## 4 Discussion  
We studied the hemodynamic implications of localized aortic valve calcifications in comparison to a healthy valve, using both uniform and helical blood inflow with realistic  
Figure 20: Iso-surfaces of the instantaneous Q-criterion for the iso-value of 100,000 s\({}^{-2}\) under uniform blood inflow. boundary conditions. To further understand the effects of helical LVOT flow, we incorporated an in-plane velocity profile alongside the through-plane waveform at the inflow boundary. For the outlet boundary condition on the aortic side, we employed the traditional three-element Windkessel model. Although this model does not capture pulse wave propagation, it offers a straightforward approach to ensuring an accurate physiological pressure at the outlet. To assess the impact of calcification on aortic valve performance, we utilized FSI simulations, through which we examined a range of hemodynamic parameters encompassing transvalvular flow fields, indices, WSS-based metrics such as TAWSS, OSI, RRT, and transWSS, and analyzed the intricacies of helical flow by quantifying helicity using various descriptors. In localized calcifications, we observed restricted leaflet movement and a decreased orifice area, fundamentally altering the valve's hemodynamics. Leaflet stiffening restricts the valve's opening, compromising blood transport efficiency and subsequently imposing additional stress on the left ventricle, aligning with clinical findings. The constricted valve opening in calcified valves leads to a flow jet at the orifice, which, in turn, promotes circulatory flow and intensifies turbulence within the aortic sinuses. The aortic orifice area typically ranges from 3.9 \(\pm\) 1.2 cm\({}^{2}\) for healthy conditions to 1.0-1.5 cm\({}^{2}\), in cases of moderate stenosis, and our findings confirm these metrics, consistent with clinical observations detailed in [4]. These different levels of calcification are notably correlated with significant disparities in resulting flow patterns, the magnitude of vorticities, and, consequently, the forces exerted on the aorta walls and valve leaflets. The asymmetrical formation of calcification deposits on one or two leaflets leads to additional stress on the remaining non-calcified leaflets. Unlike previous studies [11; 50; 51] that focused on uniformly calcified leaflets, our findings indicate that localized calcification directs the flow towards the ascending aorta's wall, and the study by [52] suggests this redirection has the potential to cause harm to the wall. Some research suggests this redirection has the potential to cause harm to the wall [52]. This redirection results in periodic elevated WSS, which may accelerate endothelial erosion and nitric oxide (NO) release over time [53]. Increasing calcification severity also leads to the formation of stronger vortices and, consequently, greater energy dissipation rates. These findings align with prior works, specifically, the studies by [PERSON] et al. [4] and [PERSON] et al. [11], but offer a more in-depth perspective by examining the localization of calcification. Alterations in blood flow directly influence the distribution of WSS on the leaflets, a factor significant for calcification progression [54]. Our simulations demonstrate that, compared to healthy scenario, calcified leaflets undergo markedly elevated WSS. Our study revealed a marked impact on WSS-based indices, with a higher TAWSS being associated with more advanced calcification grades, suggesting an increased risk of endothelial damage. The leaflet's base region, proximate to the aortic root, maintains a fairly stable and low TAWSS irrespective of calcification levels. Conversely, the calcified leaflet's tip undergoes prolonged exposure to elevated WSS and demonstrates a significant susceptibility to calcification grades. As calcification intensifies, the leaflets encounter increasingly spatially complex shear stresses, amplifying the TAWSS disparity between tip and base regions.