scholarly journals Molecular Pathogenesis and the Possible Role of Mitochondrial Heteroplasmy in Thoracic Aortic Aneurysm

Life ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1395
Author(s):  
A. V. Suslov ◽  
M. A. Afanasyev ◽  
P. A. Degtyarev ◽  
P. V. Chumachenko ◽  
M. Bagheri Ekta ◽  
...  
Keyword(s):  
Aortic Aneurysm ◽  
Thoracic Aortic Aneurysm ◽  
Aortic Wall ◽  
Morphological Changes ◽  
Genetic Disorders ◽  
Threatening Condition ◽  
Mitochondrial Pathology ◽  
Active Research ◽  
Mitochondrial Dna Heteroplasmy

Thoracic aortic aneurysm (TAA) is a life-threatening condition associated with high mortality, in which the aortic wall is deformed due to congenital or age-associated pathological changes. The mechanisms of TAA development remain to be studied in detail, and are the subject of active research. In this review, we describe the morphological changes of the aortic wall in TAA. We outline the genetic disorders associated with aortic enlargement and discuss the potential role of mitochondrial pathology, in particular mitochondrial DNA heteroplasmy, in the disease pathogenesis.

Abstract 3054: Comparison of Transforming Growth Factor-β1 Expression in Aortic Wall of Thoracic Aortic Aneurysm Versus Dissection

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Shouguo Yang ◽  
Guanggen Cui ◽  
Ramin Beygui ◽  
Fardad Esmailian ◽  
Abbas Ardehali ◽  
...  
Keyword(s):  
Aortic Aneurysm ◽  
Thoracic Aortic Aneurysm ◽  
Aortic Wall ◽  
Transforming Growth Factor ◽  
Smooth Muscle Actin ◽  
Underlying Mechanism ◽  
Transforming Growth Factor Β1 ◽  
Fluorescent Intensity ◽  
Nucleus Density ◽  
Tgf Β1

Background The underlying mechanism of thoracic aortic aneurysm (TAA) and dissection(TAD) was undetermined, and one controversy lies in whether they represent the different dvelopement period of the same disorder or totally diferent diseases. This study is in aim to compare the expression and distribution of Transforming Growth Factors(TGF) β1 in the aortic wall of TAA versus TAD patients. Method Aortic specimens were obtained from patients underwent to aortic procedures for TAA (n=38) and TAD (n=20) at UCLA , and control aorta (CN) from organ donnor (n=20). Double immunofluorescent stainning of TGF-β1 and α-smooth muscle actin were performed with paraffin embeded slides for all aortic samples and semiquantified by fluorescent intensity analysis. Histopathologic examination were performed with HE, Verhoeff van-Gieson and Masson’s trichrome stain. Results TAA and TAD patients exhibited an up-regulation of TGF-β1 to 120.3% and 109.6% compared with CN separately (P<0.05), with TAA higher than TAD (P<0.05). TGF-β1 distributed unevenly across aortic wall with the highest levels expression in tunica media, followed by intima then adventitia. In intima, TGF-β1 was expressed at the same level for TAD as CN, but was increased to 115.2% for TAA compared to CN (P<0.05). In media, TGF-β1 increased by 127.2% in TAA and 116.1% in TAD compared to CN (P<0.01), with TAA being higher than TAD (P<0.05). In adventitia, TGF- β1 was up-regulated to 119.6% and 116.7% for TAA and TAD compared to CN (P<0.05). Nucleus density analysis showed cellular plasia in adventitia of TAA and TAD than CN (P<0.05 ), while TAD patients demonstrated a higher nucleus density than TAA in intima and adventitia (P<0.05). α-actin was increased in media of TAA and TAD to 164.5% and 120% than CN (P<0.01 and P<0.05). Attenuated and interrupted elastin and mild to severe cystic medial degeneration were characteristic histopathologic finding in 29 (76.3%) TAA and 17(85%) TAD patients. Conclusions TGF- β1 expression was up-regulated in aortic wall of TAA and TAD compared to CN. The significant higher levels of TGF- β1 in intima and media in TAA versus TAD patients implicated a probable positive effect of TGF- β1 to maintain aortic wall integrity, and/or greater comsamption of TGF- β1 in the aortic dissection.

