CC BY
12
II. ХИРУРГИЯ
МРНТИ 76.29.30
ABOUT THE AUTHORS
Khanchi M. - surgeon of the department of vascular surgeon, PHD, a high level certificate physician, e-mail:khanchi.mead@yahoo.com
Matkerimov A.Zhv. - head of the department of a vascular surgery, a high level certificate physician, e-mail: oskar@mail.ru
Baubekov A.A - vascular surgeon, e-mail: baubekov81@mail.ru
Tergeussizov A.C.- vascular surgeon, e-mail: tima9_9@mail.ru
Zhakubayev M.A.- vascular surgeon, e-mail: mjakubayev@gmail.com
Tajibayev T.K.- vascular surgeon, e-mail: dr.tajibayev@gmail.com
Makkamov Rustam - vascular surgeon, e-mail: rustam_2108@mail.ru
Yerkinbaev N.N. - vascular surgeon, e-mail: Erkin_92mail.ru
Saduakas A.Y. - vascular surgeon, e-mail: almas.saduakas91@yahoo.com
Keywords
Morph functional structure of the vascular wall and its role in the pathogenesis of aneurysms, complex surgical treatment of peripheral artery aneurysms
АВТОРЛАР ТУРАЛЫ
Ханчи Миад - Ангиохирургия бел/мшес/н/ц дэргерi, PHD, xoFapbi санатты дэргер, e-mail: khanchi.mead@yahoo.com
Маткеримов А.Ж. - Ангиохирургия бел/мшес/н/ц мецгеруш/с/, жоFары санатты дэр1гер, e-mail: oskar@mail.ru
Баубеков А.А.- ангиохирург, e-mail: baubekov81@mail.ru
Тергеусизов А.С.- ангиохирург, e-mail: tima9_9@mail.ru
Жакубаев М.А.- ангиохирург, e-mail: mjakubayev@gmail.com
Таджибаев Т.К.-ангиохирург, e-mail: dr.tajibayev@gmail.com
Маккамов Р.О. - ангиохирург, e-mail: rustam_2108@mail.ru
Еркинбаев Н.Н. - ангиохирург, e-mail: Erkin_92mail.ru Садуакас А.Е. - ангиохирург, e-mail: almas.saduakas91@yahoo.com
Шамшиев А.С. - ангиохирург, e-mail: almas.26@mail.ru
Туйш сездер
Тамыр кабырасынын морфо-функциональды курылымы жэне оный, аневризма патогенез^еп рeлi, перифериялык артери-ялар аневризмасын кешенцi хирургиялык емдеу
CLINICAL AND ACADEMIC ASPECTS OF PERIPHERAL ARTERY ANEURISM (literature review) part one
Khanchi Mead, Matkerimov A.Zh, Demeuov T.N., Baubekov A.A., Zhakubayev M.A., Tergeussizov A.S., Tajibayev T.K., Yerkinbaev N.N., Makkamov R.O., Saduakas A.Y., Shamshiev A.S.
National Scientific Center of Surgery named after A.N. Syzganov, Almaty, Kazakhstan
Abstract
The review provides data on modern criteria for evaluating peripheral artery aneurysm of various etiology and localization. One of the most common causes of aneurysms the peripheral artery is an injury. Particular attention should be paid to a significant increase in the number of iatrogenic injuries. In recent years, the most complex reconstructive interventions for peripheral artery aneurysms of various etiologies have been introduced. The difficulties that the surgeon faces when performing these operations are due to the variety of anatomical variants of aneurysms. The severity of hemodynamic disorders that occur in this pathology, as well as the complexity of topographic and anatomical relationships. All of the above determines the need for further study of the etiology, pathogenesis, and clinical picture of this disease in order to improve the diagnosis and results of surgical treatment of these diseases.
Перифериялык артериялар аневризмасыньщ клиникалык-академиялык аспектшер1 (Эдебиеттерге шолу) 1-бел1м
Ханчи Миад, MaTKepiMOB А.Ж., Демеуов Т.Н., Баубеков Э.Э., Жакубаев М.А., ТергеуЫзов А.С., Тэжiбаев Т.К., Еркшбаев Н.Н., Маккамов Р.О., Садуакас А.С., Шамшиев А.С
А.Н. Сь^анов атындагы Улттык, гылыми хирургия орталыгы, Алматы, К,азак,стан
Андатпа
Шолуда турлi этиологиядагы жэне локализациядагы перифериялык артериялар аневризмасын багалаудын заманауи критерийлерi туралы мэл'шеттер берлген. Перифериялык аневризмалардын дамуынын кен таралган себептер'т'щ б'р - жаракат. Ятрогендi жаракаттар санынын артуына ерек-ше назар аудару кажет. Сонгы жылдары турлi этиологиядагы перифериялык артериялар аневриз-масы кезШде курдел'1 реконструктивт'1к араласулар енпзл^. Бул операцияларды орындау кезШде хирург кез'гетШ киындыктар аневризманын анатомиялык нускаларынын алуан турл^пне, осы патология кезШде туындайтын гемодинамикалык бузылыстардын ауырлыгына, сондай-ак топографиялык-анатомиялык эрекеттестШн курделЫпне байланысты. Жотарыда мазмундалгандардын барлыгы осы ауруларды хирургиялык емдеу^н нэтижелерiн жэне диагностикасын жаксарту максатында осы аурудын клиникалык кeрiнiсiн, патогенезн, этиологиясын ары карай зерттеудiн кажетт^пн айкындайды.
Клинико-академические аспекты аневризм периферических артерий (обзор литературы) часть 1
Ханчи Миад, Маткеримов А.Ж., Демеуов Т.Н., Баубеков А.А., Жакубаев М.А., Тергеусизов А.С., Таджибаев Т.К., Еркинбаев Н.Н., Маккамов Р.О., Садуакас А.С., Шамшиев А.С.
Национальный научный центр хирургии им. А.Н. Сызганова, Алматы, Казахстан
Аннотация
В обзоре приведены данные о современных критериях оценки аневризма периферических артерии различных этиология и локализация. Одной из наиболее распространенных причин развития аневризм периферических артерии является травма. Особое внимание необходимо уделить значительному увеличению количества ятрогенных травм. В последние годы внедрены наиболее сложные реконструктивные вмешательства при аневризмах периферические артерии различных этиология. Сложности, с которыми сталкивается хирург при выполнение этих операциях, обусловлены многообразием анатомических вариантов аневризм. Тяжестью гемодинамических нарушений, возникающих при этой патологии, а также сложностью топографо-анатомических взаимоотношений. Все выше сказанное предопределяет необходимость дальнейшего изучения этиологические, патогенеза, клинической картины этого заболевания для улучшения диагностики и результатов хирургического лечение этих заболеваний.
