Aneurysm presence at the anterior communicating artery bifurcation is associated with caliber tapering of the A1 segment

Abstract

OBJECTIVE Vessel tapering results in blood flow acceleration at downstream bifurcations (firehose nozzle effect), induces hemodynamics predisposing to aneurysm initiation, and has been associated with middle cerebral artery (MCA) aneurysm presence and rupture status. The authors sought to determine if vessel caliber tapering is a generalizable predisposing factor by evaluating upstream A1 segment profiles in association with aneurysm presence in the anterior communicating artery (ACoA) complex, the most prevalent cerebral aneurysm location associated with a high rupture risk. METHODS Three-dimensional rotational angiographic studies were analyzed for 68 patients with ACoA aneurysms, 37 nonaneurysmal contralaterals, and 53 healthy bilateral controls (211 samples total). A1 segments were determined to be dominant, codominant, or nondominant based on flow and size. Equidistant cross-sectional orthogonal cuts were generated along the A1 centerline, and cross-sectional area (CSA) was evaluated proximally and distally, using intensity-invariant edge detection filtering. The relative tapering of the A1 segment was evaluated as the tapering ratio (distal/proximal CSA). Computational fluid dynamics was simulated on ACoA parametric models with and without tapering. RESULTS Aneurysms occurred predominantly on dominant (79%) and codominant (17%) A1 segments. A1 segments leading to unruptured ACoA aneurysms had significantly greater tapering compared to nonaneurysmal contralaterals (0.69 ± 0.13 vs 0.80 ± 0.17, p = 0.001) and healthy controls (0.69 ± 0.13 vs 0.83 ± 0.16, p < 0.001), regardless of dominance labeling. There was no statistically significant difference in tapering values between contralateral A1 and healthy A1 controls (0.80 ± 0.17 vs 0.83 ± 0.16, p = 0.56). Hemodynamically, A1 segment tapering induces high focal pressure, high wall shear stress, and high velocity at the ACoA bifurcation. CONCLUSIONS Aneurysmal, but not contralateral or healthy control, A1 segments demonstrated significant progressive vascular tapering, which is associated with aneurysmogenic hemodynamic conditions at the ACoA complex. Demonstration of the upstream tapering effect in the communicating ACoA segment is consistent with its prior detection in the noncommunicating MCA bifurcation, which together form more than 50% of intracranial aneurysms. The mechanistic characterization of this upstream vascular tapering phenomenon is warranted to understand its clinical relevance and devise potential therapeutic strategies.