Abstract Details

Unruptured intracranial aneurysm (UIAs) affect approximately 3-5% of the global population. AWE is a potential biomarker that is associated with aneurysm instability and higher risk of rupture. AWE is increased in regions of the aneurysm wall where inflammatory cells are more prevalent. Aspirin may decrease AWE due to its anti-inflammatory properties.

To assess the effect of aspirin on aneurysm wall enhancement (AWE) in humans and an animal model.

Patients with IAs were analyzed for the use of aspirin, which was defined as a daily intake for at least 5 months. AWE was quantified objectively using metrics that characterize the distribution of signal intensity: 3D-AWE, focal AWE (FAWE) and specific (SAWE). These metrics, along with morphological aneurysm measurements, were analyzed for their association with aspirin consumption. A rabbit-based animal model was used to study the effects of aspirin. Aneurysms were induced with elastase as has been previously described. Four animals received aspirin for 8 weeks and were compared with 4 sham animals. Each rabbit underwent histological and high-resolution imaging to determine the presence of enhancement and inflammatory cells.

UIAs of patients who were exposed to aspirin had lower AWE= 3D-AWE (median=0.55, IQR=0.27) and FAWE (median=1.02, IQR=0.66) compared to non-exposed patients (median=0.72, IQR=0.28, p=0.027; and median=1.30, IQR=0.47, p=0.030, respectively). Among rabbits exposed to aspirin, the mean AWE was lower at 8 weeks compared to the controls (2.11 ± 0.15 vs 2.15 ± 0.37). Immunostaining of the aneurysm wall in rabbits that received aspirin revealed an absence of CD68+ or COX-2+ cells.

Aspirin therapy is associated with an objective reduction in AWE, suggesting a potential role in lowering the risk of aneurysm rupture.