Aneurysms of the aorta and peripheral arteries are a common variant of the pathology of the cardiovascular system. The choice of the vascular surgery method for the relief of peripheral vascular dysfunction aneu-rysms is largely determined by the competence of the diagnostic tool. Most scientific studies were carried out on biological models, however, they do not provide the necessary detail and analysis of the pathology of the aortic wall [de Jong M, Essers J, van Weerden WM., 2014]. However, the distinction between healthy and diseased tissue is the basis for understanding the initiation and progression of cardiovascular disease -both clinically and pre-clinical. This is why, ever since the landscape of medical imaging and diagnostics changed dramatically with the discovery of X-rays by the German physicist Wilhelm Konrad Roentgen in 1895, there has been an ongoing search to improve image resolution and contrast [Logghe G, Trachet B, Aslanidou L, et al. , 2018].
Until now, there is no clear algorithm for diagnosing patients with PAA, on the one hand, this leads to late diagnosis of the disease, after the development of its complications. On the other hand, the development of modern diagnostic methods has not yet led to a generally recognized revision of recommendations for diagnostic tactics. The most controversial issue is the mandatory use of angiography in the diagnosis of this condition.
The need for timely diagnosis of PAA is beyond doubt. However, focusing on literary sources, it can be noted that the stage of the problem is still far from being resolved. Also, many studies note that the surgical treatment of this pathology cannot be considered definitively developed. primarily associated with the variety and complexity of anatomical options, a feature of hemodynamic disorders. The availability of various and far from differently valuable methods of surgical treatment.
Thus, the clinical diagnosis of aneurysms and peripheral arteries (APA) is based on histogenetic, pathomorphological and pathophysiological features of the structure and functioning of the vascular wall. Consequently, a detailed and updated understanding of the morphological principles of the structure of blood vessels, the role and participation of the tissues forming the vascular wall is needed, which allows using high-tech diagnostic equipment to verify its pathological changes in the early stages. Although improved imaging techniques such as X-ray, ultrasound, and echocardiogram have contributed to the earlier detection of aneurysms, surgery is currently the only treatment available. There is no doubt that the volume of medical intervention, conservative or surgical, is determined taking into account the nuances listed above, which are presented in more detail in this section of the work.
ОБ АВТОРАХ
Ханчи Миад. - врач отделения ангиохирургии, PHD, врач высшей категории, e-mail: khanchi.mead@yahoo.com
Маткеримов А.Ж. - заведующий отделением ангиохирургии, врач высшей категории, e-mail: oskar@mail.ru
Баубеков А.А.- ангиохирург, e-mail: baubekov81@mail.ru
ТергеусизовА.С.- ангиохирург, e-mail: tima9_9@mail.ru
Жакубаев М.А.- ангиохирург, e-mail: mjakubayev@gmail.com
Таджибаев Т.К. - ангиохирург, e-mail: dr.tajibayev@gmail.com
Маккамов Р.О. - ангиохирург, e-mail: rustam_2108@mail.ru
Еркинбаев Н.Н. - ангиохирург, e-mail: Erkin_92mail.ru
Садуакас А.Е. - ангиохирург, e-mail: almas.saduakas91@yahoo.com
Шамшиев А.С. - ангиохирург, e-mail: almas.26@mail.ru
Ключевые слова
Морфофункциональное строение сосудистой стенке и роль ее в патогенезе аневризм, комплексное хирургическое лечение аневризм периферических артерии.
1.1. Morphofunctional structure of the vascular wall and its role in the pathogenesis of aneurysms
The peripheral vascular system (PVS) includes all the blood vessels that are outside the heart. PSS are classified as follows: (Anatomy, Blood Vessels, William D. Tucker; Kunal Mahajan.Author Information, Last Update: January 4, 2019.
1. The aorta and its branches.
2. Arterioles.
3. Capillaries.
4. Venules and veins.
The functions and structure of each PVS segment differ depending on the organ supplied by blood. However, the general plan of the structure of the vessels is represented by three layers:
1. Adventitia or outer layer that provides structural support and vessel shape.
2. The middle sheath, a media consisting of elastic and muscular tissue, which regulates the inner diameter of the vessel.
3. Intima or inner layer.
Within each layer, the number of muscle fibrils and collagen varies depending on the size and location of the vessel [Tucker WD, Bhimji SS.]
The wall of blood vessels belongs to the organs of the layered type of organization. The primary cell types of the arterial wall were described as early as the 19th century. These are endothelial cells and smooth muscle cells. In recent years, a large number of additional cell types have been identified, revealing the complex morphology of large blood vessels. The lumen of the artery is lined with a layer of endothelial cells, which, in addition to performing the main barrier function, also secrete vasodilators (for example, nitric oxide) and vasoconstrictors (endothelin-1). A thin basement membrane separates the endothelium from the surrounding tissues and the inner lining. Here, pericytes are located in a special layer, which, together with endothelial cells, form an interconnected network [Orekhov A.N., Bo-bryshev Y.V., Chistiakov D.A., 2014].
The role of pericytes located in the intima of large vessels, however, has yet to be clarified, but today their significance is postulated in the literature as an atherogenic link in the development of local inflammation [Ivanova E.A., Bobryshev Y.V., Orekhov A.N., 2015].
Pericytes can be distinguished by their secreted neuro glial antigen 2 (NG2) and CD146. In extracor-poreal experiments, pericytes can also differentiate into smooth muscle cells and various cell differen-tions of mesenchymal origin [Billaud M., Donnenberg V.S., Ellis B.W., et al., 2017]. Under natural conditions, the plasticity of pericytes is difficult to establish due to the lack of a specific trace line for transgenic models. As, for example, in the clinical
and experimental work of Manchester researchers. Using the Tbx18 (T-box 18) - CRE-ERT2 marker of pericytes, which determines their further development in the tissues of mice, extracorporeally (in vitro) it was possible to obtain a line of differentiation of pericytes that retain their perivascular characteristics, and in vivo this experiment did not show itself. even in the face of induced trauma. In addition, the available data do not exclude that other populations of perivascular cells do not perceive the influence of Tbx18, and in a living organism can act as progenitor cells. [Guimaraes-Camboa N., Cattaneo P., Sun Y., et al., 2017]. Mesangioblasts represent a subset of perivascular cells of the aorta and can also be induced to differentiate [Roostalu U, Wong JK., 2018].
The intercellular matrix of the inner shell consists of proteoglycans, and the cellular composition, in addition to endothelial and pericitis, is also represented by low-differentiated smooth muscle cells. It is known that in the wall it is the aorta certain differentions of smooth muscle cells develop in the early stages of the embryo and are preserved in an immature state until adulthood. These cells form cushion-shaped branches. It is believed that they can provide strength to the vascular wall in the areas of aneurysm deformation of the vascular wall, under the influence of blood flow turbulence and may even represent a pool of immature cells that can contribute to the development of smooth muscle cells. However, this structure of the vascular wall contributes to the development of atherosclerotic lesions, which demonstrates the importance of histological architecture in the context of cardiovascular medicine [Roostalu U, Wong JK., 2018].
In the inner lining of the arteries, intima, an internal elastic membrane is also isolated, consisting of elastic fibers and a spindle-shaped form of contractile smooth myocytes. In the middle lining of the vessel, the media, smooth myocytes are most prominent and form concentric layers of mature smooth muscle tissue. Elastin, located on the surface and surrounding smooth muscle cells, allows large arteries to expand and narrow during systole and diastole. The relative abundance of collagen (type 4 collagen in the wall of the thoracic aorta) and other extracellular matrix molecules of elastin determines the biomechanical properties of arteries [Cheng J.K., Wagenseil J.E., 2012; Xu K, Xu C, Zhang Y, et al., 2018].