Region-Specific Medial Fiber Micro-Architecture in the Longitudinal-Radial and Circumferential-Radial Planes of Ascending Thoracic Aortic Aneurysm Among Bicuspid and Tricuspid Aortic Valve Patients

2013 ◽  
Author(s):  
Alkiviadis Tsamis ◽  
Julie A. Phillippi ◽  
Ryan G. Koch ◽  
Jeffrey T. Krawiec ◽  
Antonio D’Amore ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Aortic Valve ◽  
Aortic Aneurysm ◽  
Thoracic Aortic Aneurysm ◽  
Aortic Wall ◽  
False Lumen ◽  
True Lumen ◽  
Life Threatening ◽  
The Media ◽  
Intimal Tear

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.

Abstract 667: The Role of Aortic Wall-Nuclear Factor- kappa B (NF-kB) Signaling in Formation of Dissecting Aortic Aneurysms

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Talha Ijaz ◽  
Hong Sun ◽  
Adrian Recinos ◽  
Ronald G Tilton ◽  
Allan R Brasier
Keyword(s):  
Flow Cytometry ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Aortic Rupture ◽  
Aortic Aneurysms ◽  
Tunel Staining ◽  
Abdominal Aortic ◽  
Significant Difference

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.

scholarly journals Thoracic aortic aneurysm causing aorto-esophageal fistula—our experience with a rare disease

2020 ◽  
Vol 2020 (7) ◽  
Author(s):  
Aakriti Yadav ◽  
Uttam Krishna Shrestha ◽  
Kajan Raj Shrestha ◽  
Dinesh Gurung
Keyword(s):  
Aortic Aneurysm ◽  
Thoracic Aortic Aneurysm ◽  
Sudden Onset ◽  
Massive Hemoptysis ◽  
Esophageal Fistula ◽  
Feeding Jejunostomy ◽  
Intravenous Antibiotics ◽  
Threatening Condition ◽  
Life Threatening ◽  
Upper Gastrointestinal

Abstract Aorto-esophageal fistula is a life-threatening condition, accounting for a small number of cases of upper gastrointestinal bleeding where patients present with one or more features of Chiari’s triad. We present the case of a 43-year-old woman, referred to us with symptoms of central chest pain, sudden onset dysphagia followed by massive hemoptysis. She was diagnosed with an aorto-esophageal fistula due to a ruptured thoracic aortic aneurysm and rushed for an emergency endovascular thoracic aortic stent and feeding jejunostomy with intravenous antibiotics and supportive care. After 6 weeks of surgery, the patient was re-evaluated to plan for an esophageal stent if required. The purpose of this presentation is to make the surgical fraternity aware of the gravity of this disease and novel techniques to manage it.

scholarly journals SEX DIFFERENCES IN THORACIC AORTIC ANEURYSM GROWTH: ROLE OF AORTIC STIFFNESS

2017 ◽  
Vol 69 (11) ◽  
pp. 2041
Author(s):  
Thais Coutinho ◽  
Katie Y. Cheung ◽  
Munir Boodhwani ◽  
Luc Beauchesne ◽  
Carole Dennie ◽  
...  
Keyword(s):  
Sex Differences ◽  
Aortic Aneurysm ◽  
Aortic Stiffness ◽  
Thoracic Aortic Aneurysm ◽  
Aneurysm Growth

scholarly journals TEVAR for ruptured descending thoracic aortic aneurysm: case report

2016 ◽  
Vol 15 (4) ◽  
pp. 322-327 ◽  
Author(s):  
Sthefano Atique Gabriel ◽  
Enrico Rinaldi ◽  
Marco Leopardi ◽  
Germano Melissano ◽  
Roberto Chiesa
Keyword(s):  
Case Report ◽  
Aortic Aneurysm ◽  
Thoracic Aortic Aneurysm ◽  
Thoracic Endovascular Aortic Repair ◽  
High Morbidity ◽  
Minimally Invasive Approach ◽  
Invasive Approach ◽  
Descending Thoracic Aortic Aneurysm ◽  
Threatening Condition ◽  
Life Threatening

Abstract A ruptured descending thoracic aortic aneurysm (rDTAA) is a life-threatening condition associated with high morbidity and mortality. Endovascular treatment for rDTAA promotes effective aneurysm exclusion with a minimally invasive approach. The authors report a case of a 76-year-old man with hemodynamically unstable 9-cm-diameter rDTAA treated with emergency thoracic endovascular aortic repair (TEVAR).

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