Carotid Bifurcation With Tandem Stenosis—A Patient-Specific Case Study Combined in vivo Imaging, in vitro Histology and in silico Simulation

Figure 1. Examples of collected data and data processing. (A) The collected carotid plaque tissue sample (left) and later the sample was cut into six segments with 3–4 mm thick. (B) The Hematoxylin & Eosin (H & E) staining of 6 slices. (C) At the same position of staining slices, the T1-weighted MR imaging slices with segmented contours (lumen and vessel in red color, lipid in yellow color, and calcification in green color). (D) The reconstructed 3D patient-specific carotid bifurcation, including the geometries of lumen (gray), lipid (yellow) and calcification (green).

Figure 2. The geometric model of 3D patient-specific carotid bifurcation with tandem stenosis for CFD simulation and the boundary conditions. The inlet and two outlets were extended to get fully developed flow profile. The time-dependent massflow rate boundary condition (extracted from phase-contrast MRI) was given to the CCA inlet, and the constant pressure profile was given to both ICA and ECA outlets.

Figure 3. The 3D reconstructed patient-specific carotid bifurcation models and the geometric models used in CFD. From the left to right are, the original model with tandem stenosis, the presumptive model by removing the stenosis at CCA, ICT and both locations, respectively. The inlet and outlets were extended in the CFD geometric models for the purpose of flow fully-developing.

Figure 4. The histology staining at the ICA stenosis location, the lipid, calcification, and hemorrhage could be viewed in different staining. (A1) H & E staining; (A2) Calcium in dark purple and hemorrhage in dark pink; (B1) Oil Red O; (B2) Lipids stained in red; (C1) Masson's Trichrome; (C2) Fibrous tissue in blue and hemorrhage in dark pink. (D) The lumen TaWSS contour from CFD result at the position of histology slice. WSS was found to have an association with the location of hemorrhage and calcification.

Figure 5. The massflow rate from ICA (solid line) and ECA (dashed line) outlets in the tandem stenosis model and the three presumptive models by removing stenosis at different locations. It was found the difference of flow distribution between each model enlarged at systole period, and reduced at diastole period.

Figure 6. The velocity streamline and the volume rendering of turbulence kinetic energy (TKE) in the geometric models under the maximum and minimum mass flowrate (at timestep of ~0.3 and 0.51 s, respectively).

Figure 7. The highest values of wall shear stress (WSS) at bifurcation apex through one cardiac cycle in the tandem stenosis model and the three presumptive models by removing stenosis at different locations. Similar as the curves of massflow distribution, the difference of apex WSS between each model enlarged at systole period, and reduced at diastole period, The largest gap was found at around the ejection point (~0.3 s) between the tandem stenosis model (70.58 Pa) and the non-stenosis model (27.47 Pa).

Figure 8. The contour maps of WSS concentration at local ICA part, local bifurcation part and local CCA part during one cardiac cycle in the four geometric models. (A1–A4) The WSS plot at local ICA part in the four geometric model. (B1–B4) The WSS plot at local bifurcation part in the four geometric model. (C1–C4) The WSS plot at local CCA part in the four geometric model.

Figure 9. The spatial-averaged WSS at the surface of whole carotid model, local ICA part, local bifurcation part and local CCA part during one cardiac cycle for all the four models.

Figure 10. The contours of three derived WSS parameters, TaWSS, OSI and RRT in the four geometric models.