The middle shell, the media, is surrounded by the adventitia layer, which is represented by loose connective tissue and contains many cell diferons. Identification of the cell composition of the vascular wall is of great clinical and laboratory importance for the determination of markers corresponding to discrete cell lines at different stages of differentia-
tion of one cell line. The most common markers for adventitial cells are SCA1 (stem cell antigen-1) and CD34, which identify cells around the artery itself. Similar CD34 + cells are found at the border of the middle and outer membranes [Roostalu U, Wong JK., 2018].
It is believed that some of the SCA1 + cells may also be located in the middle membrane, which suggests their ability to penetrate into the deep layers, or this indicates their smooth muscle origin. Typical adventitia cells manifest themselves as transcriptional activators and repressors of smooth muscle cells in their state. In addition, these cells decide the fate of endothelial cells. [Shen Y., Wu Y, Zheng Y., et al., 2016].
Some authors have shown in experimental studies that there are even more multipotent progenitor cells in the adventitia. They can be detected using markers of mesenchymal stromal cells (CD44 and CD90). However, it is possible that they represent the same cell population in origin, at different stages of activation and differentiation. These stromal (connective tissue) cells are able to differentiate into smooth muscle cells, they have chondrogenic and adipogenetic properties [Corselli M., Chen
C.W., Sun B., et al., 2012].
The study of adventitial cells using markers is one of the promising areas of vascular medicine. GLI1 + cells express typical markers of adventitial cells - SCA1, CD34 and, to varying degrees, markers of various mesenchymal stromal cells (CD29, CD44, CD90), as well as markers of poorly differentiated smooth myocytes, which indicates possible lineages of these cells. GLI1 + cells can differentiate into smooth myocytes, fibroblasts and osteoblasts [Kramann R., Schneider R.K., DiRocco
D.P., et al., 2015; Kramann R., Goettsch C., Wong-boonsin J., et al., 2016]. There are also progenitor / stem cells in the walls of the blood vessel, which are characterized by the release of the following markers: SRY-Box 10 (S0X10), SOX17, S100A, as well as mesenchymal stromal markers CD44 and CD29. The markers CD31, CD34, CD146 and SCA1 are found in smaller quantities. In an extracorporeal experiment, these cell populations differentiate into smooth myocytes, Schwann cells of peripheral neurons, chondrocytes, osteoblasts and adipocytes [Tang Z., Wang A., Yuan F., et al., 2012].
Large human vessels are surrounded by a dense capillary network, which is located in the adventitia membrane of the vessel wall and is called vasa va-sorum (vessels of the vessels). They are necessary for the blood supply to the outer layers of the vessel (middle and outer shells). Perivascular adipose tissue creates a kind of cushion around the artery, even extending far beyond the adventitia layer. The composition of adipose tissue in human arteries is
represented by brown and white adipocytes [Brown N.K., Zhou Z., Zhang J., et al., 2014]. Perivascu-lar adipocytes are increasingly recognized as an important vascular mediator system. They release a wide variety of signaling molecules that often promote vasodilation: adiponectin, H2, angiotensin (1-7), palmitic acid methyl ester and prostacyclins [Cheng J.K., Wagenseil J.E., 2012 and many others]. Adipocytes can also potentiate contractile smooth muscle cells and produce angiotensin II and superoxide [Owen M.K., Witzmann F.A., McKenney M.L., et al., 2013; Ramirez J.G., O'Malley E.J., Ho W.S.V., 2017]. In addition, perivascular adipocytes regulate intravascular temperature [Cheng J.K., Wagenseil J.E., 2012] and secrete a large amount of cytokines and growth factors that affect cell differentiation in the arterial wall [Nosalski R., Guzik T.J., 2017]. Finally, the arteries are richly innervated, which is necessary to modulate vascular tone.
Most tissues respond to damage with an inflammatory response, in which many different cell populations are involved. In addition, the changes also affect intracellular transformations. It was revealed that the cathepsin gene plays an important role in the pathological cascade of the pathology of cardiovascular diseases, in particular, dysfunction of the heart valves, stiffness of the aorta and its dilatation. Excessive accumulation of cathepsin in lysosomes leads to degradation of the extracellular matrix components of the aorta, cardiac muscle and heart valves, primarily due to fibroblast dysfunction. Inhibition of cathepsin improves the parameters of cardiac function, the state of the aortic wall and the valve apparatus by increasing the total activity of elastase in the aorta [Gonzalez EA, Martins GR, Tavares AMV, et al., 2018].
Other authors also wrote about the participation of intercellular components in the pathogen-esis of diseases of various parts of the aorta. Thus, K. Subramaniam and M.N. Sheppard in his works established that dilatation and subsequent rupture of the aorta occurs as a result of extensive cystic degeneration of the medial layer of the aorta and degeneration of smooth muscle cell nuclei, with disorganization, fragmentation, disappearance of elastin fibers and an increase in collagen [Subramaniam K, Sheppard MN., 2018].
Abdominal aortic aneurysm (AAA) is an enlargement of the abdominal aorta that causes serious complications and death. The development of AAA is associated with the accumulation of cells that cause inflammation in the aneurysmal vascular wall. These cells include various types of leukocytes, such as monocytes, macrophages, dendritic cells (DC), NK cells, neutrophils, B lymphocytes and T lymphocytes [Patel MJ, Blazing MA. 2013; Chang TW, Gracon AS, Murphy MP, et al. 2015]. The in-
flammatory response is a key process in the pathogenesis of AA [Peshkova IO, Schaefer G, Koltsova EK. 2016], since it increases the production of elas-tase and other proteinases (matrix metalloprotein-ases, serine proteinases, cathepsins), which are primarily responsible for the structural loss of the integrity of the vessel walls leading to the formation of AA [Sterpetti AV., 2013]. In addition, many authors noted a local increase in the level of biologically active substances:
1. chemokines
1.1. monocyte chemoattractant protein-1 [Na-kao T, Horie T, Baba O, et al., 2017];
1.2. chemokine C-C in ligand 22 (CCL22) [Jones GT, Phillips LV, Williams MJ, et al., 2016],
1.3. chemokine secreted by stromal cells (stromal cell-derived factor 1 (SDF-1) / chemo-kine (CXC motif) receptor 4 - CXCR4 and its ligand CXCL12 [Michineau S, Franck G, Wagner-Ballon O, et al., 2014; Tanios F , Pelisek J, Lutz B, et al., 2015];
2. growth factors: granulocyte colony stimulating factor (GCSF) and macrophage colony stimulating factor (MCSF) [Lu G, Su G, Davis JP, et al., 2017];
3. cytokines (TNF-a, IL-6, IL-1 p) [Lu G, Su G, Davis JP, et al., 2017; Lindberg S, Zarrouk M, Holst J, et al., 2016].
