Association of A1 Segment Morphology with the Rupture Risk and Morphology of Anterior Communicating Artery Aneurysms:...

Background/Objectives: A1 segment asymmetry, including hypoplasia and aplasia, is a well-recognized anatomical variation associated with altered hemodynamic stress and anterior communicating artery (ACoA) aneurysm formation. However, its influence on subsequent aneurysm rupture risk remains controversial. This study aimed to evaluate the relationship between A1 segment morphology and aneurysm rupture risk, as well as its association with aneurysm size and morphological complexity. Methods: A retrospective single-institution analysis was conducted on 211 patients treated for ACoA aneurysms between June 2016 and March 2025. A1 segment morphology was assessed using digital subtraction angiography and categorized as symmetric, hypoplastic (diameter < 1 mm or <50% of the contralateral vessel), or aplastic. Demographic, clinical, and radiological variables were recorded. Statistical analyses included univariate comparisons with Bonferroni correction for multiple testing and multivariable logistic regression to identify independent predictors of aneurysm rupture. Results: The study population had a mean age of 54.72 ± 10.97 years, with a male-to-female ratio of 1.24:1 (55.5% male, 44.5% female). Symmetric A1 segments were observed in 49.3% of patients, hypoplastic segments in 31.3%, and aplastic segments in 19.4%. No statistically significant association was identified between A1 morphology and aneurysm rupture rates (p = 0.251) or mean aneurysm diameter (p = 0.996). Univariate analysis demonstrated that younger age (p = 0.006), male sex (p = 0.016), and smoking (p = 0.033) were associated with rupture. However, none of these factors, including A1 morphology, remained independent predictors of rupture in the multivariable logistic regression model. Conclusions: Although A1 segment asymmetry is common in patients with ACoA aneurysms, it does not independently influence rupture risk or aneurysm morphology. Our findings suggest that rupture behavior is driven primarily by dynamic hemodynamic factors rather than static anatomical variations.