ARUP; ISBN: 978-0-9562121-5-3 - CMBBE 2012 - Cardiff University

4. RESULTS AND DISCUSSION
In order to describe the developing flow patterns within the cerebral aneurysms, an
exemplary presentation of streamlines (t = 0.9 s), seeded at the domain inlet, is shown
for both cases in Figure 3. They resemble in the fact that the flow enters the aneurysm at
its bottom and remains close to the aneurysmal wall until it divides and exits sideward
back to the arterial branches. It is conspicuous that due to the geometric situation a
helical flow pattern develops before the blood leaves the dilatations. This results in nonparabolic
velocity profiles and a twisted flow in the outflow vessels. With respect to the
velocity magnitude only small values compared to the arterial main stream could be
identified in the ROI. Nevertheless, an oscillating motion of the blood was observed in
these certain areas. This oscillation may rub against the endothelial layer and might
increase the risk of rupture.
Regarding the analyses of the time-averaged pressure distribution (see Figure 3-right),
the inlet pressure was set to 120 mmHg. The highest pressure drop can be observed
close to the bifurcation when the blood enters the outflow vessels. While case 1 shows
no increased pressure values at the dome of the aneurysm, in the ROI of case 2 slightly
elevated pressures appear in comparison to the rest of the aneurysm.
Fig. 3: Streamlines at t = 0.9 s (left) and averaged pressure (right) for both cases
For analyses of the wall shear stresses with respect to the physical time, temporal
averaging was carried out and illustrated in figure 4. Highest values mainly occur at the
neck of the aneurysm and distal to the bifurcation, respectively. On the aneurysms wall
itself and especially within the ROI only medial values are diagnosed. Comparing both
cases, the AWSS distribution of the second aneurysm appears significantly smoother due
a wider geometry, where a flow with less vorticity can evolve. The absence of high
shear regions in the ROIs indicates that elevated wall shear stresses are not primary
responsible for aneurysmal rupture.
Fig. 4: Time-averaged wall shear stresses of case 1 (left) and case 2 (right)