-based X ray phase-contrast tomography (XPCT) was used in this study to evaluate abdominal aorta specimens from patients with sac expansion without evidence of an endoleak (endotension) following endovascular aortic repair (EVAR) for an abdominal aortic aneurysm (AAA). The aim of this study was to analyze the morphologic structure of the aortic wall in patients with this condition and to establish the cause of the endotension. Methods: Human aortic specimens of the abdominal aorta were obtained during open repair, fixed with formalin, and analyzed among three groups. Group A was specimens from open abdominal aortic aneurysm repairs (n = 7). Group E was specimens from sac expansion without an evident endoleak after EVAR (n = 7). Group N was specimens from non-aneurysmal “normal” cadaveric abdominal aortas (n = 5). Using XPCT (effective voxel size, 12.5 μm; density resolution, 1 mg/cm3), we measured the density of the tunica media (TM) in six regions of each sample. Then, any changes to the elastic lamina and the vasa vasorum were analyzed pathologically. The specimens were immunohistochemically examined with anti-CD31 and vascular endothelial growth factor antibodies. Results: The time from EVAR to open aortic repair was 64.2 ± 7.2 months. There were significant differences in the thickness of the TM among three groups: 0.98 ± 0.03 mm in Group N; 0.31 ± 0.01 mm in Group A; and 0.15 ± 0.03 mm in Group E (P < .005). There were significant differences in the TM density among the groups: 1.087 ± 0.004 g/cm3 in Group N; 1.070 ± 0.001 g/cm3 in Group A; and 1.062 ± 0.007 g/cm3 in Group E (P < .005). Differences in the thickness and density of the TM correlated with the thickness of the elastic lamina; in Group N, uniform high-density elastic fibers were observed in the TM. By contrast, a thinning of the elastic lamina in the TM was observed in Group A. A marked thinness and loss of elastic fibers was observed in Group E. CD31 immunostaining revealed that the vasa vasorum was localized in the adventitia and inside the outer third of the TM in Group N, and in the middle of the TM in Group A. In Group E, the vasa vasorum advanced up to the intima with vascular endothelial growth factor-positive cells in the intimal section. Conclusions: XPCT could be used to demonstrate the densitometric property of the aortic aneurysmal wall after EVAR. We confirmed that the deformation process that occurs in the sac expansion after EVAR without evidence of an endoleak could be explained by hypoxia in the aortic wall. : Clinical Relevance: The pathophysiology of the sac expansion without evidence of an endoleak (endotension) following EVAR remains an enigma. Several theories have been proposed regarding the cause of endotension, including the presence of blood flow below the sensitivity limits of current imaging modalities, pressure transmission through a thrombus or endograft fabric, and the presence of microleak or ultrafiltration. We demonstrated the marked thinning of the elastic lamella and neovascularization in the TM and the intima and proposed that the insertion of a stent graft into an aortic aneurysm may worsen the hypoxic conditions of the aneurysmal wall. Endovascular aortic repair Sac expansion Stent graft-induced aortopathy Synchrotron radiation-based X-ray phase-contrast tomography Tissue density Diseases of the circulatory (Cardiovascular) system Takuro Tsukube, MD, PhD verfasserin aut Yuko Wada, MD, PhD verfasserin aut Masato Hoshino, PhD verfasserin aut Naoto Yagi, PhD verfasserin aut Kazunori Nakagawa, PhD verfasserin aut Yutaka Nakashima, MD, PhD verfasserin aut Kenji Okada, MD, PhD verfasserin aut Tatsuichiro Seto, MD, PhD verfasserin aut In JVS - Vascular Science Elsevier, 2021 4(2023), Seite 100123- (DE-627)1755580096 26663503 nnns volume:4 year:2023 pages:100123- https://doi.org/10.1016/j.jvssci.2023.100123 kostenfrei https://doaj.org/article/b727ca92199546b4902aaad51b00d2b1 kostenfrei http://www.sciencedirect.com/science/article/pii/S2666350323000275 kostenfrei https://doaj.org/toc/2666-3503 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 4 2023 100123- |