Such a complex interaction of immunocompe-tent cells and cytokines in the pathogenesis of ABA determines the regulation of pro-inflammatory th1 cells (producers of IL-1 p, IL-6, TNF-a and IFN-y) and anti-inflammatory th2 cells (producing IL-4, IL-5 and IL -10) [Johnston WF, Salmon M, Su G, et al., 2013].
Natural killer cells (NK lymphocytes) and a subset of other T cells express the invariant T cell receptor (TCR) and markers characteristic of these cells, which are found in abundance in the aneu-rysmal vessel wall. When activated and depending on conditions, natural killer cells can quickly and simultaneously produce large amounts of both pro-inflammatory (IFN-y, IL-2, TNF-a) and / or anti-inflammatory cytokines (IL-4, IL-5, il-10, il-13). Numerous studies have already proven the role of killer T cells in atherogenesis, but whether the presence of these cells in the aneurysmal vascular wall is directly related to the development of aneurysms is still unknown. Killer cells promote the development of aneurysms by inducing the expression of matrix enzymes that destroy smooth muscle cells and macrophages, which leads to the release of cytokines and a decrease in the viability of smooth myocytes in an angiotensin II-mediated model. [van Puijvelde GH, Kuiper J., 2017; van Puijvelde GHM, Foks AC, van Bochove RE, et al., 2018].
In addition, the literature pays attention to the development of macroautophagy as an element of
the pathogenesis of aneurysms. Autophagy is the most important cellular response to stress, manifested by the destruction of defective macromol-ecules and organelles, accompanied by the release of bioenergetic intermediates during hypoxia and lack of nutrients. Taking into account the prevalence of aneurysms in aged patients, some authors believe that the pathogenesis of aneurysms is due to thiol-dependent disorders of autophagy during aging. Losses in the covalently bound LC3 molecule damage the thiol catalytic processes mediated by the Atg3 and Atg7 proteins, which leads to inhibition of oxidation, preventing lipidolization of LC3 [Frudd K, Burgoyne T, Burgoyne JR., 2018].
Thus, the hemodynamic conditions in which the vessels function predetermine the features of their architectonics [Teregulov Yu.E., Mayanskaya SD, Teregulova ET, 2017]. In the pathogenesis of aneurysms, inflammatory reactions, including autoimmune ones, are of great importance. Theoretical experimental-academic knowledge can be applied in clinical practice, for example, in determining the cytokine profile, consisting of pro-inflammatory cytokines, chemokines, and specific growth factors in patients with aneurysms. The prospects for conservative treatment are also associated with the functioning of the vascular wall at the cellular level. By morphology: rventions. When carrying out surgical treatment, the structural features of the vascular wall described above must also be taken into account.
Classification of peripheral artery aneurysm
Classification of aneurysms is an important stage in preparation for surgery, the volume of which will directly depend on the results of auxiliary and high-tech methods of diagnostic examination of patients. For example, using CT, you can diagnose with high accuracy changes in the aorta and its branches, identify such a serious complication as dissection of the aorta [Bazhenova Yu.V., Dran-tusova N.S., Shanturov V.A., et al., 2014] ...
The main options for the classification of aneu-rysms involve taking into account such factors as etiology, morphology, localization of aneurysms, and clinical manifestations.
According to the pathogenetic principle, aneu-rysms are distinguished:
1. aneurysma verum,
2. aneurysma spurium,
3. aneurysma dissecans,
4. aneurysma congenitalis - angiodysplasias.
By morphology:
1. saccular
2. fusiform
By localization in PVS:
1. iliac,
2. Aneurysms of the visceral arteries of the abdominal cavity
3. femoral,
4. popliteal,
5. cartid
6. subclavian,
7. arteria brachialis,
8. radialis
9. ulnar,
10. tibia
11. axillary arteries.
Among the various types of peripheral vascular aneurysms, the most common are traumatic and atherosclerotic, which are of the greatest practical interest. Traumatic aneurysms are formed as a result of damage to blood vessels, mainly after bullet and shrapnel wounds. Their percentage in relation to all aneurysms of peripheral arteries is on average about 50% (A.A. Spiridonov, K.M. Morozov, 2004). It is noted that in the last 10-15 years the number of post-traumatic aneurysms has increased significantly. Most often, according to most authors, traumatic aneurysms are localized on the femoral artery, then on the popliteal, brachial, axillary and common carotid arteries. An independent group consists of pseudo-aneurysms of iatrogenic origin, and their number increases according to the spread of angiographic studies. The predominant localization of iatrogenic aneurysms: the femoral artery after its puncture according to Seldinger, the jugular and subclavian veins. Attention should also be paid to postoperative aneurysms that develop after various reconstructive operations on the vessels. False aneurysms of the anastomoses can be caused by the primary infection of the surgical wound and prosthesis, the failure of the anastomoses, the eruption of sutures due to various reasons. True aneurysms of the anastomoses area develop after endarterectomy and plasty of the autovein artery, as well as due to the ongoing degenerative process in the vascular wall. Explants aneurysms are more typical for biological and semi-biological materials. An essential role in the development of aneurysms is played by the presence of hypertension in patients. In the development of peripheral aneurysms against the background of nonspecific aortoarteri-tis, the starting point is inflammation, which begins with adventitia and leads to the destruction of the vascular wall with the subsequent formation of aneurysmal expansion.
From a tactical point of view, the Stanford classification is more convenient and justified, since it allows us to clearly distinguish which of the patients requires urgent surgical treatment (type A), who can be treated with medication until the condition stabilizes (type B), and operated on with appropriate indications in the long term.
The generally accepted classification of true (chronic) thoracoabdominal aortic aneurysms is E.S. Crawford (1986), taking into account the prevalence of the process and the involvement of the main branches of the aorta.
Aneurysms of the visceral arteries of the abdominal cavity
Aneurysms of the visceral arteries (AVA) of the abdominal cavity are rare diseases and are often a diagnostic finding during examination or are diagnosed when complications arise (ruptures, thrombosis of the distal parts). According to pathological studies, AVA are detected in 0.01-0.2%. According to the literature, the most common aneurysms of the splenic artery, hepatic artery (respectively 6080 and 20%), much less often gastroduodenal, pancreatoduodenal and superior mesenteric arteries. The causes of AVA are atherosclerosis, fibro-muscular dysplasia, disorders in the synthesis of collagen structure, trauma, etc.
Clinically, AVA can manifest itself when they rupture and are accompanied by symptoms of "acute abdomen", hypotension. Ultrasound duplex scanning plays a certain role in diagnostics. An accurate diagnosis of ABA is established by performing multispiral computed tomography, angiography of the visceral branches of the abdominal aorta.
In the treatment of AVA, endovascular, surgical methods are used. So, in case of aneurysm of the splenic artery, resection of the aneurysm is recommended, with its large size and location in the gate of the spleen - splenectomy, if possible, resection is completed by restoration of the splenic artery. In case of aneurysm of the hepatic artery, it is recommended to ligate the hepatic artery without reconstruction with the proximal extrahepatic location of the aneurysm; sometimes it becomes necessary to perform shunting operations on the distal segment of the hepatic artery [6]. Endovascular interventions - stenting, aneurysm embolization are low-traumatic, but they should be performed according to strict indications. [3, 6, 7].
