Objective Aneurysm wall enhancement (AWE) is a potential biomarker of inflammation within the aneurysm wall that has been correlated with a higher risk of rupture. Aspirin (ASA) may decrease AWE due to its anti-inflammatory properties. We aimed to assess the effect of ASA on AWE in an animal model and a cohort of patients with unruptured intracranial aneurysms (UIAs). Methods Three rabbits with elastase-induced aneurysms were exposed to ASA for 8 weeks and three rabbits were used as controls. 3 T high-resolution magnetic resonance imaging (HR-MRI) was performed at 7 days and 8 weeks to evaluate changes in AWE through histological and immunohistological analyses. Additionally, we evaluated AWE in patients who underwent imaging with a 3 T HR-MRI protocol. ASA exposure was defined as daily intake of 81 mg for at least six months prior to HR-MRI. AWE was quantified using three-dimensional AWE maps and histograms. Results Among rabbits exposed to ASA, the mean AWE was lower at 8 weeks compared to the controls (2.11 vs 2.15, p = 0.13). Immunostaining of the aneurysm wall in rabbits that received ASA revealed a reduced expression of CD68 + or cyclooxygenase-2 + cells, compared to the controls. A total of 99 patients with 120 UIAs were included in the HR-MRI analysis of UIAs. UIAs exposed to ASA (22/120) had significantly lower median AWE than those that were not exposed (0.60 vs 0.72, p = 0.032). Conclusion ASA therapy is associated with an objective reduction in AWE, suggesting a potential role in lowering the risk of aneurysm rupture.
Aspirin Effect on Aneurysm Wall Enhancement: Clinical Study and Animal-model Validation Study (S34.005)
Background: Anecdotal cases of rapidly progressing dementia in patients with dural arteriovenous fistulas (dAVFs) and cortical venous drainage have been reported in small series. However, a comprehensive description of the angiographic features of this dAVFs is lacking. We conducted an analysis of the largest cohort of dAVFs presenting with cognitive impairment (dAVFs-CI), aiming to provide a better characterization of this subset of dAVFs. Methods: The CONDOR Consortium, a multicenter repository comprising 1077 dAVFs, served as the study population. Among the dAVFs, patients with dAVFs-CI were analyzed. A propensity scores matching analysis was conducted to compare dAVFs-CI with Borden type II and type III dAVFs without cognitive impairment (controls). Logistic regression was employed to identify angiographic characteristics specific to dAVFs-CI. Post-treatment outcomes were analyzed. Results: A total of 60 patients with dAVFs-CI and 60 control dAVFs were included. Outflow obstruction leading to venous hypertension was observed in all dAVFs-CI. Sinus stenosis was significantly associated with dAVFs-CI (OR 2.85, 95% CI: 1.16-7.55, p = 0.027). dAVFs-CI were more likely to have a higher number of arterial feeders (OR 1.56, 95% CI 1.22-2.05, p < 0.001) and draining veins (OR 2.05, 95% CI 1.05-4.46, p = 0.004). Venous ectasia increased the risk of dAVFs-CI (OR 2.38, 95% CI 1.13-5.11, p = 0.024). A trend toward achieving asymptomatic status at follow-up was observed in patients with successful closure of dAVFs (OR 2.86, 95% CI 0.85-9.56, p = 0.09). Discussion: Venous hypertension is a key angiographic feature dAVFs-CI. dAVFs-CI exhibit a complex angioarchitecture characterized by an increased number of arteriovenous connections and stenosed sinuses. The presence of venous ectasia further exacerbates the impaired drainage and contributes to the development of dAVFs-CI. Notably, closure of the dAVF has the potential to reverse symptoms in certain cases (Figure).