## 3 Results and Discussion  
The model was executed for several cardiac cycles, and the results were examined after the model achieved a steady-state, as shown in Figure 4a. Figure 5 shows the velocity streamlines and structural deformation at four distinct time points throughout the cardiac cycle of the simulated 3D LV model. The filling phase (diastole) can be seen at time 1610 ms. The snapshot captured at 1760 ms displays the iso-volumetric contraction following the filling phase. Furthermore, during the closure of the MV and the subsequent opening of the AoV, the blood is directed into the after-load (systemic) circulation, as demonstrated at 1881 ms. Thereafter, the pressure in the LV decreases during the iso-volumetric relaxation as shown at 2060 ms. The occlusion of blood circulation at the LVOT is evident when the AML is shifted towards the outflow tract. Figure 5d demonstrates that obvious blockage occurs when the AML extends significantly into the outflow tract, resulting in elevated pressure gradients. In Figure 5, simulations illustrate that protrusion of AML into the LVOT leads to a higher degree of obstructed blood flow. As part of this study, we simulated the four angles of AML after the anterior leaflet splitting (laceration) in order to investigate of its impact on the flow pattern at the LVOT. After MV anterior leaflet splitting, obstruction at the LVOT diminish as the blood flows seamlessly towards the AoV (see Figure 6). Additionally, Figure 6d shows less obstruction to the LVOT flow in comparison with case (d) when AML is preserved (Figure 5). Snapshots of flow velocity profiles at different angulation of MV anterior leaflet are shown in Figure 7. It can be seen clearly the different flow profiles when displacing the AML towards LVOT from 0\({}^{\circ}\) to 30\({}^{\circ}\) (see Figure 7a). At 0\({}^{\circ}\), no flow obstruction was seen as the blood is smoothly driven into the AoV. Moreover, slight obstacle to the flow was illustrated at angle 10\({}^{\circ}\) and 20\({}^{\circ}\), while excessive simulation of the MV anterior leaflet, at 30\({}^{\circ}\) reveals higher obstruction of the blood flow in comparison with 0\({}^{\circ}\), 10\({}^{\circ}\) and 20\({}^{\circ}\). Following the division of the AML, noticeable alterations were observed in the blood flow pattern during the ejection phase through the AoV (see Figure 7b). Figure 3: The model setting for (**a**) SAM simulation by rotating the MV anterior leaflet at various angles towards the outflow tract, and (**b**) anterior leaflet after splitting. In order to examine and contrast the blood flow patterns in these different models, the blood flow were measured at a line extended perpendicularly from the center of the AoV into the LV cavity, as seen in Figure 8e. This can provide a better understanding of the impact of different simulation scenarios on the blood movement during systole. As AML protrudes into the LVOT, more obstruction can be seen in the flow pattern (see Figure 8a-d). A slight difference was found at angle 0\({}^{\circ}\) prior and post AML splitting; however, more occlusion to the blood flow is illustrated as the AML is extended to outflow tract. In this work, the flow profile at outlet boundary, the AoV, was studied. Figure 9 shows the flow profiles at different simulations. The profile was investigated by plotting the flow velocity at mid-line of AoV, as shown in Figure 9e. An obvious dropped in the flow was seen in Figure 9d in comparison with other cases (Figure 9a-c), before AML laceration. An improvement in the flow profile was existed after AML laceration, especially for case (Figure 9d). This clinical technique is used to alleviate the obstruction in the remaining area of the LVOT following the TMVI following the TMVI, hence preventing the obstruction of the LVOT [15; 16]. Figure 4: 3D model pressure waveform and gradients. (**a**) shows LV, LA, Ao and arterial pressure of 3D generic model at 0\({}^{\circ}\) (with no AML splitting), and (**b**) illustrates the pressure gradients of all simulations.