scholarly journals Features of Morphogenesis of Aortic Aneurysms on the Background of Hypertension and Associated Risk Factors

Author(s):  
V. Zakharova ◽  
O. Rudenko ◽  
V. Kravchenko

The aim. To investigate the role of hypertension and associated risk factors in the formation of aortic aneurysms. Material and methods. Retrospective analysis of 196 case histories of patients who were successively operated on for ascending aortic aneurysm at the National Amosov Institute of cardiovascular surgery. The history was analyzed, the duration and degree of hypertension were recorded, as well as other factors that may have influenced the development of ascending aortic aneurysm in some way. A pathomorphological examination of fragments of the aortic wall that were excised during the operation was performed. Out of all 294 examined patients operated for ascending aortic aneurysm, hypertension was reported in 196 (66.7%) patients. The incidence of ascending aortic aneurysm positively correlated with the duration of hypertension. The ma-jority of patients (118 [60.2%]) had signs of hypertension for more than five years. Additional ethiopathogenetic fac-tors were identified in patients with ascending aortic aneurysm and hypertension, with atherosclerosis ranking first (66 [33.6%]). The next factors that demonstrated the same incidence were the inflammatory process in the aorta and AV, and smoking: 45 cases each (22.9%). Then, in descending order, were: xenobiotics exposure (43 [21.9%]), rheumatic stenosis of AV (40 [20.4%]), chest injury (33 [16.8%]), dysplasia of AV (28 [14.3%]), alcohol abuse (13 [6.6%]), Marfan syndrome (9 [4.6%]), other (8 [4.1%]). The results of comparison of the history and pathomorphological findings allowed to develop a scheme of ascending aortic aneurysm pathogenesis in hypertension. The scheme of ascending aortic aneurysm pathogenesis in hypertension is discussed in the work. The results of morphological examination show that hypertension is associated with the dam-age to the aortic endothelium, which leads to fibromuscular proliferation of the intima with subsequent hypoxic damage to the inner layer of the media. Hypoxic damage to the media, which is associated with vasa vasorum remodeling due to hypertension, is also observed in the subventricular layer. Weakening of the aortic wall at elevated pressure causes dila-tation of the aorta, i.e. the formation of an aortic aneurysm. This process may be exacerbated by additional factors, with atherosclerosis being the most common (33.6%)

2020 ◽  
Vol 27 (4) ◽  
pp. 169-178
Author(s):  
S. S. Todorov ◽  
V. Yu. Deribas ◽  
A. S. Kaz’min ◽  
S. S. Todorov

Aim. To describe a rare occurrence of fibromuscular vasa vasorum dysplasia of the aortic aneurysm wall.Materials and methods. Surgical material from the ascending aortic aneurysm wall was examined. Longitudinal strips of the aortic wall were excised for histological examination with subsequent 24-h fixation in 10% buffered formalin. A histological isopropanol assay was performed with an automated Logos microwave tissue processor (Milestone, Italy) with subsequent sample embedding into paraffin. Sections were obtained with a rotary microtome (Leica, Germany). Staining was performed with haematoxylin-eosin, van Gieson’s picrofuchsin, orcein for elastic fibres, Hotchkiss’ PAS reaction with alcian blue for glycosaminoglycans. Histological and histochemical properties of the aortic wall were studied and imaged with a Leica DM 1000 microscope (Germany) equipped with a camera ICC50 E at magnifications 40x, 100x, 200x, 400x.Results. The conducted histological examination of the aortic aneurysm wall revealed most pronounced changes in media and adventitia layers. Elastic fibres in media were swollen, homogeneous, crimped, with pronounced dystrophic and necrobiotic changes in smooth myocytes. Regions of compromised cells and elastic fibres in media contained pockets of alcian-positive glycosaminoglycans. Specific changes were revealed in adventitia vasa vasorum in the form of a pronounced wall thickening and lumen narrowing due to dysplastic fibromuscular tissues.Conclusion. A rare form of fibromuscular dysplasia of the vasa vasorum of the ascending aortic aneurysm wall observed in a 43 years-old woman demonstrated the morbid morphology of smooth myocytes, as well as fibrous collagenous and elastic structures. The described features were likely associated with the aortic wall trophic structure and aneurysm morphogenesis.


2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Hiroaki Osada ◽  
Katsuaki Meshii ◽  
Motoaki Ohnaka ◽  
Naoki Kanemitsu ◽  
Hiroyuki Nakajima ◽  
...  

