Abstract 4354030: Progressive Flap Thickening Mediated by Wall Shear Stress in Chronic Type B Aortic Dissection

Introduction: Type B Aortic Dissection (TBAD) is a lethal disease. The dissection flap demonstrates morphologic and biomechanical changes as the dissection transitions from the acute to chronic phase. This study sought to delineate the changes in flap thickness in TBAD and to elucidate the relationship between flap thickness and patient-specific wall shear stress (WSS). Hypothesis: We hypothesized that the TBAD dissection flap thickens during the transition from acute to chronic phase, and the growth rate of the flap thickness is mediated by the WSS. Methods: A total of 18 computed tomography (CT) images were retrospectively analyzed from nine TBAD patients treated with optimal medical therapy, with each patient having two scans (Scan 1: acute phase; Scan 2: chronic phase). The flap thickness was measured from the CT cross-section (Fig. 1a and 1b) at three locations, approximately evenly distributed in the longitudinal direction of the flap, for Scan 1 and Scan 2 of each patient. Patient-specific computational fluid dynamics (CFD) was performed based on the CT-derived three-dimensional geometry of the TBAD (Scan 1), and the WSS at the same location as the measured flap thickness was obtained from the CFD flow profile. Results: The flap thickness at a total of 54 locations was obtained in the acute (n=27) and chronic (n=27) phase of the nine TBAD patients. Statistical analyses (Fig. 1c) showed that the flap thickness increased significantly as the acute TBAD transitions to the chronic phase (1.275±0.035 mm vs. 1.535±0.041 mm, p<0.001). The WSS has a strong positive correlation with the flap thickness growth rate (Fig. 1d, R=0.8261, p<0.001). Conclusions: The dissection flap thickens as the aorta transitions from the acute to chronic phase in TBAD, and regions exposed to higher WSS exhibit faster growth. These findings implicate hemodynamic loading as a key mediator of flap remodeling and highlight WSS as a potentially actionable target for risk stratification and therapeutic planning in chronic TBAD.