Aneurysm of the renal arteries is a local expansion of the diameter of the vessel in two or more times, compared with its unchanged or normal diameter. This disease is very rare. Aneurysms of the renal arteries account for only 0.8 - 1% of aneurysms of all other localizations (A. Abeshouse, 1951). However, at present, in connection with the improvement of diagnostic methods, especially screening, as well as the introduction of renal an-giography into clinical practice has led to a more frequent diagnosis of this disease (Pliskin M.J. et al., 1990).
The first preoperative diagnosis was made in 1924 by G. Soderlung, who radiographically re-
vealed a calcified aneurysm, confirmed the diagnosis pyelographically and successfully performed nephrectomy.
The main etiological causes of renal artery aneurysm are: congenital degeneration of the media, atherosclerosis, nonspecific aortoarteri-tis, fibromuscular dysplasia, periarteritis nodosa and trauma (E.K. Berezovskaya et al., 1950; N.A. Nemirovskaya, 1961; N.A. Lopatkin et al., 1969; A.A. Spiridonov, 1972; E. Poutasse, 1966; Yu.V. Belov et al., 2003).
The largest percentage of aneurysms of the renal arteries are localized in the area of the bifurcation of the main trunk or its branches (about 50%), since it is in this place that, as a result of congenital or acquired diseases, degeneration of the elastic structures of the artery wall and its media is noted (S. Ekestrom, 1964). A separate group includes poststenotic aneurysms that form distal to the narrowed segment of the renal artery, which arose on the basis of atherosclerosis, arteritis, or FMD. Constantly remitting fluctuations in blood flow velocity, changes in its shape and turbulence gradually lead to aneurysmal dilatation of the walls of the renal artery. However, not every post-stenotic dilatation of the artery should be regarded as an aneurysm. An aneurysm means only those cases where there are degenerative changes in the walls of the vessel (E.F. Poutasse, 1966).
At the initial stage of their formation, true aneu-rysms are small and thin-walled. Gradually, as the size of the aneurysm increases, its walls thicken, harden and harden and finally undergo calcification (E.F. Poutasse, 1975).
Aneurysms of interrenal localization are of particular interest, since rupture of these aneurysms can occur in 30% of cases, and 2/3 of these ruptures are fatal (W. Baker et al., 1953; B. Hogbin et al., 1969).
Clinically, aneurysms of the renal arteries can be completely asymptomatic and, in most cases, are an accidental finding during angiography (V.V. Chikov, 1972; A.A. Spiridonov, 1972), or are detected during a general image of the kidneys with calcification of the walls. Nevertheless, the main clinical symptoms are considered to be hypertension, pain, hematuria, systolic murmur in the projection of the renal artery.
Hypertensive syndrome, according to various authors, occurs from 15% - 85% of cases (B. Abe-shouse, 1951; S. Ekestrom, 1964; P. Glass et al., 1967; C. McKiel et al., 1966). Until now, the question of the causal relationship of renal artery an-eurysms and hypertensive syndrome has not been finally resolved. However, the fact that hypertension is completely stopped after nephrectomy or resection of the aneurysm with adequate reconstruction
of the renal artery indicates a certain relationship of this pathology with vaso-renal hypertension (S. McKiel et al., 1966; E. Poutasse, 1966; A.A. Spiridonov, 1972).
The most frequent clinical sign of pathology, which occurs in 50% of cases, is pain (G.G. Ara-bidze, 1969). Pain can usually be dull, indefinite in the lumbar region of the corresponding side, without a clear irradiation. However, with complications (rupture, thrombosis), they sharply increase, giving a clinic of acute abdomen, renal colic, kidney infarction, simulating complications of various diseases of the genitourinary system: kidney stones, tumor, cyst, kidney abscess, kidney rupture, acute abdomen, etc.
Another relatively common symptom of renal artery aneurysm is hematuria. In most cases of uncomplicated course, constant intermittent micro-hematuria can be observed. Clinical manifestations of complicated forms depend on the nature of the complication that has occurred: with thrombosis of an aneurysm, the picture of kidney infarction, described above, develops; when an aneurysm breaks into the renal collector, a picture of unilateral profuse bleeding through the urinary tract is observed. In general, the analysis of the uncomplicated and complicated course of the renal artery aneurysm shows that there is practically no clear clinical picture on the basis of which this diagnosis can be confidently made.
The easiest to diagnose, as mentioned above, are calcified aneurysms of the renal arteries. However, the presence of a calcified rounded shadow in the projection of the kidney on an ordinary X-ray image also requires verification of the diagnosis with urolithiasis, calcified mesenteric lymph node, tuberculous kidney abscess and many other diseases. A comparative study of the calyx-pelvic apparatus and the functional state of the kidneys based on the results of excretory urography can provide some help for the differential diagnosis in such cases.
The main method for diagnosing PA aneurysms is contrast X-ray angionography. In recent years, duplex scanning has been used as a screening method.
Aneurysms of the upper limb arteries
These aneurysms account for 34.04% of all peripheral aneurysms. Aneurysms of the subclavian artery account for 14.2%, axillary - 1.4%, brachial - 11.35%, radial - 3.55%, ulnar artery - 3.55%. In most cases, aneurysms of the upper limb arteries are of traumatic or mycotic origin. Aneurysms are localized in the subclavian, axillary and brachial arteries, other localizations are extremely rare.
Subclavian artery aneurysms often develop as a result of poststenotic dilatation caused by exter-
nal compression of the subclavian artery. Often this is joined by secondary atherosclerotic changes, and a variant of the exclusively atherosclerotic nature of aneurysmal lesion of the vessel wall is also possible. In chest exit syndrome, the cause of compression is the clavicle, I or accessory rib. The incidence of aneurysms in this pathology reaches 48.14% of all cases of exit syndrome, and in 18.5% of patients this pathology is not accompanied by embolization of the distal bed, and in 19.6% it is accompanied by distal embolization (when calculating for all cases of observation of the syndrome of exit from the chest).
The mechanism of subclavian artery aneurysm formation as a consequence of the thoracic exit syndrome,cells were first described by W.S. Hoisted in 1956. In the same year, C.J. Schein, H. Ham-ovici and H. Yang. confirmed this mechanism as a consequence of trauma to the artery when leaving the chest and described the mechanism of arterio-arterial embolism with the development of upper limb ischemia,The treatment of this pathology is the decompression of the artery by the method of resection of the compressing anatomical formation, and in some cases, cervicothoracic sympathectomy is performed to stop ischemia of the limb.
Aneurysms in exit syndrome account for approximately 6.4% of all peripheral aneurysms. This group is mainly represented by male patients.
E.S. Crawford et al. observed aneurysms of the subclavian artery only of atherosclerotic genesis only in 3 of 107 patients with peripheral aneu-rysms of various localization. With atherosclerotic genesis, treatment involves resection followed by prosthesis.
Axillary artery aneurysms are usually asymptomatic. As a rule, symptoms appear when throm-boembolism joins the peripheral arterial bed with the development of ischemia of the distal extremities.
