Different levels of spatiotemporal heterogeneity characterize the aneurysmal and healthy ascending aorta hemodynamics, reflecting on wall shear stress topological skeleton. Peculiar wall shear stress topological skeleton features are linked to local ascending thoracic aortic aneurysms stiffness. The topological shear variation index, a measure of wall shear stress luminal contraction/expansion action variation along the cardiac cycle, is an indicator of local aortic wall degradation, performing better than canonical wall shear stress-based descriptors of flow disturbances. Wall shear stress topological skeleton analysis, combined with Complex Networks theory, contributes to better determine whether arterial wall degeneration, in combination with hemodynamic insult, leads to aneurysmal progression/rupture.
We present a comprehensive and original framework for the biomechanical analysis of patients affected by ascending thoracic aorta aneurysm and aortic insufficiency. Our aim is to obtain crucial indications about the role played by deranged hemodynamics on the ATAAs risk of rupture. Computational fluid dynamics analysis was performed using patient-specific geometries and boundary conditions derived from 4D MRI. Blood flow helicity and wall shear stress descriptors were assessed. A bulge inflation test was carried out in vitro on the 4 ATAAs after surgical repair. The healthy volunteers showed no eccentric blood flow, a mean TAWSS of 1.5 ± 0.3 Pa and mean OSI of 0.325 ± 0.025. In 3 aneurismal patients, jet flow impingement on the aortic wall resulted in large TAWSS values and low OSI which were amplified by the AI degree. However, the tissue strength did not appear to be significantly reduced. The fourth patient, which showed the lowest TAWSS due to the absence of jet flow, had the smallest strength in vitro. Interestingly this patient presented a bovine arch abnormality. Jet flow impingement with high WSS values is frequent in ATAAs and our methodology seems to be appropriate for determining whether it may increase the risk of rupture or not.
Purpose. It has been reported clinically that rupture or dissections in thoracic aortic aneurysms (TAA) often occur due to hypertension which may be modelled with sudden increase of peripheral resistance, inducing acute changes of blood volumes in the aorta. There is clinical evidence that more compliant aneurysms are less prone to rupture as they can sustain such changes of volume. The aim of the current paper is to verify this paradigm by evaluating computationally the role played by the variation of peripheral resistance and the impact of aortic stiffness onto peak wall stress in ascending TAA. Methods. Fluid-Structure Interaction (FSI) analyses were performed using patient-specific geometries and boundary conditions derived from 4D MRI datasets acquired on a patient. Blood was assumed incompressible and was treated as a non-Newtonian fluid using the Carreau model while the wall mechanical properties were obtained from the bulge inflation tests carried out in vitro after surgical repair. The Navier Stokes equations were solved in ANSYS Fluent. The Arbitrary Lagrangian Eulerian formulation was used to account for the wall deformations. At the interface between the solid domain and the fluid domain, the fluid pressure was transferred to the wall and the displacement of the wall was transferred to the fluid. The two systems were connected by the System Coupling component which controls the solver execution of fluid and solid simulations in ANSYS. Fluid and solid domains were solved sequentially starting from the fluid simulations. Results. Distributions of blood flow, wall shear stress and wall stress were evaluated in the ascending thoracic aorta using the FSI analyses. We always observed a significant flow eccentricity in the simulations, in very good agreement with velocity profiles measured using 4D MRI. The results also showed significant increase of peak wall stress due to the increase of peripheral resistance and aortic stiffness. In the worst case scenario, the largest peripheral resistance (10 10 kg.s.m -4 ) and stiffness (10 MPa) resulted in a maximal principal stress equal to 702 kPa, whereas it was only 77 kPa in normal conditions. Conclusions. This is the first time that the risk of rupture of an aTAA is quantified in case of the combined effects of hypertension and aortic stiffness increase. Our findings suggest that a stiffer TAA may have the most altered distribution of wall stress and an acute change of peripheral vascular resistance could significantly increase the risk of rupture for a stiffer aneurysm.
