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Although coronary artery bypass graft (CABG) surgery is a well-established intervention, graft failure can occur, and the underlying mechanisms remain incompletely understood. The purpose of this prospective study is to utilize computational fluid dynamics (CFD) to investigate how graft hemodynamics one month post surgery may vary among graft types, which have different long-term patency rates. Twenty-four grafts from 10 participants (64.6 ± 8.5 years, 9 men) were scanned with coronary CT angiography and 4D flow MRI one month after CABG surgery. Grafts included 10 left internal mammary arteries (LIMA), 3 radial arteries (RA), and 11 saphenous vein grafts (SVG). Image-guided CFD was used to quantify blood flow rate and wall area exposed to abnormal wall shear stress (WSS). Arterial grafts had a lower abnormal WSS area than venous grafts (17.9% vs. 70.1%; p = 0.001), and a similar trend was observed for LIMA vs. SVG (13.8% vs. 70.1%; p = 0.001). Abnormal WSS area correlated positively to lumen diameter (p

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 that 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.

The degeneration of the arterial wall at the basis of the ascending thoracic aortic aneurysm (ATAA) is a complex multifactorial process, which may lead to clinical complications and, ultimately, death. Individual genetic, biological or hemodynamic factors are inadequate to explain the heterogeneity of ATAA development/progression mechanisms, thus stimulating the analysis of their complex interplay. Here the disruption of the hemodynamic environment in the ATAA is investigated integrating patient-specific computational hemodynamics, CT-based in vivo estimation of local aortic stiffness and advanced fluid mechanics methods of analysis. The final aims are (1) deciphering the ATAA spatiotemporal hemodynamic complexity and its link to near-wall topological features, and (2) identifying the existing links between arterial wall degeneration and hemodynamic insult. Technically, two methodologies are applied to computational hemodynamics data, the wall shear stress (WSS) topological skeleton analysis, and the Complex Networks theory. The same analysis was extended to the healthy aorta. As main findings of the study, we report that: (1) different spatiotemporal heterogeneity characterizes the ATAA and healthy hemodynamics, that markedly reflect on their WSS topological skeleton features; (2) a link (stronger than canonical WSS-based descriptors) emerges between the variation of contraction/expansion action exerted by WSS on the endothelium along the cardiac cycle, and ATAA wall stiffness. The findings of the study suggest the use of advanced methods for a deeper understanding of the hemodynamics disruption in ATAA, and candidate WSS topological skeleton features as promising indicators of local wall degeneration.

Objective: Ascending thoracic aortic aneu-rysm (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 analyses were performed and validated on ten patients using patient-specific data derived from CT scan and four-dimensional MRI. Systolic wall shear stress, 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 ten aTAA samples resected during surgical repair. The biomechanical and rupture properties of these samples were derived: the burst pressure, the physiological tangent elastic modulus $({{{\bf{E}}_{{\bf{physio}}}}})$ , the Cauchy stress at rupture $({{{\bf{\sigma }}_{{\bf{rupt}}}}})$ , the rupture stretch $({{{\bf{\lambda }}_{{\bf{rupt}}}}})$ , and the rupture stretch criterion $({\Upsilon_{\boldsymbol{stretch}}})$ . Statistical analysis was performed to determine correlation between all variables. Results: Statistically highly significant (p ${{\bf{\lambda }}_{{\bf{rupt}}}}$ and the TAWSS (r = 0.867 and p = 0.001) was found. Conclusion: This study shows that relatively low TAWSS significantly correlates with reduced rupture properties in aTAAs. Significance: Understanding the pathogenesis of aTAA remains crucial to reduce morbidity and mortality. Our aim is to establish possible correlations between aTAA rupture risk and hemodynamic biomarkers by combining for the first time in vivo , in vitro , and in silico analyses.

International audience; 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.

Ascending thoracic aorta aneurysm (ATAA) is the 19th common cause of human deaths. Despite important recent progress to better understand the pathogenesis and the development of the disease, the ro...

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.Computational fluid dynamics (CFD), using the finite volume method, was performed on the pRVAD DLC. For Reynolds numbers4000, the laminar model was used to describe the blood flow behavior, while shear-stress transport k-ω model was used for Reynolds numbers4000. Bench testing with a 27 Fr prototype was performed to validate the CFD calculations.There was1.3% 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.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.

We report a patient-specific case of bicuspid aortic valve with fusion of right and left coronary leaflets (R-L type I BAV), moderate aortic valve deficiency and ascending thoracic aortic aneurysms (ATAA) who was treated by only ascending aorta replacement preserving the BAV. The flow eccentricity, the helicity intensity (h2), the circumferential time averaged wall shear stress (TAWSScircumferential), the cumulative viscous energy loss at the systolic peak ( E L ' ) and the pulse wave velocity (PWV) were calculated by combining 4D flow MRI and CFD analysis before (Stage I) and after (Stage II) the surgical procedure. CFD analyses assumed rigid walls, a non-Newtonian behavior for the blood and MRI measured patient-specific blood flow profiles as inlet boundary conditions. Stage II results showed suppression of recirculation in the ascending aorta, loss of jet flow impingement onto the aortic wall, maximum TAWSScircumferential decrease (from 6.69 Pa in Stage I to 6 Pa in Stage II), reduction of flow helicity (from 10.97 in Stage I to 8.47 in Stage II) and E L ' (from 15.8 mW in Stage I to 11.2 mW in Stage II). However, Floweccentricity and PWV were found higher in Stage II due to the diameter reduction (Floweccentricity = 0.60 in Stage I and Floweccentricity = 0.91 in Stage II; PWV = 3.80 m/s in Stage I and PWV = 9.37 m/s in Stage II). Our work has permitted to compute for the first time the hemodynamic alterations obtained after restoration of normal ascending aorta and sinotubular junction geometry even preserving an R-L type I BAV with still acceptable function.