Introduction: The pathogenic mechanisms of ascending aortic aneurysm are not fully understood. The aim of this study was to identify the beginning of aortic wall dilatation based on histopathological evaluation by comparison of patients with bicuspid versus tricuspid aortic valves. Methods: Twenty-one patients (9 males, 12 females; mean age, 69±8.9 years) who underwent ascending aortic repair from 2008 to 2014 were divided into bicuspid aortic valve (n=8, Group B) and tricuspid aortic valve (n=13, Group T) subgroups. We compared the histopathological characteristics of the ascending aortic wall in these patients. Results: There were no significant differences between the two groups in age, sex, history of hypertension, and maximum diameter of the ascending aorta (Group B: 51.4±5.1 mm; Group T: 55.5±8.8 mm; p=0.247) at the time of operation. While all Group B cases exhibited aortic stenosis, there was only one case in Group T. Sclerosis or hypertrophy of the vasa vasorum was evident in both groups (Group B: 7 patients, 87.5%; Group T: 10 patients, 76.9%; p=1.000). Group B patients exhibited a much thinner aortic wall, resulting from frail smooth muscle cells of media, which induced a fragile thinner elastic lamina. The histopathological pattern of Group T was variable and included atheroma, inflammatory granulation tissue and a Marfan-like acid mucopolysaccharide pool, which produce severe fragmentation of elastic lamina. Conclusions: Degeneration of the vasa vasorum, which induces chronic ischemia or malnutrition of the aortic wall, is an important emerging substrate for the development of ascending aortic aneurysm. Bicuspid aortic valve patients exhibited congenital maldevelopment of the medial smooth muscle cells and elastic lamina. Tricuspid aortic valve patients exhibited severe fragmentation of elastic lamina, which induced by pathological changes including atheroma, inflammatory granuloma, and a Marfan-like acid mucopolysaccharide pool.


2015 ◽  
Vol 18 (4) ◽  
pp. 134 ◽  
Author(s):  
Asad A Shah

<p><strong>Background:  </strong>Bicuspid aortic valves predispose to ascending aortic aneurysms, but the mechanisms underlying this aortopathy remain incompletely characterized.  We sought to identify epigenetic pathways predisposing to aneurysm formation in bicuspid patients.</p><p><strong>Methods:  </strong>Ascending aortic aneurysm tissue samples were collected at the time of aortic replacement in subjects with bicuspid and trileaflet aortic valves.  Genome-wide DNA methylation status was determined on DNA from tissue using the Illumina 450K methylation chip, and gene expression was profiled on the same samples using Illumina Whole-Genome DASL arrays.  Gene methylation and expression were compared between bicuspid and trileaflet individuals using an unadjusted Wilcoxon rank sum test.  </p><p><strong>Results:  </strong>Twenty-seven probes in 9 genes showed significant differential methylation and expression (P&lt;5.5x10<sup>-4</sup>).  The top gene was protein tyrosine phosphatase, non-receptor type 22 (<em>PTPN22</em>), which was hypermethylated (delta beta range: +15.4 to +16.0%) and underexpressed (log 2 gene expression intensity: bicuspid 5.1 vs. trileaflet 7.9, P=2x10<sup>-5</sup>) in bicuspid patients, as compared to tricuspid patients.  Numerous genes involved in cardiovascular development were also differentially methylated, but not differentially expressed, including <em>ACTA2</em> (4 probes, delta beta range:  -10.0 to -22.9%), which when mutated causes the syndrome of familial thoracic aortic aneurysms and dissections</p><p><strong>Conclusions:  </strong>Using an integrated, unbiased genomic approach, we have identified novel genes associated with ascending aortic aneurysms in patients with bicuspid aortic valves, modulated through epigenetic mechanisms.  The top gene was <em>PTPN22</em>, which is involved in T-cell receptor signaling and associated with various immune disorders.  These differences highlight novel potential mechanisms of aneurysm development in the bicuspid population.</p>


Author(s):  
Andre Y. Son ◽  
Nicole M. DeMarais ◽  
S. Chris Malaisrie ◽  
Jon W. Lomasney ◽  
Maurice Pradella ◽  
...  

Author(s):  
Alkiviadis Tsamis ◽  
Julie A. Phillippi ◽  
Ryan G. Koch ◽  
Jeffrey T. Krawiec ◽  
Antonio D’Amore ◽  
...  

Aortic dissection is a life-threatening cardiovascular emergency with a high potential for death. It usually begins with an intimal tear which permits blood to enter the wall, split the media and create a false lumen, which can reenter the true lumen or exit through the adventitia causing complete rupture. A possible mechanism for dissection of ascending thoracic aortic aneurysm (ATAA) can be the occurrence of blood pressure-induced wall stresses in excess to the adhesive strength between the degenerated aortic wall layers.