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10.1016/j.jvssci.2023.100123 doi (DE-627)DOAJ097968978 (DE-599)DOAJb727ca92199546b4902aaad51b00d2b1 DE-627 ger DE-627 rakwb eng RC666-701 Takateru Yamamoto, MD verfasserin aut Mechanism of sac expansion without evident endoleak analyzed with X ray phase-contrast tomography 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective: Synchrotron radiation-based X ray phase-contrast tomography (XPCT) was used in this study to evaluate abdominal aorta specimens from patients with sac expansion without evidence of an endoleak (endotension) following endovascular aortic repair (EVAR) for an abdominal aortic aneurysm (AAA). The aim of this study was to analyze the morphologic structure of the aortic wall in patients with this condition and to establish the cause of the endotension. Methods: Human aortic specimens of the abdominal aorta were obtained during open repair, fixed with formalin, and analyzed among three groups. Group A was specimens from open abdominal aortic aneurysm repairs (n = 7). Group E was specimens from sac expansion without an evident endoleak after EVAR (n = 7). Group N was specimens from non-aneurysmal “normal” cadaveric abdominal aortas (n = 5). Using XPCT (effective voxel size, 12.5 μm; density resolution, 1 mg/cm3), we measured the density of the tunica media (TM) in six regions of each sample. Then, any changes to the elastic lamina and the vasa vasorum were analyzed pathologically. The specimens were immunohistochemically examined with anti-CD31 and vascular endothelial growth factor antibodies. Results: The time from EVAR to open aortic repair was 64.2 ± 7.2 months. There were significant differences in the thickness of the TM among three groups: 0.98 ± 0.03 mm in Group N; 0.31 ± 0.01 mm in Group A; and 0.15 ± 0.03 mm in Group E (P < .005). There were significant differences in the TM density among the groups: 1.087 ± 0.004 g/cm3 in Group N; 1.070 ± 0.001 g/cm3 in Group A; and 1.062 ± 0.007 g/cm3 in Group E (P < .005). Differences in the thickness and density of the TM correlated with the thickness of the elastic lamina; in Group N, uniform high-density elastic fibers were observed in the TM. By contrast, a thinning of the elastic lamina in the TM was observed in Group A. A marked thinness and loss of elastic fibers was observed in Group E. CD31 immunostaining revealed that the vasa vasorum was localized in the adventitia and inside the outer third of the TM in Group N, and in the middle of the TM in Group A. In Group E, the vasa vasorum advanced up to the intima with vascular endothelial growth factor-positive cells in the intimal section. Conclusions: XPCT could be used to demonstrate the densitometric property of the aortic aneurysmal wall after EVAR. We confirmed that the deformation process that occurs in the sac expansion after EVAR without evidence of an endoleak could be explained by hypoxia in the aortic wall. : Clinical Relevance: The pathophysiology of the sac expansion without evidence of an endoleak (endotension) following EVAR remains an enigma. Several theories have been proposed regarding the cause of endotension, including the presence of blood flow below the sensitivity limits of current imaging modalities, pressure transmission through a thrombus or endograft fabric, and the presence of microleak or ultrafiltration. We demonstrated the marked thinning of the elastic lamella and neovascularization in the TM and the intima and proposed that the insertion of a stent graft into an aortic aneurysm may worsen the hypoxic conditions of the aneurysmal wall. Endovascular aortic repair Sac expansion Stent graft-induced aortopathy Synchrotron radiation-based X-ray phase-contrast tomography Tissue density Diseases of the circulatory (Cardiovascular) system Takuro Tsukube, MD, PhD verfasserin aut Yuko Wada, MD, PhD verfasserin aut Masato Hoshino, PhD verfasserin aut Naoto Yagi, PhD verfasserin aut Kazunori Nakagawa, PhD verfasserin aut Yutaka Nakashima, MD, PhD verfasserin aut Kenji Okada, MD, PhD verfasserin aut Tatsuichiro Seto, MD, PhD verfasserin aut In JVS - Vascular Science Elsevier, 2021 4(2023), Seite 100123- (DE-627)1755580096 26663503 nnns volume:4 year:2023 pages:100123- https://doi.org/10.1016/j.jvssci.2023.100123 kostenfrei https://doaj.org/article/b727ca92199546b4902aaad51b00d2b1 kostenfrei http://www.sciencedirect.com/science/article/pii/S2666350323000275 kostenfrei https://doaj.org/toc/2666-3503 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 4 2023 100123- |
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Takateru Yamamoto, MD @@aut@@ Takuro Tsukube, MD, PhD @@aut@@ Yuko Wada, MD, PhD @@aut@@ Masato Hoshino, PhD @@aut@@ Naoto Yagi, PhD @@aut@@ Kazunori Nakagawa, PhD @@aut@@ Yutaka Nakashima, MD, PhD @@aut@@ Kenji Okada, MD, PhD @@aut@@ Tatsuichiro Seto, MD, PhD @@aut@@ |