Surgical treatment of aneurysms of this localization involves resection followed by an end-to-end anastomosis or replacement of the resected segment with a synthetic or auto-vein.
Aneurysms of the brachial artery and radialis, ulnar arteries
In most cases, aneurysms of this localization are the result of trauma. S. Matas in 1888 described the classic symptomatology of aneurysms of this localization. Clinical manifestations include both symptoms of vascular origin and peripheral neurological symptoms.
Aneurysms of the radial and ulnar arteries are also based on post-traumatic origin. S. Thorrens, having examined a large group of patients, revealed the atherosclerotic nature of the aneurysms of this
localization in only a small number of them. Clinical symptoms and diagnosis are similar to those of brachial artery aneurysm.
Treatment consists in resection of the aneurysm followed by prosthetics. In the treatment of radialis. ulnar aneurysms, resection or alloying is often performed without restoring the patency of the affected segment, but this procedure is possible only if the patency of the palmar arch is preserved.
Carotid aneurysm is a local expansion of the diameter of the carotid artery with a thinning of the vessel wall. Such an aneurysm is especially dangerous due to the fact that blood supply to the brain is carried out through the carotid arteries and any complication of an aneurysm can cause a stroke. This pathology presents great difficulties in treatment, therefore, many vascular departments try to refuse such patients. Few clinics confidently perform surgical and endovascular interventions for carotid aneurysms. An innovative vascular center among them.
An aneurysm can develop in the cervical part of the carotid artery, or its intracerebral part. Any localization is dangerous to life. A ruptured cervical aneurysm is rare, but a blood clot can form that blocks blood flow through the artery, or pieces of it can cause ischemic strokes. Intracerebral aneu-rysms are often complicated by ruptures with the development of hemorrhagic stroke.
Numerous articles in the medical literature describe possible complications and prove that timely treatment avoids adverse outcomes associated with the disease.
The reasons: The main cause of aneurysm development is congenital weakness of connective tissue, connective tissue diseases. Sometimes The starting point for the development of dilatation of the carotid artery can be radiation therapy for neck tumors. Dilation of the internal carotid artery is sometimes observed after stenting or removal of an atherosclerotic plaque.
Types of aneurysms
By localization:
• Carotid artery aneurysm in the bifurcation area
• Internal carotid artery aneurysm
• Aneurysm of the external carotid artery
• Aneurysm of the intracranial section of the internal carotid artery
The form of aneurysm of the carotid artery is:
1. saccular
2. fusiform
Symptoms
The main symptoms of aneurysm of the carotid arteries in the neck are associated with its complications. An aneurysm may not cause any sensa-
tions and is detected by chance during a medical examination or ultrasound of the neck.
• Visual impairment
because of repeated separation of small blood clots, ocular symptoms of an aneurysm of the carotid artery can develop: blurred vision, double vision, dilated pupils, loss of visual fields.
• Headache
Sudden and severe headache pain can be a sign of a ruptured carotid aneurysm as well as other arteries in the brain. This pain is so intense that most patients describe it as "unbearable and most excruciating pain." The headache is usually accompanied by nausea and vomiting, tension in the occipital muscles, often loss of consciousness and coma. Intracranial aneurysm rupture is associated with a very high mortality rate. Therefore, if such aneurysms are detected, they must be operated as early as possible.
Complications
• Transient ischemic attack (microstroke)
One of the important symptoms of the disease is a microstroke or transient ischemic attack (TIA). Clinically, this is manifested by signs of cerebral circulation disorders, which disappear within a day. This may be weakness in an arm or leg, impaired facial expressions, impaired speech, balance, ability to walk, sensitivity in half of the body. The cause of this complication is the detachment of small blood clots from the aneurysm cavity and their transfer to the brain.
• Ischemic stroke
Thrombosis of an aneurysm or separation of a large blood clot leads to the cessation of blood circulation in a large area of the brain and the death of this area. In connection with a stroke, persistent paralysis or cerebral coma develops. Mortality with this complication is at least 40%.
• Compression of the organs of the neck
Large aneurysms can exert pressure on nearby
anatomical structures, such as the jugular vein, larynx, vagus nerve, and recurrent nerve. This leads to the appearance of symptoms such as swelling of the face, hoarseness of voice, difficulty in swallowing and speaking, decreased sensitivity of the skin of the neck and face. A ruptured aneurysm can cause sudden compression of the trachea and death of the patient from asphyxiation.
Prognosis
The likelihood of developing fatal complications with carotid aneurysm is very high. Ischemic stroke occurs in half of patients, rupture within a cerebral aneurysm develops in 25% of patients per year. These complications require timely surgery. After surgical treatment, patients in most cases get rid of
the risks associated with an aneurysm of the carotid artery and live a normal life.
Aneurysm of the femoral and popliteal arteries is a complex and very important problem in modern vascular surgery. According to the literature, aneurysms Diagnosis and surgical treatment of patients with atherosclerotic aneurysms of this localization account for about 70 - 80% of the number of aneurysms of all peripheral arteries (Troitsky A.B. et al., 2005).
Aneurysms of the femoral and popliteal arteries are important nosological units, which is associated with their potential danger of developing complications that threaten not only the limb, but also the patient's life. B.S. Gulter and R.G. Darling, when analyzing 45 clinical observations of patients with femoral artery aneurysms in 47% of them, revealed a complicated clinical course. G.E. Tolsted et al. found thrombosis in 43% of patients with aneurysms of the femoral arteries (Spiridonov A.A. et al., 2004),
There are conflicting opinions about the tactics of treating asymshoma aneurysms. Some authors recommend conservative treatment of such aneu-rysms. It is estimated that 14 to 24% of asymptomatic popliteal aneurysms become symptomatic annually (Antonello M. et al. 2007). According to R. Pulli et al., 2006, the incidence of acute ischemia of the lower extremities due to thrombosis of the popliteal artery aneurysm was! from 7 to 68% of cases.
Ideally, recommendations should be based on knowledge of the natural course of the disease, but there are practically no such observations. It is known that with an increase in the duration of the disease, the number of complications increases. A. Roggoetal. (1993) report that all patients with 45 aneurysms of the popliteal arteries who were treated "conservatively" developed symptoms of limb ischemia, and this required surgical intervention on average within 4.2 years after diagnosis, with half of the patients during the first two years old. However, there are currently no large enough studies to determine the rate of complications or limb loss.
The results of surgical treatment depend on the underlying conditions. The best long-term results are observed in patients with asymptomatic aneu-rysms. There is evidence that surgical treatment of asymptomatic aneurysms is significantly better than symptomatic aneurysms (J.Ruch et al., 2006).
Thus, until now there is no clear algorithm for the surgical treatment of patients with femoral and popliteal aneurysms, which leads in a large number of cases to the development of complications (rupture, thrombosis, thromboembolism). In addition, despite the development of a large number of different types of treatment for patients with this disease, there is no unified tactics for the treatment of patients with femoral and popliteal aneurysms,
depending on their location, prevalence and severity of hemodynamic disorders.
All of the above determines the need for further study of the clinical picture of this disease in order to improve the diagnosis and results of surgical treatment of patients with aneurysms of the femoral and popliteal arteries.
