SUMMARY: In animal models, treatment with
aspirin and genetic inactivation of COX-2 decreases
aneurysm formation and
rupture. Selective inhibition of COX-1 did not decrease
aneurysm rupture, suggesting that selection inhibition of COX-2 may be critical in thwarting
aneurysm progression. Walls of ruptured human
intracranial aneurysms have higher levels of COX-2 and microsomal
prostaglandin E2 synthase 1 (mPGES-1), both of which are known to be inhibited by
aspirin. In a pilot study, patients undergoing microsurgical clipping had attenuated expression of COX-2, mPGES-1, and macrophages in
aneurysm walls after 3 months of
aspirin therapy versus those that did not receive
aspirin. Additionally, in patients undergoing endovascular
therapy, local circulating expression of
chemokines and COX-2 were increased in blood samples taken from within
aneurysm domes as compared to peripheral blood sample controls. Treatment with
aspirin also resulted in decreased expression of COX-2 within leukocytes within
aneurysms as compared to peripheral blood samples. Novel molecular imaging with
ferumoxytol-enhanced MRI may help in the identification of patients at increased risk for
aneurysm rupture and assessment of a response to
aspirin therapy. Key Messages:
Aspirin has been found to be a safe in patients harboring
cerebral aneurysms and clinical studies provide evidence that it may decrease the overall rate of
rupture. Furthermore,
aspirin is an accessible and inexpensive medicine for patients who may not have access to endovascular or microsurgical treatment or for patients who are deemed low risk of
aneurysm rupture, high risk for intervention, or both. Future clinical trials are indicated to determine the overall effect of
aspirin on
aneurysm progression and
rupture. This review provides an update on the potential mechanisms and benefits of
aspirin in the treatment of
cerebral aneurysms.