Internal carotid artery bifurcation aneurysms are probably formed to decrease the abnormally-enhanced hemodynamic stresses caused by direct flow impaction.

The hemodynamic parameters associated with the presence of internal carotid artery (ICA) bifurcation saccular aneurysms are unknown. This study was conducted to investigate this association using computational fluid dynamic (CFD) analysis of patients' specific three-dimensional (3D) imaging datasets. Patients with ICA bifurcation saccular aneurysms were retrospectively enrolled, and the 3D angiographic datasets were used for CFD analysis with aneurysm presence and virtual aneurysm removal. A total of 20 patients with ICA bifurcation aneurysms were enrolled, including 15 (75%) female and 5 (25%) male patients aged 26-76 (50.0±13.4) years. Compared with the hemodynamic parameters on the aneurysm dome, the dynamic (median 1.65 vs. 12.79±5.74 Pa) and total pressure (198.90±22.90 vs. 288.85±57.08 Pa), vorticity (2,507.00±1,237.53 vs. 5,717.17±2,210.72), cell (median 3.92 vs. 9.06±4.41) and turbulence Reynolds numbers (median 0.08 vs. 0.27), turbulence kinetic energy (median 0.00001 vs. 0.0002), turbulence intensity (median 0.002 vs. 0.011±0.004), turbulence dissipation rate (median 0.05 vs. 1.09), wall shear stress (WSS; median 2.26 vs. 6.44±2.53), and strain rate (2,566.32±1,350.56 vs. 5,920.91±2,186.03) on the bifurcation after aneurysm removal were significantly (P<0.0001) increased. On the line for sampling hemodynamic parameters, the dynamic (median 1.28 vs. 18.23±8.09 Pa) and total (201.73±31.35 vs. 299.97±76.61 Pa) pressure, vorticity (median 1,821.63 vs. 6,873.31±1,930.62), cell Reynolds number (median 3.39 vs. 9.14±2.69), turbulence kinetic energy (median 7.31e-6 vs. 0.0003±0.0001 m2/S2), turbulence intensity (median 0.002 vs. 1.74±0.82), turbulence dissipation rate (median 0.03 vs. 1.76±0.37 m2/S3), turbulence Reynolds number (median 0.08 vs. 0.33±0.15), WSS (median 1.86 vs. 7.45±2.70 Pa), and strain rate (median 1,919.79 vs. 7,677.92±1,966.70) were significantly (P<0.0001) decreased on the aneurysm dome compared with those on the bifurcation apex wall after aneurysm removal. Two peaks of hemodynamic parameters appeared when flow moved towards the anterior cerebral artery (ACA) and middle cerebral artery (MCA) branches. On the line across the aneurysm dome, the hemodynamic parameters remained very low except for the aneurysm part with strong hemodynamic parameters. At peak 1, the dynamic and total pressure, vorticity, WSS, strain rate, and cell Reynolds number were all significantly (P<0.0001) greater than those on line 3 at direct flow impinging center (DFIC) or line 1 on the smaller ACA, whereas all the turbulence parameters were significantly (P<0.0001) greater than those on line 1 but smaller than those on line 3. At peak 2, all hemodynamic parameters were significantly (P<0.0001) greater than those at line 3 at the DFIC or on line 5 on the larger MCA. ICA bifurcation aneurysm formation is closely associated with significantly decreased hemodynamic stresses, and aneurysm formation occurs to decrease the abnormally-enhanced hemodynamic parameters on the bifurcation apex caused by direct flow impingement.