The aim of this study was to improve the results of surgical treatment of patients with atherosclerotic aneurysms of the femoral and popliteal arteries.
In accordance with this goal, the following research objectives are formulated:
1. To assess the likelihood of complications in patients with atherosclerotic aneurysm of the femoral and popliteal arteries, depending on the duration of existence.
2. To evaluate the immediate results of surgical treatment of atherosclerotic aneurysms of the femoral and popliteal arteries.
3. To carry out a comparative analysis of the long-term results of surgical treatment of atherosclerotic aneurysms of the femoral and popliteal arteries in asymptomatic patients and patients with a complicated course of the disease.
References
1. Gerlinde Logghe (UGent), Bram Trachet (UGent), Lydia Aslanidou, Pablo Villaneuva-Perez, Julie De Backer (UGent), Nikolaos Stergiopulos, Marco Stam-panoni, Hiroki Aoki and Patrick Segers, Propagation-based phase-contrast imaging of aortic dissection in mice: from individual elastic lamella to 3D analysis. (UGent).(2018) Biomechanics, 8th World congress, Abstracts.
2. William D. Tucker; Yingyot Arora; Kunal Mahajan. Anatomy, Blood Vessels Treasure Island (FL): Stat-Pearls Publishing; 2020 Jan. PubMed]
3. Tucker, W. D., and Bhimji, S. S. (2018). Anatomy, Blood Vessels. Treasure Island, FL: StatPearls.
4. Orekhov A.N., Bobryshev Y.V., Sobenin I.A., Mel-nichenko A.A., Chistiakov D.A. Int J Mol Sci. 2014 Jul 21;15(7):12807-41.
5. Ekaterina A. Ivanova, Yuri V. Bobryshev, and Alexander N. Orekhov. ntimal pericytes as the second line of immune defence in atherosclerosis. Department of Development and Regeneration, Biomedical Sciences Group, KU Leuve, Leuven, Belgium. World J Cardiol. 2015 Oct 26; 7(10): 583-593
6. Marie Billaud 1, Vera S Donnenberg 2, Bradley W Ellis 3, E Michael Meyer 4, Albert D Donnenberg 5, Jennifer C Hill 3, Tara D Richards 3, Thomas G Gleason 1, Julie A Phillippi 6Classification and Functional Characterization of Vasa Vasorum-As-sociated Perivascular Progenitor Cells in Human Aorta7-2017 Jul 11;9(1):292-303. doi: 10.1016/j. stemcr.2017.04.028. Epub 2017 May 25
7. Urmas Roostalu 1, Bashar Aldeiri 2, Alessandra Al-bertini 2, Neil Humphreys 2, Maj Simonsen-Jackson
4. To carry out a comparative analysis of long-term results of surgical treatment of atherosclerotic aneurysms of the femoral and popliteal arteries, depending on the state of the distal arterial! about the channel.
5. To conduct a comparative analysis of long-term results of surgical treatment of atherosclerotic aneurysms of the femoral and popliteal arteries, depending on the type of graft.
6. To clarify the indications and tactics of treatment of atherosclerotic aneurysms of the femoral and popliteal artery.
The expediency of active surgical tactics in patients with atherosclerotic aneurysms of the femoral and popliteal arteries has been substantiated. It has been shown that in patients with atherosclerotic aneurysm of the femoral and popliteal arteries, examination of the abdominal aorta and other peripheral arteries is necessary to exclude their aneurysmal lesions.
The optimal variant of surgical treatment is the operation of resection of the aneurysm of the popliteal arteries with prosthetics, which provides better patency of shunts in the long-term period compared to bypass and ligation of the popliteal artery aneurysm.
2, Jason K F Wong 2, Giulio Cossu 2 Distinct Cellular Mechanisms Underlie Smooth Muscle Turnover in Vascular Development and Repair.2018 Jan 19;122(2):267-281. doi:
8. Roostalu U1,Wong JK2.Developmental Biology, Arterial smooth muscle dynamics in development and repair 15 Feb 2018, 435(2):109-121
9. Cheng JK1 ,Wagenseil JE Extracellular matrix and the mechanics of large artery development..Biomechan-ics and Modeling in Mechan Department of Biomedical Engineering, Washington University, St. Louis, MO 63103, USA, 15 May 2012, 11(8):1169-1186
10. Shen Y, Cheng X, Ying M. Prophylactic amiodarone: Use it or not? The Journal of Thoracic and Cardiovascular Surgery. 151: 891-2. PMID.
11. Corselli M, Chen C-W, Sun B, Yap S, Rubin JP, Pwault B. The tunica adventitia of human arteries and veins as a source of mesenchymal stem cells. Stem Cells and Development. 2012 May 20;21(8):1299-308. https://doi.org/10.1089/scd.2011.0200
12. Kramann R, Goettsch C, Wongboonsin J, et al. Adventitial MSC-like Cells Are Progenitors of Vascular Smooth Muscle Cells and Drive Vascular Calcification in Chronic Kidney Disease. Cell Stem Cell 2016;19:628-642. 10.1016/j.stem.2016.08.001
13. Kramann R, Schneider RK, DiRocco DP, et al. Perivascular Gli1+ progenitors are key contributors to injury-induced organ fibrosis. Cell Stem Cell 2015;16:51-66. 10.1016/j.stem.2014.11.004
14. Zhenyu Tang,1,2,4 Aijun Wang,1,4 Falei Yuan,1 Zhiq-iang Yan,1 Bo Liu,3 Julia S. Chu,1 Jill A. Helms,3 and Song Li.Differentiation of Multipotent Vascular Stem
Cells Contributes to Vascular Diseases. Nat Commun. 2012; 3: 875.Published online 2012 Jun 6. doi: 10.1038/ncomms1867
15. Brown NK, Zhou Z, Zhang J, Zeng R, Wu J, Eitzman DT, Chen YE, Chang L. Perivascular adipose tissue in vascular function and disease: a review of current research and animal models. Arterioscler Thromb Vasc Biol. 2014;34:1621-30. [PMC free article] [PubMed] [Google Scholar]
16. Meredith Kohr Owen, Frank A. Witzmann, Mikaela L. Mckenney, Xianyin Lai, Zachary C. Berwick, Steven P. Moberly, Mouhamad Alloosh, Michael Sturek, Johna-than D. Tune. Perivascular adipose tissue potentiates contraction of coronary vascular smooth muscle: Influence of obesity Meredith Kohr Owen, 2013Cellular & Integrative Physiology,Family Medicine
17. J G Ramirez 1, E J O'Malley 1, W S V Ho Procontractile effects of perivascular fat in health and disease2017 Oct;174(20):3482-3495. doi: 10.1111/ bph.13767. Epub 2017 Apr 3.
18. Nosalski, R. and Guzik, T. J. (2017) Perivascular adipose tissue inflammation in vascular disease. British Journal of Pharmacology, 174(20), pp. 3496-3513
19. Gonzalez EA, Martins GR, Tavares AMV, et al. Ca-thepsin B inhibition attenuates cardiovascular pathology in mucopolysaccharidosis I mice.Lice Science. 2018;196:102-109.
