Aortic dissection leads to late complications due tochronic degeneration and dilatation of the false lumen. This study examines the interaction between hemodynamics and long-term remodeling of a patient's aortic dissection, tracked from pre-dissection to the chronic phase using CT angiography. Fluid–structure interaction models with 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. Aortic dilatation was most significant distal to the left subclavian artery, reaching 6 cm in the chronic phase. Simulations quantified the flow jet velocity through the entry tear, which peaked at 185 cm/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 2 mmHg in the subacute and chronic phases, with 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 1.8 mm as disease progressed, which was associated with an overall increase in aortic diameter. Simulations with a significant reduction in flap stiffness during the subacute phase resulted in increased flap motion up to 9.5 mm. Although these results are based on a single patient, they suggest a strong relationship between hemodynamics and aortic growth.