## 3 Results and Discussion
### Flow Rate
\begin{table}
\begin{tabular}{c c c c c} \hline \hline  & **Model 1** & **Model 2** & **Model 3** & **Model 4** \\ \hline flow rate at LCX (g/s) & 0.4113 & 0.4249 & 0.4016 & 0.4092 \\ flow rate percentage at LCX (\%) & 32.73 & 33.82 & 31.89 & 32.66 \\ flow rate at DB (g/s) & 0.1915 & 0.1832 & 0.1944 & 0.1892 \\ flow rate percentage at DB (\%) & 15.24 & 14.58 & 15.44 & 15.10 \\ flow rate at LAD (g/s) & 0.6536 & 0.6484 & 0.6632 & 0.6543 \\ flow rate percentage at LAD (\%) & 52.02 & 51.60 & 52.67 & 52.23 \\ \hline \hline \end{tabular}
\end{table} 
Table 1: Blood flow rate of each branch in different models. Figure 7: Flow rate distribution of each branch: (**a**) LCX, (**b**) LAD, and (**c**) DB. locations of the plaques led to different sizes of the vortices behind the plaques. At the LCX section, the velocity distribution trends in the section were basically the same, but the magnitudes of the velocities were different. The reason for this phenomenon is that before the blood flow enters the LCX branch, the speed of the blood flow is different due to the different levels of energy consumption in the vortex region. The same interpretation can be found at the LAD section. However, this explanation does not apply to model 3, in which the velocity was small at the LCX section but large at the LAD section. In model 3, the vortex area behind the block not only consumed the kinetic energy of the fluid but also hindered the flow of the fluid into the LCX, which led to more blood flowing into the LAD; so, in the LAD section, the blood flow velocity in model 3 was significantly higher than other models. In the late diastole, the blood velocity increased significantly, and the velocity distribution in each section was basically consistent with the peak systolic period. However, the greater blood flow velocity resulted in a larger area of low velocity near the vessel wall, especially in the LAD section, which is easily observed from Figure 8. In Table 2, the maximum and average velocities quantify the information in Figure 9, and the standard deviation reflects the difference in velocity gradients at the cross-section. Figure 8: Velocity streamline diagram of the peak systolic phase. Figure 9: Velocity contours of each branch section during the peak systole and late diastole. The following conclusions can be drawn from the flow, velocity streamlines, and cross-sectional velocity: the presence of plaque causes the blood flow velocity to rise sharply at the plaque, and a vortex forms behind the plaque. The existence of vortices lowers the kinetic energy of the fluid, and at the same time hinders the movement of the fluid in this direction. The plaques are distributed in different circumferential positions, and vortices of different shapes and degrees are generated behind them. Under the combined action of the plaque and the eddy current, plaques at different circumferential positions in coronary arteries cause changes in the blood flow and velocity in each branch. Due to the different parts of the heart supplied by blood in the corresponding coronary branch (the LCX supplies the left edge of the left ventricle to the apex of the heart, the LAD supplies part of the anterior ventricular septum, most of the left and right ventricles, and part of the left bundle branch, and the DB supplies the anterior wall of the left ventricle), differently distributed plaques may cause different degrees of heart disease.