20. Kunasilan Subramaniam, Mary N Sheppard.Tho-racic aortic dissection. Death may not always be due to rupture with haemorrhage. Unusual complications which can be missed at autopsy.Publication date2018/2/1Journal.Journal of forensic and legal medicine
21. Patel, M.J., Blazing, M.A. Inflammation and Atherosclerosis: Disease Modulating Therapies. Curr Treat Options Cardio Med 15, 681-695 (2013). https://doi. org/10.1007/s11936-013-0268-z
22. Chang,1 Adam S. A. Gracon,1 Michael P. Murphy,1* and David S. Wilkes2 .Exploring autoimmunity in the pathogenesis of abdominal aortic aneurysms Tiffany W.* 1 Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana; and 2 Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana Submitted 14 April 2015; accepted in final form 22 June 2015.
23. Iuliia O. Peshkova .Giulia Schaefer .Ekaterina K. Koltsova.Atherosclerosis and aortic aneurysm - is inflammation a common denominator? The FEBS Journal: 24 December 2015
24. Sterpetti AV. UNIVERSITY OF ROME.Etiology of inflammatory abdominal aortic aneurysms. Surgery, 15 Mar 2013, 153(5):741-742
25. Nakao, T, Horie, T, Baba, O. Genetic ablation of mi-croRNA-33 attenuates inflammation and abdominal aortic aneurysm formation via several antiinflammatory pathways. Arterioscler Thromb Vasc Biol 2017; 37: 2161-2170
26. Jones GT, Phillips LV, Williams MJ, et al., 2016,che-mokine C-C in ligand 22 (CCL22) [
27. Michineau S, Franck G, Wagner-Ballon O, et al.,Chemokine (C-X-C motif) receptor 4 blockade by AMD3100 inhibits experimental abdominal aortic aneurysm expansion through anti-inflammatory
effects.Arterioscler Thromb Vasc Biol. 2014 Aug; 34(8):1747-55
28. F. Tanios a, J. Pelisek a,* B. Lutz a , B. Reutersberg a , E. Matevossian b, K. Schwamborn c, V. H^el d, H.H. Eckstein a, C. Reeps a a Department of Vascular and Endovascular Surgery, Klinikum rechts der Isar, Munich, Germany. A Potential Marker for Inflammatory Activity in Abdominal Aortic Aneurysm Wall. Eur J Vasc Endovasc Surg (2015) 50, 745e753.
29. Guanyi Lu 1, Gang Su 1, John P Davis 1, Basil Scha-heen 1, Emily Downs 1, R Jack Roy 2, Gorav Ailawadi
1, Gilbert R Upchurch Jr .A novel chronic advanced stage abdominal aortic aneurysm murine model.J Vasc Surg.. 2017 Jul;66(1):232-242.e4.
30. William F. Johnston.Morgan Salmon.Nicolas H. Pope. Akshaya Meher.Gang Su., Matthew L. Stone,Guanyi Lu.,Gary K. Owens, Gilbert R. UpchurchJr, and Gorav Ailawadi. Response to Letter Regarding Article, "Inhibition of Interleukin-1 p Decreases Aneurysm Formation and Progression in a Novel Model of Thoracic Aortic Aneurysm"Originally published7 Apr 2015 .
31. van Puijvelde GHM, Foks AC, van Bochove RE, et al., CD1d deficiency inhibits the development of abdominal aortic aneurysms in LDL receptor deficient mice. January 2018.D0I: 10.1371/journal.pone.0190962
32. Karen Frudd1 , Thomas Burgoyne2,3 & Joseph Robert Burgoyne. Frudd, K; Burgoyne, T; Burgoyne, JR; (2018) Oxidation of Atg3 and Atg7 mediates inhibition of autophagy. Nature Communications , 9 Article 95. 10.1038/s414 67-017-02352-z. Published online 2018 May 10.
33. Julia V. Bazhenova1, Natalia Sergeevna Drantuso-va2, Victor Anatolievich Shanturov1,2, Boris I. Poda-shev1. COMPUTER TOMOGRAPHY IN DIAGNOSTICS OF AORTIC ANEURYSM. Siberian Medical Journal (Irkutsk), 2014, № 7.
34. Bazhenova Ju.V., Drantusova N.S., Shanturov V.A., Podashev B.I. Computed tomography in the diagnosis of aortic aneurysms. Sibirskij medicinskij zhur-nal (Irkutsk)=Siberian Medical Journal (Irkutsk). 2014;7:37-41 (In Russ.
35. Spiridonov, A. A. V. S. Arakelyan, T. V. Sukhareva Historical aspects of surgical treatment of vasorenaal hypertension (in Russian) // Bul. scientific center for cardiac surgery named after V.S. Arakelyan. A. N. Bakulev Scientific Center for Heart Surgery RAMS. - - 2006. - - Т. 7, № 4. - - С. 61-68.
36. Dagherty M.J., Calligaro K.D. Visceral artery aneurysms. In book: Ashera E. (ed.). Vascular Surgery for Chaimovich: Per. from English M.: Beene, 2010, vol.
2, 236-246.
37. Pokrovsky A.V., Shubin A.A. Aneurysms of visceral arteries. In book: Pokrovskiy A.V. (ed.). Clinical An-giology: A Manual. Moscow: Medicine, 2004, т. 2, 117-128.
38. Ferneiii I. De externis corporis affectibus. In: Ambi-ani Pathologiae. Venetiis: P. Bosellus, 1555, Lib. VII, 165-180
39. Maillard M., Novellas S., Baudin G. et al. Anйvrisme de l'artMre sp^nique: diagnostic et Mrapeutique endovas-culaire. J. Radiol. 2010, 91, 1103-1111
40. Burkey S.H., Vazquez M.A., Valentine R.J. De novo renal artery aneurysms presenting 6 years after
transplantation: a complication of recurrent arterial stenosis? // J. Vasc. Surgery.-2000.- Vol. 32.-P. 388-391.
41. Cohen J.R., Shamash F.S. Ruptured renal artery aneurysms during pregnancy // J. Vasc. Surg.—1987.— Vol. 6.—P. 51-59.
42. Callicutt C., Rush B., Eubancks T. et al. Idiopathic renal artery and infrarenal aortic aneurysms in a 6-year-old child: case report and literature review // J. Vasc. Surg.-2005.-Vol. 41.—P. 893-896.
43. D e Bakey M.E., Lefrak E.A., Garcia-Rinaldi R. et al. Aneurysms of the renal artery // Arch. Surg.—1973.— Vol. 106.—P. 438-443.
44. khanchi, mead Surgical treatment of vasorenal hypertension in combined occlusal arterial lesions Dissertation for a degree, PhD, Republic of Kazakhstan, Almaty., 2007
45. E F Poutasse, Renal artery aneurysms: their natural history and surgery, 1966 PT - Journal Article,PL - United States,TA - J Urol,JT - The Journal of urology,PG - 297-306
46. Antonello M, Frigatti P, Battocchio P, et al. Endo-vascular treatment of asymptomatic popliteal an-eurysms: 8-year concurrent comparison with open repair. J Cardiovasc Surg (Torino). 2007;48(3):267-274
