**3.2 Velocity streamlines along the cardiac cycle**

After evaluating the velocity profiles, velocity streamlines were created to better visualize and understand how blood flow behaves, as shown in **Figure 4**.

The results indicate the existence of fluid recirculation downstream of the stenosis for both CFD and FSI models, but the recirculation zones are longer in FSI simulations, and this is due to the considerable vessel expansion driven by the pulsatile blood flow.

#### **3.3 WSS and its indices**

The magnitude of the WSS predicted by FSI and rigid model along the artery wall for both systole and diastole are compared in **Figure 5**. In this case, it is observed that the differences between compliant and rigid-wall models are remarkable. In CFD simulations, WSS values estimated in the stenosis throat are approximately twice of those obtained with FSI simulations. This indicates that the WSS distributions were substantially affected by arterial wall compliance, which is in agreement with previous research [25, 26, 41].

**Figure 4.**

*Velocity streamlines obtained during systole and diastole for both CFD and FSI simulations.*

**Figure 5.** *Wall shear stress profiles obtained along artery wall at (a) systole and (b) diastole.*

Taking into account that WSS-related hemodynamic parameters, such as OSI and TAWSS, play an important role in atherogenesis, these were also evaluated. **Figure 6** depicts the TWASS profiles obtained in both CFD and FSI simulations.

The results evidence high values of TAWSS at the stenosis throat, due to flow acceleration and high-velocity gradient near the wall, and, as expected the TAWSS is overestimated by the CFD model as previously explained for WSS distributions. In spite of these observations, the overall TAWSS distributions for the FSI and rigid-wall cases are identical.

Regarding the OSI profiles depicted in **Figure 7**, it can be observed that for both CFD and FSI simulations, the maximum values (≈0*:*5) are obtained downstream of the stenosis, which indicates the presence of unsteady and oscillatory flow, commonly associated with higher susceptibility to atherosclerotic plaque development [27, 40]. Nonetheless, although the OSI profiles for the two cases look similar and unaffected by wall distensibility, in the distal region, OSI values for the FSI case are slightly higher than for the rigid wall [25]. These differences may be due to the occurrence of longer recirculation areas with the elastic model.

In general, it was found that for both rigid and compliant models the poststenotic region presents lower TAWSS and higher OSI values, which constitute risk factors for the incidence and abnormal plaque formation [16, 27].

#### **3.4 Displacement**

**Figure 8** represents the arterial wall displacement contours of the FSI simulations during systole and diastole.

**Figure 6.**

*Time-averaged wall shear stress profiles obtained in CFD and FSI simulations.*

**Figure 7.** *Oscillatory shear index obtained in CFD and FSI simulations.*

*Comparison of CFD and FSI Simulations of Blood Flow in Stenotic Coronary Arteries DOI: http://dx.doi.org/10.5772/intechopen.102089*

#### **Figure 8.**

*Displacement profile at the arterial wall obtained in CFD and FSI simulations.*

In the first place, it is noted that the displacements are similar for both cycle phases. This is a consequence of the assumption of the constant outlet pressure, which is a limitation of this work. In this case, the deformations are slightly bigger in the region upstream of the stenosis, and as there is a pressure drop in the throat, the displacements are somewhat lower in the downstream region.

It is also noteworthy that the displacements of the arterial wall are approximately 1.5–2% of the vessel thickness, which is in agreement with the hypothesis that arteries become stiffer with the development of atherosclerosis. Despite this order of magnitude of the displacement values, these still bring considerable differences in the calculations of the velocity and WSS-related variables.
