BACKGROUND AND PURPOSE: The anterior communicating artery (ACoA) is a site of predilection for intracranial saccular aneurysms causing subarachnoid hemorrhage. ACoA aneurysms are frequently associated with an asymmetrical circle of Willis. In such cases, the ACoA is probably exposed to high hemodynamic stress caused by a considerable shunt flow across the ACoA to the distal segment of the contralateral anterior cerebral artery (ACA). In the present study, the flow pattern and flow-induced shear stress in the ACoA complex that may initiate aneurysmal lesions were studied under steady and pulsatile flow conditions. METHODS: Flow visualization was studied with dye injection and birefringent flow visualization in symmetrical and asymmetrical models of various sizes of ACoA. The distribution of wall shear stress was measured using an electrochemical method based on a diffusion-controlled reaction of ferricyanide ion to ferrocyanide ion at a platinum electrode embedded in the wall of the ACoA model. RESULTS: With equal flow rate (Reynolds number 150 to 600), vortical flow was formed in the mouth of the ACoA, and no cross flow through the ACoA was observed. The wall shear stress on the mid-wall of the ACoA was almost zero. However, as soon as the flow rate became unequal, a cross flow through the ACoA was observed. The stagnation point also appeared at the medial junction of the ACoA and ACA. The wall shear stress increased to a very high level at the wall of the ACoA and around the stagnation point. CONCLUSIONS: Geometric changes from the symmetrical to the asymmetrical ACoA develop higher shear stress on the ACoA than critical values and the stagnation point at the ACoA junction. A combination of these hemodynamic factors is considered to play an important role in initiation of aneurysm.
BACKGROUND AND PURPOSE: The anterior communicating artery (ACoA) is a site of predilection for intracranial saccular aneurysms causing subarachnoid hemorrhage. ACoA aneurysms are frequently associated with an asymmetrical circle of Willis. In such cases, the ACoA is probably exposed to high hemodynamic stress caused by a considerable shunt flow across the ACoA to the distal segment of the contralateral anterior cerebral artery (ACA). In the present study, the flow pattern and flow-induced shear stress in the ACoA complex that may initiate aneurysmal lesions were studied under steady and pulsatile flow conditions. METHODS: Flow visualization was studied with dye injection and birefringent flow visualization in symmetrical and asymmetrical models of various sizes of ACoA. The distribution of wall shear stress was measured using an electrochemical method based on a diffusion-controlled reaction of ferricyanide ion to ferrocyanide ion at a platinum electrode embedded in the wall of the ACoA model. RESULTS: With equal flow rate (Reynolds number 150 to 600), vortical flow was formed in the mouth of the ACoA, and no cross flow through the ACoA was observed. The wall shear stress on the mid-wall of the ACoA was almost zero. However, as soon as the flow rate became unequal, a cross flow through the ACoA was observed. The stagnation point also appeared at the medial junction of the ACoA and ACA. The wall shear stress increased to a very high level at the wall of the ACoA and around the stagnation point. CONCLUSIONS: Geometric changes from the symmetrical to the asymmetrical ACoA develop higher shear stress on the ACoA than critical values and the stagnation point at the ACoA junction. A combination of these hemodynamic factors is considered to play an important role in initiation of aneurysm.