Image-based biomechanical modeling of aortic wall stress and vessel deformation: response to pulsatile arterial pressure simulations

Author(s):  
Dilana Hazer ◽  
Miriam Bauer ◽  
Roland Unterhinninghofen ◽  
Rüdiger Dillmann ◽  
Götz-M. Richter
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.


2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Uwe Raaz ◽  
Alexander M Zöllner ◽  
Ryuji Toh ◽  
Futoshi Nakagami ◽  
Isabel N Schellinger ◽  
...  

Stiffening of the aortic wall is a phenomenon consistently observed in abdominal aortic aneurysm (AAA). However, its role in AAA pathophysiology is largely undefined. Using an established murine elastase-induced AAA model, we demonstrate that segmental aortic stiffening (SAS) precedes aneurysm growth. Finite elements analysis (FEA)-based wall stress calculations reveal that early stiffening of the aneurysm-prone aortic segment leads to axial (longitudinal) stress generated by cyclic (systolic) tethering of adjacent, more compliant wall segments. Interventional stiffening of AAA-adjacent segments (via external application of surgical adhesive) significantly reduces aneurysm growth. These changes correlate with reduced segmental stiffness of the AAA-prone aorta (due to equalized stiffness in adjacent aortic segments), reduced axial wall stress, decreased production of reactive oxygen species (ROS), attenuated elastin breakdown, and decreased expression of inflammatory cytokines and macrophage infiltration, as well as attenuated apoptosis within the aortic wall. Cyclic pressurization of stiffened aortic segments ex vivo increases the expression of genes related to inflammation and extracellular matrix (ECM) remodeling. Finally, human ultrasound studies reveal that aging, a significant AAA risk factor, is accompanied by segmental infrarenal aortic stiffening. The present study introduces the novel concept of segmental aortic stiffening (SAS) as an early pathomechanism generating aortic wall stress and thereby triggering AAA growth. Therefore monitoring SAS by ultrasound might help to better identify patients at risk for AAA disease and better predict the susceptibility of small AAA to further growth. Moreover our results suggest that interventional mechanical stiffening of the AAA-adjacent aorta may be further tested as a novel treatment option to limit early AAA growth.


2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Nathan Couper ◽  
Michael Richards ◽  
Ankur Chandra

INTRODUCTION: TEVAR has been seen to cause acute and chronic stent-induced tears of the adjacent aortic wall after treatment in 10-25% of cases with increasing frequency as the stent is placed closer to the aortic valve. The underlying cause for these tears and the ability to predict their occurrence is poorly understood. We hypothesize the cause of these tears is related to stent-induced changes in the adjacent aortic wall which could be quantified and predicted through finite element analysis (FEA) of stent-aorta interface. METHODS: Abaqus TM was used to resolve the FEA model of the stent-aorta interface in three configurations. The maximum principal stress in the vessel wall was averaged over the volume around the stent attachment point and the curvature of the stent was calculated at both the distal and proximal ends. (Figure 1). RESULTS: As the curvature of the attachment site increased, an increase in adjacent aortic wall stress was noted. These ranged from mean curvature (1/m) of 0.1 with wall stress of 49kPa for the distal attachment, position #2 to mean curvature of 6.7 and wall stress of 82kPa for the distal attachment site in position #3. There was an increase in maximum stress distribution as the TEVAR approached the aortic root of 104kPa, 109kPa, and 112kPa for positions 1-3 repectively. CONCLUSIONS: An increase in adjacent aortic wall stress and stress distribution was noted as TEVAR were placed closer to the aortic root which corresponds to the increase in stent-induced aortic tears observed in clinical series. This approach provides the basis for a predictive clinical tool to allow for patient-specific TEVAR planning with associated aortic wall stress analysis to minimize adjacent aortic trauma and assist in future stent design.


2020 ◽  
pp. 1753495X1990041
Author(s):  
Govind Krishna Kumar Nair ◽  
Catriona Bhagra ◽  
Mathew Sermer ◽  
Candice K Silversides ◽  
Birgit Pfaller

Pregnancy increases aortic wall stress and, for a woman with a chronic dissection, this can lead to extension of the dissection, aortic rupture, and death. We report a pregnancy in a woman with a history of a chronic type B aortic dissection. As a child, she had repeat balloon dilation of aortic coarctation, and one of the procedures was complicated by an iatrogenic dissection at the dilation site. At the age of 27 years, she had a planned pregnancy.


2007 ◽  
Vol 33 (5) ◽  
pp. 592-598 ◽  
Author(s):  
H. Åstrand ◽  
Å. Rydén-Ahlgren ◽  
G. Sundkvist ◽  
T. Sandgren ◽  
T. Länne

2011 ◽  
Vol 92 (4) ◽  
pp. 1384-1389 ◽  
Author(s):  
Derek P. Nathan ◽  
Chun Xu ◽  
Ted Plappert ◽  
Benoit Desjardins ◽  
Joseph H. Gorman ◽  
...  

2020 ◽  
Vol 57 (6) ◽  
pp. 1061-1067
Author(s):  
Ignas B Houben ◽  
Nitesh Nama ◽  
Frans L Moll ◽  
Joost A van Herwaarden ◽  
David A Nordsletten ◽  
...  

Abstract OBJECTIVES Maximal aortic diameter is commonly used to assess aortic risk but poorly predicts the timing and location of dissection events in patients with connective tissue disease who undergo regular imaging surveillance. Hence, we aimed to use available surveillance computed tomography angiography (CTA) scans to investigate the correlation between 3-dimensional (3D) growth and cyclic transmural wall stress with the location of intimal tear formation. METHODS Three type B aortic dissection patients with 2 available electrocardiogram (ECG)-gated pre-dissection CTA scans and without surgical repair during the pre-dissection interval were retrospectively identified at our institution. Vascular deformation mapping was used to measure 3D aortic growth between 2 pre-dissection clinical CTA studies. In addition, we performed a computational analysis to estimate cyclic transmural wall stress in patient-specific baseline CTA geometries. RESULTS In all 3 connective tissue disease patients, the site of type B aortic intimal tear co-localized with areas of peak 3D aortic wall growth. Aortic growth was detected by clinical radiological assessment in only 1 case. Co-localization of peak transmural stress and the site of intimal tear formation were found in all cases. CONCLUSIONS Focal areas of growth and transmural wall stress co-localized with the site of intimal tear formation. These hypothesis-generating results suggest a possible new analytic pathway for a more sophisticated assessment of the factors leading to the initiation of dissection in patients with connective tissue disease. These methods could improve on current risk-stratification techniques.


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