Aortic Wall Stress in Hypertension and Ascending Thoracic Aortic Aneurysms: Implications for Antihypertensive Therapy

2013 ◽  
Vol 20 (4) ◽  
pp. 265-271 ◽  
Author(s):  
Simon W. Rabkin ◽  
Michael T. Janusz
2021 ◽  
Vol 108 (Supplement_3) ◽  
Author(s):  
R J Burgos Lázaro ◽  
N Burgos Frías ◽  
S Serrano-Fiz García ◽  
V Ospina Mosquera ◽  
F Rojo Pérez ◽  
...  

Abstract INTRODUCTION The surgical indication for ascending aortic aneurysms (AAA) is established when the maximum diameter > 50 mm; It responds to Laplace's Law (T wall = P × r / 2e). The aim of the study is to define wall stress in AAA. MATERIAL AND METHODS 218 ascending aortic walls have been studied: 96 from organ donors, and 122 from AAA: Marfán 58 (47.5%), bicuspid aortic valve 26 (21.4%), and atherosclerosis 38 (31.1%). The samples were studied "in vitro", according to the model Young's (relationship between stress and deformed area), by means of the mechanical traction test (Tension = Force / Area). The analysis was performed with the stress-elongation curve (d Tension / d Elongation). RESULTS The stress of the aortic wall, classified from highest to lowest according to pathology and age was: cystic necrosis of the middle layer, arteriosclerosis, age > 60 years, between 35 and 59, and < 34 years. The stress of “control aortas” wall increased directly in relation to the age of the donors. CONCLUSIONS The maximum diameter of the ascending aorta, the patient's type of pathology and age are factors that affect the maximum tension of the aortic wall and resistance, factors that allow differentiation and prediction of the risk of rupture of the AAA. The validation of the results obtained through numerical simulation was significant and the uniaxial analysis has modeled the response of the vessels to their internal pressure.


2013 ◽  
pp. 6-11
Author(s):  
Alberto Milan ◽  
Francesco Tosello ◽  
Sara Abram ◽  
Ambra Fabbri ◽  
Alessandro Vairo ◽  
...  

Introduction: Acute and chronic aortic syndromes are associated with substantial morbidity and mortality. Silent risk factors such as arterial hypertension and aortic root dilatation can increase the likelihood of aortic dissection or rupture. The relationship between arterial hypertension and the dimensions of the aortic root dimension is a topic of active debate. Materials and methods: We reviewed the literature on the physiopathology, diagnosis, natural history, and management of thoracic aortic aneurysms. Results: Biological variables influencing the size of the aorta include age, sex, body surface area, pressure values, and stroke volume. Pathologic enlargement of the thoracic aorta can be caused by genetic, degenerative, inflammatory, traumatic, or toxic factors. Studies investigating the correlation between aortic dimensions and arterial pressures (diastolic, systolic, or pulse) have produced discordant results. Discussion: Classically, emphasis has been placed on the importance of hypertension-related degeneration of the medial layer of the aortic wall, which leads to dilatation of the thoracic aorta, reduced aortic wall compliance, and increased pulse pressures. However, there are no published data that demonstrate unequivocally the existence of a pathogenetic correlation between arterial hypertension and aortic root dilatation. Furthermore, there is no evidence that antihypertensive therapy is effective in the management of nonsyndromic forms of aortic root dilatation. An interesting branch of research focuses on the importance of genetic predisposition in the pathogenesis of thoracic aortic aneurysms. Different genetic backgrounds could explain differences in the behaviour of aortic walls exposed to the same hemodynamic stress. Further study is needed to evaluate these focal physiopathological aspects.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Imon Rahaman ◽  
Zhongjie Wang ◽  
Yue XUAN ◽  
Liang Ge ◽  
Elaine E Tseng

Introduction: Current guidelines for elective surgery of ascending thoracic aortic aneurysms (aTAAs) use aneurysm size as primary determinant for risk stratification of adverse events. Biomechanically, dissection may occur when wall stress exceeds wall strength. A widespread method for stress analysis is structural finite-element analysis (FEA). Patient-specific aortic geometries are easily obtainable and stress distributions can potentially predict risk of dissection. However, FEA is a time-consuming and difficult procedure. To bypass this issue, a recent study has developed the first deep learning (DL) approach for a fast and accurate estimation of aortic wall stress distributions. Hypothesis: In this study, we assessed the hypothesis that this deep learning approach can be applied to a large clinical dataset. Model performance was measured by comparing FEA and DL stress predictions in parallel. Methods: Patients with aTAA (n = 169) were studied. Patient-specific aneurysm geometries were obtained from ECG-gated computed tomography. Shapes were represented by hexahedral meshes with 9648 nodes and 6336 solid elements. FEA peak wall stresses and stress distributions were determined using LS-DYNA software with user-defined fiber-embedded material models under systolic pressure. The DL model was implemented in Julia and consisted of unsupervised and supervised learning algorithms. Training was performed on a training set of 152 shapes and testing set of 17 shapes with 10-fold cross-validation. Mean absolute error (MAE) and absolute error of peak stress values (APE) were used to compare DL model predictions with FEA values considered to be ground truth. Results: Average stress values predicted by our DL model were 175.64 ± 4.17 kPa and 95.69 ± 2.15 kPa in the circumferential and longitudinal direction, respectively. We computed a MAE of 5.06 ± 1.08 kPa and APE of 2.58 ± 1.39 kPa in the circumferential direction and MAE of 4.51 ± 0.98 kPa and APE of 2.32 ± 1.84 kPa in the longitudinal direction. Conclusions: DL model trained exclusively on clinical data was able to accurately predict stress distributions on complex aortic geometries. Fast and accurate stress predictions will facilitate real-time clinical applications for the risk assessment of aTAAs.


Circulation ◽  
2013 ◽  
Vol 128 (11_suppl_1) ◽  
pp. S157-S162 ◽  
Author(s):  
E. K. Shang ◽  
D. P. Nathan ◽  
S. R. Sprinkle ◽  
R. M. Fairman ◽  
J. E. Bavaria ◽  
...  

2020 ◽  
Vol 26 ◽  
Author(s):  
Salvatore Campisi ◽  
Raja Jayendiran ◽  
Francesca Condemi ◽  
Magalie Viallon ◽  
Pierre Croisille ◽  
...  

Abstract:: Guidelines for the treatment of aortic wall diseases are based on measurements of maximum aortic diameter. However aortic rupture or dissections do occur for small aortic diameters. Growing scientific evidence underlines the importance of biomechanics and hemodynamics in aortic disease development and progression. Wall shear stress (WWS) is an important hemodynamics marker which depends on aortic wall morphology and on the aortic valve function. WSS could be helpful to interpret aortic wall remodeling and define personalized risk criteria. The complementarity of Computational Fluid Dynamics and 4D Magnetic Resonance Imaging as tools for WSS assessment is a promising reality. The potentiality of these innovative technologies will provide maps or atlases of hemodynamics biomarkers to predict aortic tissue dysfunction. Ongoing efforts should focus on the correlation between these non-invasive imaging biomarkers and clinico-pathologic situations for the implementation of personalized medicine in current clinical practice.


2018 ◽  
Vol 156 (2) ◽  
pp. 492-500 ◽  
Author(s):  
Yue Xuan ◽  
Zhongjie Wang ◽  
Raymond Liu ◽  
Henrik Haraldsson ◽  
Michael D. Hope ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Anna Malashicheva ◽  
Daria Kostina ◽  
Aleksandra Kostina ◽  
Olga Irtyuga ◽  
Irina Voronkina ◽  
...  

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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