## 3 Results and Discussion
### Wall Shear Stress (WSS)  
It is well known that the WSS is associated with the occurrence and development of intimal hyperplasia and atherosclerotic plaques. Smaller WSS areas are prone to plaque growth, while larger WSSs can cause plaque rupture. The degree of WSS oscillation during the cardiac cycle is related to the endothelial cell damage. The higher the degree of oscillation, the greater the risk of endothelial damage. The WSS distribution of each model at the peak systolic period is shown in Figure 10.  
No matter where the plaques were located, there was a large WSS in front of the plaque, a small WSS behind the plaque, a large WSS at the LCX bifurcation, and a small WSS at the DB bifurcation. Combining the velocity streamlines in Figure 8, it is not difficult to see that there was a certain correlation between the WSS and the blood flow velocity of the blood vessel wall. The WSS value was consistent with the variation trend of the velocity. Behind the plaque, the eddy current caused the blood flow to be disordered and the flow velocity was low, forming a low WSS area. At the LCX bifurcation, the blood flow impacted the top of the bifurcation and caused a high WSS there. When entering the DB, the blood flow rate was further reduced due to the existence of the bifurcation, forming a low WSS area. Comparing between different models, there were obvious differences in the low WSS area behind the plaque, which was the result of the combined effect of the vortex behind the plaque and the separation of the blood flow. The WSS distributions at the DB forks were similar, and there was no significant difference. In order to further compare \begin{table}
\begin{tabular}{c c c c c c} \hline
**Time** & **Parameter** & **Model 1** & **Model 2** & **Model 3** & **Model 4** \\ \hline \multirow{8}{*}{peaksy stop} & LM. average velocity (cm/s) & 4.63 & 4.97 & 4.50 & 4.79 \\  & LM. maximum velocity (cm/s) & 24.31 & 25.64 & 26.87 & 23.81 \\  & LM. standard deviation (cm/s) & 5.74 & 6.12 & 6.15 & 5.98 \\  & LCX. average velocity (cm/s) & 9.52 & 9.66 & 9.19 & 9.25 \\  & LCX. maximum velocity (cm/s) & 27.19 & 28.93 & 26.70 & 27.11 \\  & LCX. standard deviation (cm/s) & 7.58 & 7.84 & 7.42 & 7.48 \\  & LAD. average velocity (cm/s) & 5.45 & 5.75 & 5.93 & 5.44 \\  & LAD. maximum velocity (cm/s) & 18.49 & 18.60 & 19.95 & 17.79 \\  & LAD. standard deviation (cm/s) & 4.95 & 4.93 & 5.33 & 4.77 \\ \hline \multirow{8}{*}{latedia stop} & LM. average velocity (cm/s) & 12.35 & 12.75 & 12.25 & 12.47 \\  & LM. maximum velocity (cm/s) & 51.43 & 53.65 & 56.34 & 50.06 \\  & LM. standard deviation (cm/s) & 13.45 & 13.87 & 14.14 & 13.99 \\  & LCX. average velocity (cm/s) & 21.20 & 23.23 & 19.45 & 21.83 \\  & LCX. maximum velocity (cm/s) & 56.02 & 62.17 & 52.27 & 60.26 \\  & LCX. standard deviation (cm/s) & 16.13 & 17.60 & 14.89 & 16.53 \\  & LAD. average velocity (cm/s) & 14.75 & 15.75 & 15.72 & 13.34 \\  & LAD. maximum velocity (cm/s) & 47.27 & 46.44 & 48.32 & 46.06 \\  & LAD. standard deviation (cm/s) & 13.37 & 12.68 & 14.90 & 12.45 \\ \hline \end{tabular}
\end{table} 
Table 2: Velocity values of each section during the peak systole and late diastole. the distribution of the WSS among each model, a representative position in the model was taken to quantify the change in WSS in the complete cardiac cycle, as shown in Figure 11.  
At the shoulder of the LCX bifurcation, that is, point 1, the variation trend of the WSS under different models was similar, but the WSS value was different. The WSS values were sorted from high to low; the highest were model 2 and model 4, and their WSS changes were almost the same; the second was model 1; the lowest was model 3, which was significantly different from the other models. At the apex of the LCX bifurcation, that is, point 2, the trend of the WSS changes was similar to that at point 1. The difference was that the amplitude of the WSS was larger here, and the maximum amplitudes from model 1 to model 4 were 26.54 Pa, 22.79 Pa, 37.36 Pa, and 21.84 Pa, respectively.