Quantitative not qualitative histology differentiates aneurysmal from nondilated ascending aortas and reveals a net gain of medial components
Abstract Medial degeneration is a common histopathological finding in aortopathy and is considered a mechanism for dilatation. We investigated if medial degeneration is specific for sporadic thoracic aortic aneurysms versus nondilated aortas. Specimens were graded by pathologists, blinded to the cli...
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oai:doaj.org-article:5b389f7fa447400a85fff10e77f7f93f2021-12-02T17:45:18ZQuantitative not qualitative histology differentiates aneurysmal from nondilated ascending aortas and reveals a net gain of medial components10.1038/s41598-021-92659-12045-2322https://doaj.org/article/5b389f7fa447400a85fff10e77f7f93f2021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-92659-1https://doaj.org/toc/2045-2322Abstract Medial degeneration is a common histopathological finding in aortopathy and is considered a mechanism for dilatation. We investigated if medial degeneration is specific for sporadic thoracic aortic aneurysms versus nondilated aortas. Specimens were graded by pathologists, blinded to the clinical diagnosis, according to consensus histopathological criteria. The extent of medial degeneration by qualitative (semi-quantitative) assessment was not specific for aneurysmal compared to nondilated aortas. In contrast, blinded quantitative assessment of elastin amount and medial cell number distinguished aortic aneurysms and referent specimens, albeit with marked overlap in results. Specifically, the medial fraction of elastin decreased from dilution rather than loss of protein as cross-sectional amount was maintained while the cross-sectional number, though not density, of smooth muscle cells increased in proportion to expansion of the media. Furthermore, elastic lamellae did not thin and interlamellar distance did not diminish as expected for lumen dilatation, implying a net gain of lamellar elastin and intralamellar cells or extracellular matrix during aneurysmal wall remodeling. These findings support the concepts that: (1) medial degeneration need not induce aortic aneurysms, (2) adaptive responses to altered mechanical stresses increase medial tissue, and (3) greater turnover, not loss, of mural cells and extracellular matrix associates with aortic dilatation.Sameh YousefNana MatsumotoIssam DabeMakoto MoriAlden B. LandryShin-Rong LeeYuki KawamuraChen YangGuangxin LiRoland AssiPrashanth VallabhajosyulaArnar GeirssonGilbert MoeckelJay D. HumphreyGeorge TellidesNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021) |
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Medicine R Science Q Sameh Yousef Nana Matsumoto Issam Dabe Makoto Mori Alden B. Landry Shin-Rong Lee Yuki Kawamura Chen Yang Guangxin Li Roland Assi Prashanth Vallabhajosyula Arnar Geirsson Gilbert Moeckel Jay D. Humphrey George Tellides Quantitative not qualitative histology differentiates aneurysmal from nondilated ascending aortas and reveals a net gain of medial components |
description |
Abstract Medial degeneration is a common histopathological finding in aortopathy and is considered a mechanism for dilatation. We investigated if medial degeneration is specific for sporadic thoracic aortic aneurysms versus nondilated aortas. Specimens were graded by pathologists, blinded to the clinical diagnosis, according to consensus histopathological criteria. The extent of medial degeneration by qualitative (semi-quantitative) assessment was not specific for aneurysmal compared to nondilated aortas. In contrast, blinded quantitative assessment of elastin amount and medial cell number distinguished aortic aneurysms and referent specimens, albeit with marked overlap in results. Specifically, the medial fraction of elastin decreased from dilution rather than loss of protein as cross-sectional amount was maintained while the cross-sectional number, though not density, of smooth muscle cells increased in proportion to expansion of the media. Furthermore, elastic lamellae did not thin and interlamellar distance did not diminish as expected for lumen dilatation, implying a net gain of lamellar elastin and intralamellar cells or extracellular matrix during aneurysmal wall remodeling. These findings support the concepts that: (1) medial degeneration need not induce aortic aneurysms, (2) adaptive responses to altered mechanical stresses increase medial tissue, and (3) greater turnover, not loss, of mural cells and extracellular matrix associates with aortic dilatation. |
format |
article |
author |
Sameh Yousef Nana Matsumoto Issam Dabe Makoto Mori Alden B. Landry Shin-Rong Lee Yuki Kawamura Chen Yang Guangxin Li Roland Assi Prashanth Vallabhajosyula Arnar Geirsson Gilbert Moeckel Jay D. Humphrey George Tellides |
author_facet |
Sameh Yousef Nana Matsumoto Issam Dabe Makoto Mori Alden B. Landry Shin-Rong Lee Yuki Kawamura Chen Yang Guangxin Li Roland Assi Prashanth Vallabhajosyula Arnar Geirsson Gilbert Moeckel Jay D. Humphrey George Tellides |
author_sort |
Sameh Yousef |
title |
Quantitative not qualitative histology differentiates aneurysmal from nondilated ascending aortas and reveals a net gain of medial components |
title_short |
Quantitative not qualitative histology differentiates aneurysmal from nondilated ascending aortas and reveals a net gain of medial components |
title_full |
Quantitative not qualitative histology differentiates aneurysmal from nondilated ascending aortas and reveals a net gain of medial components |
title_fullStr |
Quantitative not qualitative histology differentiates aneurysmal from nondilated ascending aortas and reveals a net gain of medial components |
title_full_unstemmed |
Quantitative not qualitative histology differentiates aneurysmal from nondilated ascending aortas and reveals a net gain of medial components |
title_sort |
quantitative not qualitative histology differentiates aneurysmal from nondilated ascending aortas and reveals a net gain of medial components |
publisher |
Nature Portfolio |
publishDate |
2021 |
url |
https://doaj.org/article/5b389f7fa447400a85fff10e77f7f93f |
work_keys_str_mv |
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