Contribution of the Hemodynamics of A1 Dysplasia or Hypoplasia to Anterior Communicating Artery Aneurysms

Abstract

To explore the association between the hemodynamics and formation, growth, and rupture of aneurysms in anterior communicating arteries (ACoA) with A1 dysplasia or hypoplasia. A series of 3-dimensional numerical simulation models of the anterior communicating artery complex (ACoAC) were designed geometrically. The diameter of A1 was fixed on one side and decreased gradually on the other side. Three groups of ACoA aneurysm model growth were constructed with different positions to the dominant bifurcation. Blood flow was modeled as an incompressible Newtonian fluid described by the unsteady Navier-Stokes equations. Vessel walls were assumed to be rigid; no slip boundary conditions were applied at the walls. Wall shear stress (WSS), flow velocity, and pressure were influenced by the dynamic variations of A1 diameter. When the diameter of the nondominant A1 gradually decreased, WSS and flow velocity dynamically increased in the dominant bifurcation and pressure decreased. Wall shear stress differences were significant between the dominant and nondominant bifurcations (t = 6.543; P < 0.05). With aneurysm growth, WSS and flow velocity gradually decreased, and turbulence appeared. Wall shear stress was lower at the bifurcation than that 0.02 mm and 0.1 mm to the bifurcation, whereas flow velocity and turbulent flow were more obvious. A1 dysplasia/hypoplasia is a potential risk factor in the formation of ACoA aneurysms. Wall shear stress increase may contribute to aneurysm formation. Wall shear stress decrease and turbulent flow may be responsible for the growth and rupture of ACoA aneurysms. The hemodynamic mechanism in the growth and rupture of aneurysms in different locations might be different.