Abstract 672: Histopathological Comparison of Ascending Aortic Aneurysm: Bicuspid versus Tricuspid Aortic Valve Patients

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Hiroaki Osada ◽  
Katsuaki Meshii ◽  
Motoaki Ohnaka ◽  
Naoki Kanemitsu ◽  
Hiroyuki Nakajima ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Aortic Valve ◽  
Aortic Aneurysm ◽  
Smooth Muscle Cells ◽  
Aortic Wall ◽  
Vasa Vasorum ◽  
Ascending Aortic Aneurysm ◽  
Tricuspid Aortic Valve ◽  
Group B ◽  
Elastic Lamina

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.

scholarly journals Genetic and Epigenetic Mechanisms Underlying Vascular Smooth Muscle Cell Phenotypic Modulation in Abdominal Aortic Aneurysm

2020 ◽  
Vol 21 (17) ◽  
pp. 6334
Author(s):  
Rijan Gurung ◽  
Andrew Mark Choong ◽  
Chin Cheng Woo ◽  
Roger Foo ◽  
Vitaly Sorokin
Keyword(s):  
Smooth Muscle ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Smooth Muscle Cells ◽  
Aortic Wall ◽  
Epigenetic Mechanisms ◽  
Phenotypic Modulation ◽  
Abdominal Aortic

Abdominal aortic aneurysm (AAA) refers to the localized dilatation of the infra-renal aorta, in which the diameter exceeds 3.0 cm. Loss of vascular smooth muscle cells, degradation of the extracellular matrix (ECM), vascular inflammation, and oxidative stress are hallmarks of AAA pathogenesis and contribute to the progressive thinning of the media and adventitia of the aortic wall. With increasing AAA diameter, and left untreated, aortic rupture ensues with high mortality. Collective evidence of recent genetic and epigenetic studies has shown that phenotypic modulation of smooth muscle cells (SMCs) towards dedifferentiation and proliferative state, which associate with the ECM remodeling of the vascular wall and accompanied with increased cell senescence and inflammation, is seen in in vitro and in vivo models of the disease. This review critically analyses existing publications on the genetic and epigenetic mechanisms implicated in the complex role of SMCs within the aortic wall in AAA formation and reflects the importance of SMCs plasticity in AAA formation. Although evidence from the wide variety of mouse models is convincing, how this knowledge is applied to human biology needs to be addressed urgently leveraging modern in vitro and in vivo experimental technology.

scholarly journals Fibromuscular dysplasia of aortic aneurysm vasa vasorum (a rare case report)

2020 ◽  
Vol 27 (4) ◽  
pp. 169-178
Author(s):  
S. S. Todorov ◽  
V. Yu. Deribas ◽  
A. S. Kaz’min ◽  
S. S. Todorov
Keyword(s):  
Aortic Aneurysm ◽  
Histological Examination ◽  
Fibromuscular Dysplasia ◽  
Aortic Wall ◽  
Vasa Vasorum ◽  
Wall Thickening ◽  
Elastic Fibres ◽  
Ascending Aortic Aneurysm ◽  
Aneurysm Wall ◽  
Smooth Myocytes

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.

Proteomics of Ascending Aortic Aneurysm with Bicuspid or Tricuspid Aortic Valve

2007 ◽  
Vol 15 (3) ◽  
pp. 185-190 ◽  
Author(s):  
Peter Matt ◽  
Anne von Orelli ◽  
Franziska Bernet ◽  
Thomas Grussenmeyer ◽  
Ivan Lefkovits ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Aortic Aneurysm ◽  
Ascending Aortic Aneurysm ◽  
Tricuspid Aortic Valve

Abstract 397: Analysis of Cell Phenotype in Relation to TGFβ Treatment of Aortic Smooth Muscle Cells and Myofibroblasts Isolated from Aortas and Valves of Thoracic Aortic Aneurysm Patients with a Tricuspid or a Bicuspid Valve