Author(s):  
Marie Billaud ◽  
Jennifer C. Hill ◽  
Tara D. Richards ◽  
Thomas G. Gleason ◽  
Julie A. Phillippi

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Talha Ijaz ◽  
Hong Sun ◽  
Adrian Recinos ◽  
Ronald G Tilton ◽  
Allan R Brasier

Introduction: Abdominal aortic aneurysm is a devastating disease since it can lead to aortic rupture and instantaneous death. We previously demonstrated that IL-6 secreted from the aortic wall is necessary for the development of abdominal aortic aneurysm and dissection (AAD). Since IL-6 is a NF-kB/RelA dependant gene, we investigated the role of aortic wall- NF-kB/RelA signaling in the development of AAD. Methods and Results: To test the role of aortic wall-RelA, we utilized Cre-Lox technology to delete RelA from aortic cells. Tamoxifen-inducible, Col1a2-promoter driven Cre mice (Col1a2-Cre) were crossed with mT/mG Cre-reporter mice to determine which aortic cells undergo genetic recombination after Cre activation. Flow cytometry analysis of the aortic wall indicated that 88% of the genetically recombined cells were SMCs and 8% were fibroblasts. Next, RelA floxed (RelA f/f) mice, generated in our lab, were crossed with Col1a2-Cre mice. RelA f/f Cre+ and RelA f/f Cre- were stimulated with tamoxifen for 10 days to generate aortic-RelA deficient (Ao-RelA-/-) or wild-type (Ao-RelA+/+) transgenics. Flow cytometry, qRT-PCR, and immunohistochemistry analysis suggested a depletion of aortic-RelA greater than 60%. To test the role of Ao-RelA in AAD, Ao-RelA -/- (n= 20) and Ao-RelA +/+ (n=14) mice were infused with angiotensin II for 7 days. Surprisingly, 20% of Ao-RelA-/- mice died from development of AAD and aortic rupture while no deaths were observed in Ao-RelA+/+ group. In addition, 40% of Ao-RelA-/- mice developed AAD compared to 14% of Ao-RelA+/+ mice. There was no significant difference in TUNEL staining or ERTR7+ fibroblast population between the two groups. Conclusion: Our studies suggest that aortic wall-RelA may be necessary for protection from AAD.


2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Valerie R. Ramiro ◽  
Carmegie C. Saliba ◽  
John Anthony D. Tindoc ◽  
Marinette R. Jambaro ◽  
Enrique M. Chua ◽  
...  

Aortic aneurysms are not commonly reported among patients with systemic lupus erythematosus (SLE). We report a case of a 47-year-old Filipino female diagnosed with SLE 17 years ago maintained on prolonged oral steroids, azathioprine, and hydroxychloroquine. She also had lupus nephritis, secondary hypertension, and dyslipidemia. She initially presented with a week-long watery nonbloody diarrhea with associated diffuse crampy abdominal pain and generalized weakness. She was admitted for a week at a provincial hospital and was given an unrecalled antibiotic with resolution of symptoms. Upon discharge, however, she experienced two weeks of severe right lower quadrant pain radiating to the back and left lower quadrant, with no history of diarrhea, vomiting, dysuria, and fever. Complete blood count showed slight leukocytosis and elevated C-reactive protein. Abdominal imaging revealed a saccular infrarenal aneurysm with dissection. An atherosclerotic mechanism was primarily considered, but a vasculitic process was likewise considered due to elevated acute phase reactants. The initial plan was Endovascular Aneurysm Repair (EVAR) but due to financial limitations, an exploratory laparotomy with infrarenal endoaneurysmorrhaphy was eventually performed. Intraoperative findings were a saccular infrarenal aneurysm with dissection up to the proximal right common iliac artery and an abscess compartment within the false lumen in the anterior aortic wall. Abscess culture yielded high growth of Salmonella group B. Micrographs of the aortic wall biopsy showed fibrin deposition necrosis and calcification with peripheral viable cellular infiltrates consisting of neutrophils and foamy macrophages. Inadvertently placing an endovascular graft in an infected aortic aneurysm would have led to graft infection and catastrophic morbidity. We highlight the significance of having a high index of suspicion for infectious causes of aortitis among immunocompromised patients presenting with aneurysm prior to pursuing an endovascular versus an open approach for repair.


Vascular ◽  
2014 ◽  
Vol 23 (4) ◽  
pp. 411-418 ◽  
Author(s):  
Erasmo S da Silva ◽  
Vitor C Gornati ◽  
Ivan B Casella ◽  
Ricardo Aun ◽  
Andre EV Estenssoro ◽  
...  

Objective To analyze the characteristics of patients with abdominal aortic aneurysms referred to a tertiary center and to compare with individuals with abdominal aortic aneurysm found at necropsy. Methods We have retrospectively analyzed the medical records of 556 patients with abdominal aortic aneurysm and 102 cases abdominal aortic aneurysm found at necropsy. Results At univariated analysis, hypertension, tobacco use and maximum diameter were significant risk factors for symptomatic aneurysm, while diabetes tended to be a protective factor for rupture. By logistic regression analysis, the largest transverse diameter was the only one significantly associated with abdominal aortic aneurysm rupture ( p < .0001, odds ratio 1.7, 95% confidence interval 1.481–1.951). Intact abdominal aortic aneurysm found at necropsy showed similarities with outpatients in relation to abdominal aortic aneurysm diameter and risk factors. Conclusion Intact abdominal aortic aneurysm at necropsy and at outpatients setting showed similarities that confirmed that abdominal aortic aneurysm repair is less offered to women, and they died more frequently with intact abdominal aortic aneurysm from other causes.


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