Cardiovascular Engineering and Technology

, Volume 9, Issue 4, pp 707–722 | Cite as

Evaluation of Peak Wall Stress in an Ascending Thoracic Aortic Aneurysm Using FSI Simulations: Effects of Aortic Stiffness and Peripheral Resistance

  • Rossella Campobasso
  • Francesca Condemi
  • Magalie Viallon
  • Pierre Croisille
  • Salvatore Campisi
  • Stéphane Avril



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.


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.


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 (1010 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.


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.


4D MRI Thoracic aortic aneurysm Fluid–structure interactions Peak wall stress Risk of rupture Aortic stiffness 



We thank Dr Morbiducci and Dr Gallo from Polytechnic of Turin (Italy) who provided insight and expertise that greatly assisted the model development. We are also grateful to Ansys, Inc. for providing Ansys-Fluent (ANSYS® Academic Research, Release 17.2). This research was supported by the European Research Council (ERC grant biolochanics, grant number 647067).


This research was supported by the European Research Council (ERC grant biolochanics, grant number 647067, grant holder: SA).

Conflict of interest

All the authors declare they have no conflict of interest.

Ethical approval

All procedures performed in this study were in accordance with the ethical standards of the 1964 Helsinki declaration and its later amendments. The study was approved by the Institutional Review Board of the University Hospital Center of Saint-Étienne (France). After informed consent, a 59-year-old man was enrolled. The patient was scanned on a 3T MRI scanner (Siemens Magnetom Prisma) without contrast agent using a 4D flow phase contrast protocol and sequence.


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Copyright information

© Biomedical Engineering Society 2018

Authors and Affiliations

  1. 1.Mines Saint-Etienne, Univ Lyon, Univ Jean Monnet, INSERMSaint-EtienneFrance
  2. 2.Centre Hospitalo-UniversitaireSaint-EtienneFrance
  3. 3.Univ Lyon, UJM-Saint-Etienne, INSA, CNRS, UMR 5520, INSERM U1206, CREATISSaint-EtienneFrance
  4. 4.Department of Electrical and Computer EngineeringUniversity of TorontoTorontoCanada

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