Histological peculiarities of degenerative changes in the dilated ascending aorta
AbstractBackground. Currently, an established indication for surgical repair of an ascending aortic aneurysm is the aortic diameter greater than 55 mm without hereditary connective tissue disorders and bicuspid aortic valve. The aortic size from 40 to 54 mm, regardless of the body surface area, is classified as aortic dilation. Histopathological changes in the dilated ascending aorta without genetic diseases still remain poorly investigated. There are no specific guidelines determining the surgical strategy in patients with the pathology concerned.
Objective. This study was undertaken to investigate histopathological alterations in the wall of the dilated ascending aorta.
Material and methods. A total of 25 gross specimens of the ascending aorta were obtained from corpses after sudden death. They were divided into two groups. The first group (n=5) included the samples of the dilated ascending aorta (diameter of 40 to 54 mm) and the second group (n=20) consisted of the samples of the ascending aorta of less than 40 mm in diameter. Three samples of the aortic wall were taken from each gross specimen at the level of the ascending aorta in the most dilated area. The obtained samples were fixed, stained with hematoxylin-eosin, Van Gieson, Weigert–Van Gieson stains and analyzed by means of light microscopy. Degenerative changes in the aortic wall were assessed according to the Consensus «Noninflammatory degenerative diseases – nomenclature and diagnostic criteria» (2016). The groups were compared using the Student’s t-test for the quantitative data and Chi-squared test and Fisher’s exact test for categorical variables. The statistical significance threshold was set at p<0.05.
Results. The obtained findings revealed a more severe grade of accumulation and distribution of the intralamellar mucoid extracellular matrix in the dilated ascending aorta (р=0.007; p=0.005, respectively), as well as a more pronounced grade and extent of elastic fiber degradation (р<0.001; p<0.001). Moreover, in the first group multifocal medial fibrosis was observed more frequently (p=0.027). The groups were not statistically different in the grade of translamellar mucoid extracellular matrix accumulation and distribution (p=0.103; p=0.504), the extent of smooth muscle cell alterations (p=0.179), and the grade of medial fibrosis (p=0.074).
Conclusion. Dilation of the ascending aorta is related with degenerative changes of the aortic wall. Mucoid extracellular matrix accumulation and elastic fiber alterations are the first degenerative manifestations. Thus, dilation of the ascending aorta is indicative of morphological alterations of the aortic wall and should be taken into consideration while determining the surgical strategy.
Funding. The study had no financial support.
Conflict of interest. The authors declare no conflicts of interest.
Authors’ contribution. Study conception and design – Vachev A.N., Kozin I.I.; data collection and handling – Kozin I.I., Poletaeva S.V., Kulakhmetova N.F., Ivanova O.V.; statistical processing – Kozin I.I.; manuscript revision – Vachev A.N., Frolova E.V.
For citation: Kozin I.I., Poletaeva S.V., Kulakhmetova N.F., Ivanova O.V., Frolova E.V., Vachev A.N. Histological peculiarities of degenerative changes in the dilated ascending aorta. Angiology and Vascular Surgery. Journal named after Academician A.V. Pokrovsky. 2023; 29 (4): 7–13. DOI: https://doi.org/10.33029/1027-6661-2023-29-4-7-13
Keywords:ascending aorta dilation; intralamellar mucoid extracellular matrix accumulation; translamellar mucoid extracellular matrix accumulation; elastic fiber alterations; smooth muscle cell alterations; medial fibrosis; medial degeneration
References
1. Guidelines for the diagnosis and treatment of aortic diseases (2017). Russian Journal of Cardiology and Cardiovascular Surgery. 2018; 11 (1): 7–67. (in Russian)
2. Erdheim J. Medionecrosis aortae idiopathica cystica. Virchows Archiv. 1930; 276 (1): 187–229.
3. Konstantinov B.A., Belov Yu.V., Kuznechevsky F.V. Aneurysms of the ascending department and the aortic arch. M.: Аstrel. 2006; 335. (in Russian)
4. Halushka M.K., Angelini A., Bartoloni G., et al. Consensus statement on surgical pathology of the aorta from the Society for Cardiovascular Pathology and the Association For European Cardiovascular Pathology: II. Noninflammatory degenerative diseases – nomenclature and diagnostic criteria. Cardiovascular Pathology. 2016; 25 (3): 247–257. DOI: https://doi.org/10.1016/j.carpath.2016.03.002
5. Hagan P.G., Neinaber C.A., Isselbacher E.M., et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000; 283 (7): 897–903. DOI: https://doi.org/10.1001/jama.283.7.897
6. Neri E., Barabesi L., Buklas D., et al. Limited role of aortic size in the genesis of acute type A aortic dissection. European Journal of Cardio-Thoracic Surgery. 2005; 28 (6): 857–863. DOI: https://doi.org/10.1016/j.ejcts.2005.10.013
7. Parish L.M., Gorman J.H., Kahn S., et al. Aortic size in acute type A dissection: implications for preventive ascending aortic replacement. European Journal of Cardio-Thoracic Surgery. 2009; 35 (6): 941–945. DOI: https://doi.org/10.1016/j.ejcts.2008.12.047
8. Shen Y.H., Lu H.S., LeMaire S.A., Daugherty A. Unfolding the Story of Proteoglycan Accumulation in Thoracic Aortic Aneurysm and Dissection. Arteriosclerosis, Thrombosis, and Vascular Biology. 2019; 39 (10): 1899–1901. DOI: https://doi.org/10.1161/ATVBAHA.119.313279
9. Ware A.L., Miller D.V., Erickson L.K., Menon S.C. Marfan syndrome associated aortic disease in neonates and children: a clinical-morphologic review. Cardiovascular Pathology. 2016; 25 (5): 418–422. DOI: https://doi.org/10.1016/j.carpath.2016.06.002
10. Grewal N., Gittenberger–de Groot A.C. Pathogenesis of aortic wall complications in Marfan syndrome. Cardiovascular Pathology. 2018; 33: 62–69. DOI: https://doi.org/10.1016/j.carpath.2018.01.005
11. Mackay C.D.A., Jadli A.S., Fedak P.W.M., Patel V.B. Adventitial Fibroblasts in Aortic Aneurysm: Unraveling Pathogenic Contributions to Vascular Disease. Diagnostics (Basel). 2022; 12 (4): 871. DOI: https://doi.org/10.3390/diagnostics12040871
All articles in our journal are distributed under the CC BY-NC-ND 4.0 (Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International)
п?? GEOTAR-Media Publishing Group. The use of textual and illustrative content from this publication for the training of any artificial intelligence systems п?? including machine learning models and neural networks п?? is strictly prohibited without the prior written consent of the copyright holder.