A longitudinal study of aortic remodeling in chronic type B dissection with patient-specific fluid-structure interaction models
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Aortic dissection is a life-threatening condition characterized by the sudden formation of a new parallel flow channel, the false lumen. Degeneration and dilatation of the false lumen in the chronic phase are the main cause of late adverse events. However, the interplay between anatomic remodeling, which in turn is associated with microstructural remodeling, and hemodynamics during disease progression is not yet well understood [1]. Therefore, in this study, we examine the evolution of a patient’s aortic dissection captured by surveillance imaging with CTA over a period of seven years, from pre-dissection to the chronic phase. We use two-way fluid--structure interaction models with tissue pre-stress, anisotropy, external support, and 4D-flow MRI-derived flow conditions [2] to realistically investigate growth-related hemodynamic markers. In addition, the extracted wall geometries differentiate between tissue layers and thus enable layer-specific material properties. The computational results demonstrate that as the disease progresses, the velocity of the observed blood jet through the entry tear decreases. This blood jet results in locally increased wall shear stresses and blood pressures at the false lumen wall and correlates with regions of aortic dilatation. Additionally, as the disease progresses, the pressure difference between the true and false lumina decreases. This difference becomes negative, particularly in the distal false lumen. These results support the widely accepted notion that growth and remodeling during dissection are likely driven by altered mechanosensation resulting from changes in wall shear stresses and responses to hypertension or wound healing.
