Introduction and purpose Current methods to risk stratify patients with unruptured cerebral aneurysms are based on limited natural history data. Circle of Willis variations are thought to contribute to aneurysm development via hemodynamic changes, including increased blood flow. The impact of circle of Willis anomalies on risk of aneurysm rupture is not known. We hypothesized that a circle of Willis anomaly is more commonly seen in ruptured cerebral aneurysms. Our aim was to compare the frequency of circle of Willis anomalies that contribute to increased flow between ruptured and unruptured cerebral aneurysms.
Methods Over a 2 year period, we identified all patients with an ICD-9 diagnosis code for subarachnoid hemorrhage or non-ruptured cerebral aneurysm admitted to a single urban tertiary care institution. Only patients with anterior communicating artery (ACoA) or posterior communicating artery (PCoA) aneurysms were included in the analysis. Demographic and clinical information was abstracted from patient charts. Catheter cerebral angiograms for all patients were independently reviewed on a picture archiving and communications system (PACS) for aneurysm location and morphology. A submillimeter measurement tool was used on magnified images for measurements of vessel diameter and aneurysm size. Circle of Willis anomalies of the ACoA group were defined as hypoplasia (diameter ≤50% of the dominant A1) or absence of the contralateral A1 segment of the anterior cerebral artery. A circle of Willis anomaly in the PCoA group was defined as the presence of a fetal origin posterior cerebral artery (PCoA diameter greater than the P1 segment of the ipsilateral posterior cerebral artery). χ2 test, Student's t test and multivariate logistic regression analyses were performed to evaluate the association between circle of Willis anomalies and ruptured aneurysms.
Results During 2008 and 2009, of the 587 patients with ruptured and unruptured cerebral aneurysms, 113 had either an ACoA or PCoA aneurysm and were included in the analysis. Mean age was 57.5 years, 83 (73.5%) patients were female and 85 (75.2%) cases were ruptured aneurysms. Hypertension was present in 77 (68.1%) patients and 70 (61.9%) patients were smokers. There were 49 (43.4%) PCoA aneurysms and 64 (56.6%) ACoA aneurysms. Aneurysm shape was non-spherical in 74 (65.5%) cases. Mean aneurysm size was 5.65 mm (SD 3.31) and mean vessel diameter within anomaly groups was 2.31 mm (SD 0.39) and 1.96 mm (SD 0.52) for the dominant A1 and PCoA, respectively. A circle of Willis anomaly was identified in 46 (40.7%) of all patients. Multivariate regression analysis revealed a higher risk of aneurysm rupture when a circle of Willis anomaly was present (p=0.0245, OR 3.72, CI (1.18 to 11.66)).
Conclusions This series suggests that aneurysms associated with a circle of Willis anomaly have an increased risk of rupture compared with aneurysms associated with a normal circle of Willis. Circle of Willis anomalies may increase the risk of aneurysm rupture through hemodynamic changes involving increased flow. Physiologic characterization of blood flow associated with circle of Willis anomalies is warranted. Future studies could establish circle of Willis anomalies as an important determinant in patient selection for preventative aneurysm treatment.
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Competing interests None.
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