PATHOGISTOLOGICAL CHANGES OF THE ATHEROSCLEROTIC AORTA AS BIOMECHANICAL RISKS OF RUPTURE OF ITS WALL

Radomychelski I.-M., Piddubnyi A., Domashenko M., Moskalenko R.

PATHOMORPHOLOGY

Scentific article

Introduction. Pathological biomineralization is associated with increased morbidity and mortality from cardiovascular disease. Pathological modifications of the fibrous component and intercellular substance affect the elasticity, extensibility, strength of the aortic wall, but much less attention is given for their study. The aim of work is to study the pathomorphological properties of atherosclerotic-changed aorta under conditions of various forms of pathological biomineralization. Materials and methods. The study was performed on 60 samples of atherosclerotic-changed aorta. 30 samples of abdominal mineralized aortas (group M) were examined, which were divided after histological examination according to the size of calcifications into group M1 (macroscopic calcifications) and M2 (microscopic calcifications), with 15 samples in each group. Calcification up to ≤2 mm was considered to be microscopic, >2 mm – macroscopic30 aortic tissue samples without signs of biomineralization (group C) were used as control group. Methods of macroscopic description, histology, histochemistry were used to study the histopathological changes of aortic tissue. Results. The average age of the patients group with pathological aortic biomineralization significantly exceeds the mean age of the control group – 68.43±1.32 (M) and 51.8±2.56 (C) years (p<0.05), which corresponds to the idea of the temporal intervals of complicated atherosclerosis development. The important changes in aortic tissues around biomineral deposits were identified in our study. Histological examination, as well as histochemical staining of the studied samples with alcyan blue, PAS-reagent, revealed an uneven distribution of glycoproteins and acidic GAGs in the fibrous and intercellular components. The occurrence of mucoid edema elements in the areas of calcification formation was noted. Pathohistological changes in the form of edema and defibrillation of elastic fibrils in the areas adjacent to the calcifications were detected, which visually didn´t show any signs of direct damage.

atherosclerosis, aorta, pathological biomineralization, histology, histochemistry, biomechanical properties.

1. Libby P, Buring JE, Badimon L, Hansson GK, Deanfield J, Bittencourt MS, et al. Atherosclerosis. Nat Rev Dis Primers. 2019 Aug 16;5(1):56. DOI: 10.1038/s41572-019-0106-z.
2. Yahagi K, Kolodgie FD, Lutter C, Mori H, Romero ME, Finn AV, et al. Pathology of Human Coronary and Carotid Artery Atherosclerosis and Vascular Calcification in Diabetes Mellitus. Arterioscler Thromb Vasc Biol. 2017 Feb;37(2):191-204. DOI: 10.1161/ATVBAHA.116.306256.
3. Petsophonsakul P, Furmanik M, Forsythe R, Dweck M, Schurink GW, Natour E, et al. Role of Vascular Smooth Muscle Cell Phenotypic Switching and Calcification in Aortic Aneurysm Formation. Arterioscler Thromb Vasc Biol. 2019 Jul;39(7):1351-1368. DOI: 10.1161/ ATVBAHA.119.312787.
4. GBD 2013 Mortality and Causes of Death Collaborators. Global, regional, and national age–sex specific all-cause and cause-specific mortality for 240 causes of death, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2015;385:117- 171. DOI: 10.1016/S0140-6736(14)61682-2.
5. Soldozy S, Norat P, Elsarrag M, Chatrath A, Costello JS, Sokolowski JD, et al. The biophysical role of hemodynamics in the pathogenesis of cerebral aneurysm formation and rupture. Neurosurg Focus. 2019 Jul 1;47(1):E11. DOI: 10.3171/2019.4.FOCUS19232.
6. Ahmadi A, Argulian E, Leipsic J, Newby DE, Narula J. From Subclinical Atherosclerosis to Plaque Progression and Acute Coronary Events: JACC State-of-the-Art Review. J Am Coll Cardiol. 2019 Sep 24;74(12):1608-1617. DOI: 10.1016/j.jacc.2019.08.012.
7. Brown AJ, Teng Z, Evans PC, Gillard JH, Samady H, Bennett MR. Role of biomechanical forces in the natural history of coronary atherosclerosis. Nat Rev Cardiol. 2016 Apr;13(4):210-20. DOI: 10.1038/nrcardio.2015.203.
8. Pugliese G, Iacobini C, Blasetti Fantauzzi C, Menini S. The dark and bright side of atherosclerotic calcification. Atherosclerosis. 2015 Feb;238(2):220-30. DOI: 10.1016/j.atherosclerosis.2014.12.011.
9. Radomychelski I, Piddubnyi A, Danilchenko S, Maksymova O, Moskalenko Y, Moskalenko R. Morphological and Crystal-Chemical Features of Macro- and Microcalcifications of Human Aorta. Microscopy and Microanalysis. 2021;27(6):1539-1546. DOI:10.1017/ S1431927621012721.
10. Moskalenko RA. Rolʹ patolohichnoyi biomineralizatsiyi pry aterosklerotychnomu urazhenni aorty. Aktualʹni problemy suchasnoyi medytsyny. 2017;2(5):56-62. [in Ukrainian].
11. Lok ZSY, Lyle A. Osteopontin in vascular disease: friend or foe? Arterioscler Thromb Vasc Biol. 2019;39:613-622. DOI: 10.1161/ ATVBAHA.118.311577.
12. Stary HC, Chandler AB, Glagov S, Guyton JR, Insull WJr, Rosenfeld ME, et al. A definition of initial, fatty streak, and intermediate lesions of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation. 1994 May;89(5):2462-78. DOI: 10.1161/01.cir.89.5.2462.
13. Menini S, Iacobini C, Ricci C, Blasetti Fantauzzi C, Salvi L, Pesce CM, et al. The galectin-3/RAGE dyad modulates vascular osteogenesis in atherosclerosis. Cardiovasc Res. 2013 Dec 1;100(3):472-80. DOI: 10.1093/cvr/cvt206.

«Bulletin of problems biology and medicine» Issue 4 (162), 2021 year, 285-290 pages, index UDK 616.13-004.6-091.8-073.756.8

10.29254/2077-4214-2021-4-162-285-290