Investigating the role of structural wall stress in aortic growth prognosis in acute uncomplicated type B aortic dissection.

False lumen expansion is a major factor that determines long-term survival of uncomplicated type B aortic dissection (TBAD). The objective of this study was to investigate whether structural wall stress distributions computed from patient-specific acute TBAD geometries can be used to predict aortic growth rates. Three-dimensional (3D) computed tomography angiography (CTA) of 9 patients with acute uncomplicated TBAD was obtained at initial hospital admission and at their most recent follow-up visits. Patient-specific structural wall stress distributions were computed from the initial baseline CTA using a forward penalty method. Spatially varying blood pressure distributions, derived from computational fluid dynamics (CFD) simulations informed by patient-specific brachial blood pressure (BP) measurements, were incorporated into the forward penalty stress analysis. For 5 patients, transthoracic echocardiography (TTE) data were also available and used to prescribe patient-specific inlet flow conditions in the CFD simulations. Aortic growth rates were quantified and visualized within the 3D TBAD geometries using the initial baseline and follow-up scans. Linear mixed-effects regression analyses were performed to evaluate the spatial correlations between biomechanical markers (structural wall stress, wall shear stress, and pressure) and aortic growth rates. Utilizing initial baseline patient-specific CTA and BP data, along with TTE data when available, the forward penalty analyses revealed hemodynamic and structural mechanics insights of acute uncomplicated TBADs. The linear mixed-effects model indicated that the fixed-effect association between acute structural wall stress and estimated aortic growth rate distributions was statistically significant (p = 0.036), which demonstrated that aortic segments experiencing higher structural stress in the acute phase exhibited more rapid growth. Fixed-effect associations were not significant when predicting growth rate using wall shear stress (p = 0.88) or pressure (p = 0.65) distributions computed from the acute TBAD geometry. Significant Pearson correlation coefficients (p < 0.05) were observed between acute structural wall stress and aortic growth rate in all patients. Higher structural wall stress in the acute TBAD geometry was associated with regions of increased aortic growth rates. When modeled as a solid, false lumen thrombus was linked to lower structural wall stress and may have a protective effect against rapid aortic growth. Further studies are needed to investigate the biphasic nature of thrombus. Structural stress, which in this study was derived using the forward penalty approach, may be a novel predictor of aortic growth rate in acute TBAD.