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There were significant differences in the thickness of the TM among three groups: 0.98 ± 0.03 mm in Group N; 0.31 ± 0.01 mm in Group A; and 0.15 ± 0.03 mm in Group E (P < .005). There were significant differences in the TM density among the groups: 1.087 ± 0.004 g/cm3 in Group N; 1.070 ± 0.001 g/cm3 in Group A; and 1.062 ± 0.007 g/cm3 in Group E (P < .005). Differences in the thickness and density of the TM correlated with the thickness of the elastic lamina; in Group N, uniform high-density elastic fibers were observed in the TM. By contrast, a thinning of the elastic lamina in the TM was observed in Group A. A marked thinness and loss of elastic fibers was observed in Group E. CD31 immunostaining revealed that the vasa vasorum was localized in the adventitia and inside the outer third of the TM in Group N, and in the middle of the TM in Group A. In Group E, the vasa vasorum advanced up to the intima with vascular endothelial growth factor-positive cells in the intimal section. Conclusions: XPCT could be used to demonstrate the densitometric property of the aortic aneurysmal wall after EVAR. We confirmed that the deformation process that occurs in the sac expansion after EVAR without evidence of an endoleak could be explained by hypoxia in the aortic wall. : Clinical Relevance: The pathophysiology of the sac expansion without evidence of an endoleak (endotension) following EVAR remains an enigma. Several theories have been proposed regarding the cause of endotension, including the presence of blood flow below the sensitivity limits of current imaging modalities, pressure transmission through a thrombus or endograft fabric, and the presence of microleak or ultrafiltration. 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Takateru Yamamoto, MD |
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Takateru Yamamoto, MD misc RC666-701 misc Endovascular aortic repair misc Sac expansion misc Stent graft-induced aortopathy misc Synchrotron radiation-based X-ray phase-contrast tomography misc Tissue density misc Diseases of the circulatory (Cardiovascular) system Mechanism of sac expansion without evident endoleak analyzed with X ray phase-contrast tomography |
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RC666-701 Mechanism of sac expansion without evident endoleak analyzed with X ray phase-contrast tomography Endovascular aortic repair Sac expansion Stent graft-induced aortopathy Synchrotron radiation-based X-ray phase-contrast tomography Tissue density |
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misc RC666-701 misc Endovascular aortic repair misc Sac expansion misc Stent graft-induced aortopathy misc Synchrotron radiation-based X-ray phase-contrast tomography misc Tissue density misc Diseases of the circulatory (Cardiovascular) system |
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Takateru Yamamoto, MD |
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Takateru Yamamoto, MD Takuro Tsukube, MD, PhD Yuko Wada, MD, PhD Masato Hoshino, PhD Naoto Yagi, PhD Kazunori Nakagawa, PhD Yutaka Nakashima, MD, PhD Kenji Okada, MD, PhD Tatsuichiro Seto, MD, PhD |
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mechanism of sac expansion without evident endoleak analyzed with x ray phase-contrast tomography |
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Mechanism of sac expansion without evident endoleak analyzed with X ray phase-contrast tomography |
| abstract |
Objective: Synchrotron radiation-based X ray phase-contrast tomography (XPCT) was used in this study to evaluate abdominal aorta specimens from patients with sac expansion without evidence of an endoleak (endotension) following endovascular aortic repair (EVAR) for an abdominal aortic aneurysm (AAA). The aim of this study was to analyze the morphologic structure of the aortic wall in patients with this condition and to establish the cause of the endotension. Methods: Human aortic specimens of the abdominal aorta were obtained during open repair, fixed with formalin, and analyzed among three groups. Group A was specimens from open abdominal aortic aneurysm repairs (n = 7). Group E was specimens from sac expansion without an evident endoleak after EVAR (n = 7). Group N was specimens from non-aneurysmal “normal” cadaveric abdominal aortas (n = 5). Using XPCT (effective voxel size, 12.5 μm; density resolution, 1 mg/cm3), we measured the density of the tunica media (TM) in six regions of each sample. Then, any changes to the elastic lamina and the vasa vasorum were analyzed pathologically. The specimens were immunohistochemically examined with anti-CD31 and vascular endothelial growth factor antibodies. Results: The time from EVAR to open aortic repair was 64.2 ± 7.2 months. There were significant differences in the thickness of the TM among three groups: 0.98 ± 0.03 mm in Group N; 0.31 ± 0.01 mm in Group A; and 0.15 ± 0.03 mm in Group E (P < .005). There were significant differences in the TM density among the groups: 1.087 ± 0.004 g/cm3 in Group