Patient-specific bicuspid aortic valve hemodynamics study based on computer simulation and in vitro experiment.

Bicuspid aortic valve (BAV) is a common congenital malformation of the aortic valve with various structural characteristics. Different types of BAV can cause secondary aortic diseases, including calcific aortic valve stenosis and aortic dilation, although their pathogenesis remains unclear. In this study, we first established patient-specific BAV simulation models and silicone models (Type 0 A-P, Type 1 R-N, and Type 1 L-R) based on clinical computed tomography angiography (CTA) and pressure data. Next, we applied a research method combining fluid-structure interaction (FSI) simulation and digital particle image velocimetry (DPIV) experiment to quantitatively analyze the hemodynamic, structural mechanical, and flow field characteristics of patients with different BAV types. Simulation-based hemodynamic parameters and experimental results were consistent with clinical data, affirming the accuracy of the model. The location of the maximum principal strain in the patient-specific model was associated with the calcification site, which characterized the mechanism of secondary aortic valve stenosis. The maximum wall shear stress (WSS) of the patient-specific model (>67.1 Pa) exceeded 37.9 Pa and could cause endothelial surface injury as well as remodeling under long-term exposure, thus increasing the risk of aortic dilation. The distribution of WSS was mainly caused by BAV type, resulting in different degrees of dilation in different parts guided by the type. The patient-specific model revealed a maximum viscous shear stress (VSS) value of 5.23 Pa, which was smaller than the threshold for shear-induced hemolysis of red blood cells (150 Pa) and platelet activation (10 Pa), but close to the threshold for platelet sensitization (6 Pa). The results of flow field characteristics revealed a low risk of hemolysis but a relative high risk of thrombus formation in the patient-specific model. This study not only provides a basis for future comprehensive research on BAV diseases, but also generates relevant insights for theoretical guidance for calcific aortic valve stenosis and aortic dilation caused by different types of BAV, as well as biomechanical evidence for the potential risk of hemolysis and thrombus formation in BAV, which is of great value for clinical diagnosis and treatment of BAV. [ABSTRACT FROM AUTHOR]