Assessment of aortic dissection remodeling with patient-specific fluid-structure interaction models.

Abstract

Aortic dissection leads to late complications due to chronic degeneration and dilatation of the false lumen. However, the interaction between hemodynamics and microstructural remodeling driving long-term changes is not fully understood. This study examines the progression of a patient's aortic dissection, tracked from pre-dissection to the chronic phase using computed tomography angiography. Fluid-structure interaction models that account for tissue prestress, external support, and anisotropic properties were used to analyze hemodynamic markers. Each aortic wall layer had distinct thicknesses and material properties. The boundary conditions were guided by in vitro 4D-flow MRI and the patient's blood pressure. Quantitative measurements during routine clinical care showed that aortic dilatation was most significant distal to the left subclavian artery, reaching 6cm in the chronic phase. Simulations resulted in a flow jet velocity through the entry tear that peaked at 185cm/s in the subacute phase and decreased to 123 to 133 cm/s in the chronic phase, corresponding to an increased entry tear size. Flow jet impingement on the false lumen resulted in a localized pressure increase of 11 and 2mmHg in the subacute and chronic phases, with the wall shear stress reaching 4,Pa. These hemodynamic changes appear to be the main drivers of aortic growth and morphological changes. Despite moderate overall flap movement, in-plane displacement increased from 0.6 to 1.8mm as disease progressed, which was associated with an overall increase in aortic diameter. Additional simulations with a significant reduction in flap stiffness during the subacute phase resulted in increased flap motion up to 9.5mm. Although these results are based on a single patient, they suggest a strong relationship between hemodynamics and aortic growth.