N; 1.070 ± 0.001 g/cm3 in Group A; and 1.062 ± 0.007 g/cm3 in Group E (P < .005). Differences in the thickness and density of the TM correlated with the thickness of the elastic lamina; in Group N, uniform high-density elastic fibers were observed in the TM. By contrast, a thinning of the elastic lamina in the TM was observed in Group A. A marked thinness and loss of elastic fibers was observed in Group E. CD31 immunostaining revealed that the vasa vasorum was localized in the adventitia and inside the outer third of the TM in Group N, and in the middle of the TM in Group A. In Group E, the vasa vasorum advanced up to the intima with vascular endothelial growth factor-positive cells in the intimal section. Conclusions: XPCT could be used to demonstrate the densitometric property of the aortic aneurysmal wall after EVAR. We confirmed that the deformation process that occurs in the sac expansion after EVAR without evidence of an endoleak could be explained by hypoxia in the aortic wall. : Clinical Relevance: The pathophysiology of the sac expansion without evidence of an endoleak (endotension) following EVAR remains an enigma. Several theories have been proposed regarding the cause of endotension, including the presence of blood flow below the sensitivity limits of current imaging modalities, pressure transmission through a thrombus or endograft fabric, and the presence of microleak or ultrafiltration. We demonstrated the marked thinning of the elastic lamella and neovascularization in the TM and the intima and proposed that the insertion of a stent graft into an aortic aneurysm may worsen the hypoxic conditions of the aneurysmal wall. |
| abstractGer |
Objective: Synchrotron radiation-based X ray phase-contrast tomography (XPCT) was used in this study to evaluate abdominal aorta specimens from patients with sac expansion without evidence of an endoleak (endotension) following endovascular aortic repair (EVAR) for an abdominal aortic aneurysm (AAA). The aim of this study was to analyze the morphologic structure of the aortic wall in patients with this condition and to establish the cause of the endotension. Methods: Human aortic specimens of the abdominal aorta were obtained during open repair, fixed with formalin, and analyzed among three groups. Group A was specimens from open abdominal aortic aneurysm repairs (n = 7). Group E was specimens from sac expansion without an evident endoleak after EVAR (n = 7). Group N was specimens from non-aneurysmal “normal” cadaveric abdominal aortas (n = 5). Using XPCT (effective voxel size, 12.5 μm; density resolution, 1 mg/cm3), we measured the density of the tunica media (TM) in six regions of each sample. Then, any changes to the elastic lamina and the vasa vasorum were analyzed pathologically. The specimens were immunohistochemically examined with anti-CD31 and vascular endothelial growth factor antibodies. Results: The time from EVAR to open aortic repair was 64.2 ± 7.2 months. There were significant differences in the thickness of the TM among three groups: 0.98 ± 0.03 mm in Group N; 0.31 ± 0.01 mm in Group A; and 0.15 ± 0.03 mm in Group E (P < .005). There were significant differences in the TM density among the groups: 1.087 ± 0.004 g/cm3 in Group N; 1.070 ± 0.001 g/cm3 in Group A; and 1.062 ± 0.007 g/cm3 in Group E (P < .005). Differences in the thickness and density of the TM correlated with the thickness of the elastic lamina; in Group N, uniform high-density elastic fibers were observed in the TM. By contrast, a thinning of the elastic lamina in the TM was observed in Group A. A marked thinness and loss of elastic fibers was observed in Group E. CD31 immunostaining revealed that the vasa vasorum was localized in the adventitia and inside the outer third of the TM in Group N, and in the middle of the TM in Group A. In Group E, the vasa vasorum advanced up to the intima with vascular endothelial growth factor-positive cells in the intimal section. Conclusions: XPCT could be used to demonstrate the densitometric property of the aortic aneurysmal wall after EVAR. We confirmed that the deformation process that occurs in the sac expansion after EVAR without evidence of an endoleak could be explained by hypoxia in the aortic wall. : Clinical Relevance: The pathophysiology of the sac expansion without evidence of an endoleak (endotension) following EVAR remains an enigma. Several theories have been proposed regarding the cause of endotension, including the presence of blood flow below the sensitivity limits of current imaging modalities, pressure transmission through a thrombus or endograft fabric, and the presence of microleak or ultrafiltration. We demonstrated the marked thinning of the elastic lamella and neovascularization in the TM and the intima and proposed that the insertion of a stent graft into an aortic aneurysm may worsen the hypoxic conditions of the aneurysmal wall. |
