ArticleInternational journal for numerical methods in biomedical engineering2025
A Fluid-Structure Interaction Computational Study of Residual Aortic Dissection to Investigate the Influence of Mechanical Behaviour of Wall and Flap on Flows.
Article in International journal for numerical methods in biomedical engineering, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Patient-Specific Fluid-Structure Interaction Simulations Suggest Wall-Shear-Stress-Related Biomarkers in Type B Dissection Associated with Marfan Syndrome.Annals of biomedical engineering · 2026Article
- A Fluid-Structure Interaction Computational Study of Residual Aortic Dissection to Investigate the Influence of Mechanical Behaviour of Wall and Flap on Flows.International journal for numerical methods in biomedical engineering · 2025Article
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2 authors.
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Abstract
Residual thoracic aortic dissection (RTAD) is a pathology whose patient-dependent evolution is an important clinical issue, and for which numerical fluid-structure interaction (FSI) models can be helpful. However, the proposal of an ad hoc mechanical wall and flap model remains a challenge. To make progress on this issue, we seek to understand the respective influence of the flap and the wall in interaction with the flow in RTAD. Based on a patient's RTAD geometry, we established different FSI models to simulate the mechanical behaviour of the wall and flap. We varied the Young's modulus of the wall between 1.2 MPa (W12) and 2.7 MPa (W27) and the Young's modulus of the flap between 0.6 MPa (F06) and 1.2 MPa (F12), resulting in 3 different cases to study (F06W12, F12W12 and F06W27) and allowing a relative comparison. Structural displacements and stresses are equivalent in F06W12 and F12W12, resulting in equivalent flow characteristics. When comparing F06W12 with F06W27, we show that a stiffer wall reduces flap motion by 49.8%, 51% and 52% respectively, around the first entry tear, second and third one respectively. The difference in flow pressure between channels, which reflects the resistance to flow, is very small (about 1-2 mmHg) and similar for all 3 cases. This result seems to be highly related to the current geometry with one entry and two re-entry tears. Our results show that the wall is the main driver of the overall mechanical behaviour of the RTAD. We demonstrated that a stiffer pathological wall leads to smaller flap displacements, which is consistent with clinical observations in the chronic phase.
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