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Ascending thoracic aortic aneurysm (aTAA) is a major cause of human deaths. Despite important recent progress to better understand its pathogenesis and development, the role played by deranged hemodynamics on aTAA risk of rupture is still partially unknown. Our aim was to develop and apply a novel methodology to assess the correlation between aTAA rupture risk and hemodynamic biomarkers combining for the first time in vivo, in vitro and in silico analyses. Methods: Computational fluid dynamic (CFD) analyses were performed and validated on 10 patients using patient-specific data derived from CT scan and 4D MRI. Systolic wall shear stress (WSS), time-averaged wall shear stress (TAWSS), flow eccentricity (Floweccentricity) and helicity intensity (h2) were assessed. A bulge inflation test was carried out in vitro on the 10 aTAA samples resected during surgical repair. The biomechanical and rupture properties of these samples were derived: the burst pressure, the physiological tangent elastic modulus (), the Cauchy stress at rupture (), the rupture stretch () and the rupture stretch criterion (ϒ). Statistical analysis was performed to determine correlation between all variables. Results: Statistically highly significant (p<0.01) positive correlation between and the TAWSS (r=0.867 and p=0.001) was found.
Objectives Our goal is to develop a double lumen cannula (DLC) for a percutaneous right ventricular assist device (pRVAD) in order to eliminate two open chest surgeries for RVAD installation and removal. The objective of this study was to evaluate the performance, flow pattern, blood hemolysis, and thrombosis potential of the pRVAD DLC. Methods Computational fluid dynamics (CFD), using the finite volume method, was performed on the pRVAD DLC. For Reynolds numbers <4000, the laminar model was used to describe the blood flow behavior, while shear-stress transport k-ω model was used for Reynolds numbers >4000. Bench testing with a 27 Fr prototype was performed to validate the CFD calculations. Results There was <1.3% difference between the CFD and experimental pressure drop results. The Lagrangian approach revealed a low index of hemolysis (0.012% in drainage lumen and 0.0073% in infusion lumen) at 5 l/min flow rate. Blood stagnancy and recirculation regions were found in the CFD analysis, indicating a potential risk for thrombosis. Conclusions The pRVAD DLC can handle up to 5 l/min flow with limited potential hemolysis. Further modification of the pRVAD DLC is needed to address blood stagnancy and recirculation.
The aim of the present work is to propose a robust computational framework combining computational fluid dynamics (CFD) and 4D flow MRI to predict the progressive changes in hemodynamics and wall rupture index (RPI) induced by aortic morphological evolutions in patients harboring ascending thoracic aortic aneurysms (ATAAs). An analytical equation has been proposed to predict the aneurysm progression based on age, sex, and body surface area. Parameters such as helicity, wall shear stress (WSS), time‐averaged WSS, oscillatory shear index, relative residence time, and viscosity were evaluated for two patients at different stages of aneurysm growth, and compared with age‐sex‐matched healthy subjects. The study shows that evolution of hemodynamics and RPI, despite being very slow in ATAAs, is strongly affected by morphological alterations and, in turn could impact biomechanical factors and aortic mechanobiology. An aspect of the current work is that the patient‐specific 4D MRI data sets were obtained with a follow‐up of 1 year and the measured time‐averaged velocity maps and flow eccentricity were compared with the CFD simulation for validation. The computational framework presented here is capable of capturing the blood flow patterns and the hemodynamic descriptors during the various stages of aneurysm growth. Further investigations will be conducted in order to verify these results on a larger cohort of patients and with long follow‐up times to finally elucidate the link between deranged hemodynamics, AA geometry, and wall mechanical properties in ATAAs.
The AvalonElite double lumen cannula (DLC) provides total cavopulmonary assist (CPA) in failing Fontan sheep, but recirculation limits reliability. To improve CPA performance, a two-valve extracardiac conduit (ECC) was used to bracket infusion blood toward pulmonary artery (PA). A total cavopulmonary connection with failing Fontan circulation adult sheep model was created with valved ECC (n = 6). The valved ECC was connected to superior/inferior venae cavae (SVC/IVC) and right PA. The AvalonElite DLC was inserted from right jugular vein with infusion opening between the ECC valves. The DLC drainage lumen withdrew blood from SVC/IVC, and the infusion lumen returned blood to ECC. A failing Fontan sheep model with valved ECC was successfully created. Central venous pressure increased from 9 ± 1 to 17 ± 1 mm Hg, systolic arterial pressure decreased from 103 ± 9 to 51 ± 13 mm Hg, and cardiac output decreased from 3.6 ± 0.3 to 1.4 ± 0.2 L/min. Serum lactate significantly increased, indicating poor tissue perfusion. At 4 L/min pumping flow, the AvalonElite DLC returned hemodynamics/lactate to baseline levels throughout 6 hour CPA. Necropsy revealed intact/well-functioning ECC valves and well-positioned DLC with no visible thrombosis. The AvalonElite DLC provides reliable CPA performance in failing Fontan sheep with valved ECC.
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