Abstract W MP46: Novel In Vivo Assessment of Unruptured Intracranial Aneurysm Inflammatory Factors: Prospective Analysis of Intra-Aneurysmal Serum Inflammatory Markers in a University Hospital
Background: There are known correlations between intracranial aneurysm size as well as underlying demographic risk factors that lead to aneurysm rupture. The treatment of unruptured aneurysms is predicated on this, however selecting which unruptured aneurysms should be treated can be difficult. It is thought that formation, growth and eventual rupture of aneurysms is due to an underlying inflammatory process, which has been shown in pathological studies to exist within aneurysmal walls. The inflammatory milieu within a live aneurysmal sac and its implications for aneurysmal rupture is not currently known.
Objective: To determine the presence of inflammatory markers within unruptured aneurysm sacs.
Methods: We analyzed prospectively collected data from a database of patients who presented for unruptured aneurysm coil embolization over the span of 25 months to a University Hospital. These patients had blood samples withdrawn from the aneurysm sac immediately prior to coil embolization. This blood was sent for testing, with controls provided by blood sampled from the aneurysm parent vessel. Complement C3 and C4 levels from the aneurysm and parent vessel were then compared using column tables with paired t-test analysis.
Results: A total of 8 patients were enrolled. The mean age (± SD) of treated patients was 68 (±15.3) years and 7 (87.5%) were women. 5 aneurysms (62.5%) were in the anterior circulation. Aneurysm size ranged from 5mm to 14mm, mean size 8.9mm (± 3.1mm). 5 patients (62.5%) were white while 7 patients (87.5%) had history of hypertension. C3 and C4 analysis showed a consistent decrease of complement values within the aneurysm as compared to the parent vessel. (For C3, mean of differences [MD] was 9.375, 95% confidence interval [CI] 5.56-13.19. For C4, MD was 1.500, 95% CI 0.50-2.50.)
Conclusion: There is an observed decrease in complement values within unruptured aneurysms, suggestive of ongoing classic complement pathway activation. This supports the aneurysm inflammation model, which shows complement deposition in aneurysm walls. Our data suggests that this process is ongoing in live unruptured aneurysms and could be possibly targeted in future aneurysm trials. Further investigation is needed.
Author Disclosures: S.M. Cordina: None. W. Gerthoffer: None. A. Martino: None. R. Wilson: None. D.K. Naritoku: None.
- © 2015 by American Heart Association, Inc.