Impact of Circle of Willis Anatomical Variations on Outcomes in Aneurysmal Subarachnoid Hemorrhage
摘要
Anatomical variations in the Circle of Willis (CoW) may influence hemodynamics and aneurysmal subarachnoid hemorrhage (aSAH) outcomes. We hypothesized that incomplete CoW could alter cerebral blood flow and reduce symptomatic vasospasm risk due to underlying arteriosclerotic changes.
MethodsWe analyzed imaging data from patients with aSAH admitted to an academic center from 2015–2022. Patients were categorized by CoW anatomy into two (complete vs. incomplete) and three groups (complete, partial [missing an anterior or posterior component], and disconnected [missing both an anterior and posterior component]). Primary outcomes included radiologic vasospasm (transcranial Doppler [TCD] criteria) and symptomatic vasospasm. Secondary outcomes included delayed cerebral ischemia and three-month functional outcomes (modified Rankin Scale).
ResultsAmong 286 patients with aSAH (61.5% female; mean age 56.2 ± 13.4 years), 79% had incomplete CoW anatomy and were older than complete CoW patients (57.6 ± standard deviation vs. 50.7 ± standard deviation years, P = 0.003). Univariate analysis revealed lower incidence of symptomatic vasospasm in incomplete CoWs (36% vs. 59%, P = 0.013) without significant differences in TCD-diagnosed vasospasm or functional outcomes. Multivariate analysis confirmed incomplete and disconnected CoWs were associated with lower symptomatic vasospasm risk (odds ratio [OR] 0.43, 95% confidence interval [CI] 0.19–0.93, P = 0.03 and OR 0.27, 95% CI 0.10–0.68, P = 0.007, respectively) with no differences in TCD elevation, delayed cerebral ischemia, or three-month functional outcomes (OR 1.01, 95% CI 0.5–2.0 and OR 0.87, 95% CI 0.37–2.07, respectively).
ConclusionsIncomplete CoW is associated with lower symptomatic vasospasm risk but not with functional outcomes. These findings may reflect physiological arteriosclerotic changes influencing vasospasm risk. Understanding CoW anatomy could assist risk stratification of patients with aSAH, warranting further research into these mechanisms.