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Valentina Paloschi ◽  
Lasse Folkersen ◽  
Sanela Kurtovic ◽  
Dick Wagsater ◽  
Anders Franco Cereceda ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Aortic Valve ◽  
Aortic Aneurysm ◽  
Smooth Muscle Cells ◽  
Thoracic Aortic Aneurysm ◽  
Muscle Cells ◽  
Cell Types ◽  
Cell Phenotype ◽  
Matrix Remodeling ◽  
Exon Arrays

Background Thoracic aortic aneurysm (TAA) is a pathological widening of the aorta, due to degeneration of extracellular matrix (ECM) and loss of smooth muscle cells (SMCs). Bicuspid aortic valve (BAV) is a congenital disorder present in 1-2 % of the population which makes TAA associated with BAV a common complication. Previously we showed that aortas isolated from BAV and normal tricuspid aortic valve (TAV) patients are different both at gene and protein levels. Particularly, differences in the TGFβ pathway seem to be crucial players in aneurysm development, affecting matrix remodeling and wound healing. Since SMCs and myofibroblasts are the critical cells responsible for these activities, we evaluated different properties of the cells focusing on fibronectin (FN) and its spliced versions, a target gene of TGFβ. Interestingly, extra domain A of FN (EDA) was previously described for its roles in vascular morphogenesis, as well as in processes like migration and proliferation. Methods and results Biopsies from the thoracic aorta and Aortic valves were collected during Elective Aortic Valve Replacement Surgery. mRNA expression was analyzed in the ascending aorta by Affymetrix Exon arrays in patients with TAV (n=46) and BAV (n=77). Expression of EDA was found increased only in dilated aortas from TAV patients but not in BAV patients. Primary SMCs were isolated with the explant outgrowth technique from aortas of BAV and TAV patients (n=15). Myofibroblasts were isolated by collagenase digestion from BAV and TAV valves (n=30). Cells were cultured and treated with TGFβ at a concentration of 20 ng/ml for 6h. TGFβ treatment influenced the splicing of FN and enhanced the formation of EDA-containing FN in SMCs from TAV patients but not in cells derived from BAV patients. We have not observed clear differences in SMC proliferation and migration. Myofibrolasts analysis is ongoing. Conclusions So far, our results suggest that despite a decreased EDA-fibronectin expression in BAV cells, the phenotype of SMCs isolated from BAV and TAV patients in culture does not differ. However, impaired TGFβ signaling that may result in the increased susceptibility of BAV patients to develop TAA could be due to effects on other cell types.

scholarly journals Phenotypic and Functional Changes of Endothelial and Smooth Muscle Cells in Thoracic Aortic Aneurysms

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Anna Malashicheva ◽  
Daria Kostina ◽  
Aleksandra Kostina ◽  
Olga Irtyuga ◽  
Irina Voronkina ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Aortic Valve ◽  
Smooth Muscle Cells ◽  
Aortic Wall ◽  
Muscle Cells ◽  
Aortic Aneurysms ◽  
Cell Phenotype ◽  
Functional Markers ◽  
Thoracic Aortic Aneurysms

Thoracic aortic aneurysm develops as a result of complex series of events that alter the cellular structure and the composition of the extracellular matrix of the aortic wall. The purpose of the present work was to study the cellular functions of endothelial and smooth muscle cells from the patients with aneurysms of the thoracic aorta. We studied endothelial and smooth muscle cells from aneurysms in patients with bicuspid aortic valve and with tricuspid aortic valve. The expression of key markers of endothelial (CD31, vWF, and VE-cadherin) and smooth muscle (SMA, SM22α, calponin, and vimentin) cells as well extracellular matrix and MMP activity was studied as well as and apoptosis and cell proliferation. Expression of functional markers of endothelial and smooth muscle cells was reduced in patient cells. Cellular proliferation, migration, and synthesis of extracellular matrix proteins are attenuated in the cells of the patients. We show for the first time that aortic endothelial cell phenotype is changed in the thoracic aortic aneurysms compared to normal aortic wall. In conclusion both endothelial and smooth muscle cells from aneurysms of the ascending aorta have downregulated specific cellular markers and altered functional properties, such as growth rate, apoptosis induction, and extracellular matrix synthesis.

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