## 1 Introduction  
AD is a deadly cardiovascular emergency. Under the Stanford classification, AD is divided into type A and type B. If not diagnosed and treated properly in time, the mortality rate of AD patients increases by 1-2% per hour, with over 35% dying within 24 h and 50% within 48 h [1]. While AD's exact pathogenesis remains unclear, it is widely accepted to involve blood and vessel biodynamics [2]. Hypertension is found in 67.3-76.6% of AD patients and in as high as 86% of Stanford type B aortic dissection (TBAD) patients [3, 4]. It is considered a significant risk factor for the occurrence and evolution of AD [5, 6]. Therefore, studying the effect of hypertension on the progression of TBAD is of great practical significance. When the aortic intima of AD patients is torn, blood flows out of the intimal tear under bp, causing the aortic wall to separate into inner and outer layers. The intimal flap divides the aorta into true lumens (TLs) and false lumens (FLs) [7], with the outer wall of the FL called the FL wall. Previous studies have simulated and analyzed the biodynamic effects of hypertension on AD, confirming the effectiveness of simulations in studying AD formation and evolution. These studies have not only clarified the determinants of bp but also offered more precise clinical data. The findings reveal that while hypertension has limited effects on AD blood flow velocity, patterns, and wall shear stress, it significantly elevates vascular wall pressure [8]. [PERSON] et al. dissected healthy pig aortas to create AD and performed uniaxial tensile tests on tissue samples revealing significant regional variations in the biomechanical response of porcine aortic tissue [9]. [PERSON] et al. (2021) found that the aortic material is stiffer longitudinally than circumferentially [10]. [PERSON] et al. (2014) reviewed the hemodynamic numerical simulation of AD, emphasizing that vessel wall properties, complex geometric features, and biomechanical factors are closely related to the occurrence and evolution of tears [11]. [PERSON] et al. (2015) studied the hemodynamic characteristics of TBAD, showing that the distal tear significantly impacts lumen pressure, with larger distal tears reducing the pressure difference between the TL and FL [12]. [PERSON] et al. (2025) [13] studied the FL formation in AD. They found that slow blood flow enters the FL, creating vortices that worsen thrombus formation. [PERSON] et al. (2024) observed the gradual expansion of the FL, with its surface area increasing from 82.63 cm\({}^{2}\) to 98.84 cm\({}^{2}\) and volume from 45.12 mL to 63.40 mL [14]. [PERSON] et al. (2012) [15] used CFD to study the stress on the FL wall in AD under different bps. Their research shows that as bp rises, the stress on the FL wall increases. [PERSON] et al. (2012) also used CFD, revealing a close link between the hemodynamic behavior of AD and bp, though the impact of bp on wall shear stress distribution is minimal [16]. [PERSON] et al. (2019) [17] experimentally studied AD hemodynamics under varied mean pressures in vitro. They found that mean pressure changes barely affect AD vortex and retrograde flow patterns. [PERSON] et al. (2020) and [PERSON] et al. (2020) used the FSI method to study the von Mises stress and intimal flap deformation in a single-layer model of AD [18; 19]. Previous studies have simplified the model material properties, such as by treating the vascular wall as a single-layer rigid material, which may compromise the credibility of simulation results. This study, based on tests of fresh aortas of 5-7-month-old Yorkshire pigs, used ABAQUS-ISIGHT inversion to refine the hyperelastic anisotropic constitutive model parameters for AD, creating an HGO-based model closest to human AD. Using FSI and CFD, it simulated blood flow and biodynamic features of TBAD with higher physiological fidelity, analyzing the effect of hypertension on the evolution of TBAD.