Article
Determinants for the size of ruptured intracranial aneurysms – A retrospective cohort analysis
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Authors
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Amr Abdulazim
- Neurochirurgische Klinik, Universitätsklinikum Düsseldorf, Düsseldorf, Deutschland
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Kerim Beseoglu
- Neurochirurgische Klinik, Universitätsklinikum Düsseldorf, Düsseldorf, Deutschland
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Hans-Jakob Steiger
- Neurochirurgische Klinik, Universitätsklinikum Düsseldorf, Düsseldorf, Deutschland
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Daniel Hänggi
- Neurochirurgische Klinik, Universitätsklinikum Düsseldorf, Düsseldorf, Deutschland
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Nima Etminan
- Neurochirurgische Klinik, Universitätsklinikum Düsseldorf, Düsseldorf, Deutschland
| Published: | June 2, 2015 |
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Outline
Text
Objective: We previously reported a detrimental effect of cardiovascular risk factors (smoking or hypertension) on the size of ruptured intracranial aneurysms. However, it remains unclear whether the actual parent vessel diameter at the aneurysm neck is an additional determinant for the aneurysm size at the time of rupture.
Method: We performed a retrospective analysis based on the following inclusion criteria: 1) aneurysmal subarachnoid hemorrhage (aSAH) 2) accurate 3-dimensional (3D) catheter or CT-angiography. The maximum aneurysm diameters, neck size, as well as the exact parent vessel calibres before and after the aneurysm neck (V1 and V2, respectively) were measured. Additionaly, aspect and size ratio were calculated and dichotomized (smooth or irregular/daughter-sack-like protrusion) aneurysm lobulation was assessed based on 3-dimensional reconstruction images. Correlation analysis was performed using SPSS.
Results: 467 patients were included in the present study. Mean aneurysm size was 6.100 ± 3.541 mm (mean ± SD). The majority of aneurysms were localized on the anterior communicating artery (AcomA: 41.1%), middle cerebral artery (MCA: 17.6%), posterior communicating artery (PcomA: 16.3%), and basilar artery (BA: 9.6%). There was a significant correlation between mean parent vessel diameter and maximum aneurysm diameter (r= 0,270; p<0.0001). 228 aneurysms (48.1%) showed multilobarity. There was no significant difference between the aneurysm size of lobulated (6.038 ± 3.374 mm) and non-lobulated (6.160 ± 3.699 mm) ruptured aneurysms (p<0.711).
Conclusions: The data in the present analysis, derived from a large clinical cohort underline the increasing assumption that the actual parent artery diameter at the origin of an aneurysm is a main determinant for its size at the time of rupture. Interestingly, at least for ruptured aneurysms the parent vessel diameter seems to be a stronger determinant than aneurysm lobulation. These finding support the increasing concept that the aneurysm diameter is only one of many determinants for natural history of intracranial aneurysms.