| abstract_unstemmed |
Objective: Synchrotron radiation-based X ray phase-contrast tomography (XPCT) was used in this study to evaluate abdominal aorta specimens from patients with sac expansion without evidence of an endoleak (endotension) following endovascular aortic repair (EVAR) for an abdominal aortic aneurysm (AAA). The aim of this study was to analyze the morphologic structure of the aortic wall in patients with this condition and to establish the cause of the endotension. Methods: Human aortic specimens of the abdominal aorta were obtained during open repair, fixed with formalin, and analyzed among three groups. Group A was specimens from open abdominal aortic aneurysm repairs (n = 7). Group E was specimens from sac expansion without an evident endoleak after EVAR (n = 7). Group N was specimens from non-aneurysmal “normal” cadaveric abdominal aortas (n = 5). Using XPCT (effective voxel size, 12.5 μm; density resolution, 1 mg/cm3), we measured the density of the tunica media (TM) in six regions of each sample. Then, any changes to the elastic lamina and the vasa vasorum were analyzed pathologically. The specimens were immunohistochemically examined with anti-CD31 and vascular endothelial growth factor antibodies. Results: The time from EVAR to open aortic repair was 64.2 ± 7.2 months. There were significant differences in the thickness of the TM among three groups: 0.98 ± 0.03 mm in Group N; 0.31 ± 0.01 mm in Group A; and 0.15 ± 0.03 mm in Group E (P < .005). There were significant differences in the TM density among the groups: 1.087 ± 0.004 g/cm3 in Group N; 1.070 ± 0.001 g/cm3 in Group A; and 1.062 ± 0.007 g/cm3 in Group E (P < .005). Differences in the thickness and density of the TM correlated with the thickness of the elastic lamina; in Group N, uniform high-density elastic fibers were observed in the TM. By contrast, a thinning of the elastic lamina in the TM was observed in Group A. A marked thinness and loss of elastic fibers was observed in Group E. CD31 immunostaining revealed that the vasa vasorum was localized in the adventitia and inside the outer third of the TM in Group N, and in the middle of the TM in Group A. In Group E, the vasa vasorum advanced up to the intima with vascular endothelial growth factor-positive cells in the intimal section. Conclusions: XPCT could be used to demonstrate the densitometric property of the aortic aneurysmal wall after EVAR. We confirmed that the deformation process that occurs in the sac expansion after EVAR without evidence of an endoleak could be explained by hypoxia in the aortic wall. : Clinical Relevance: The pathophysiology of the sac expansion without evidence of an endoleak (endotension) following EVAR remains an enigma. Several theories have been proposed regarding the cause of endotension, including the presence of blood flow below the sensitivity limits of current imaging modalities, pressure transmission through a thrombus or endograft fabric, and the presence of microleak or ultrafiltration. We demonstrated the marked thinning of the elastic lamella and neovascularization in the TM and the intima and proposed that the insertion of a stent graft into an aortic aneurysm may worsen the hypoxic conditions of the aneurysmal wall. |
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Mechanism of sac expansion without evident endoleak analyzed with X ray phase-contrast tomography |
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https://doi.org/10.1016/j.jvssci.2023.100123 https://doaj.org/article/b727ca92199546b4902aaad51b00d2b1 http://www.sciencedirect.com/science/article/pii/S2666350323000275 https://doaj.org/toc/2666-3503 |
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Takuro Tsukube, MD, PhD Yuko Wada, MD, PhD Masato Hoshino, PhD Naoto Yagi, PhD Kazunori Nakagawa, PhD Yutaka Nakashima, MD, PhD Kenji Okada, MD, PhD Tatsuichiro Seto, MD, PhD |
| author2Str |
Takuro Tsukube, MD, PhD Yuko Wada, MD, PhD Masato Hoshino, PhD Naoto Yagi, PhD Kazunori Nakagawa, PhD Yutaka Nakashima, MD, PhD Kenji Okada, MD, PhD Tatsuichiro Seto, MD, PhD |
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1755580096 |
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RC - Internal Medicine |
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10.1016/j.jvssci.2023.100123 |
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RC666-701 |
| up_date |
2024-07-03T14:43:59.821Z |
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