467. Magnetic Resonance Vessel Wall Imaging in Human Intracranial Aneurysms: A Histological Analysis
Features NREF-funded Author
Authors: Joseph Scott Hudson; Mario Zanaty, MD; Daichi Nakagawa, MD; David Kung, MD; Pascal Jabbour, MD; Edgar Samaniego, MD, MS; David Hasan, MD (Iowa City, IA)
Introduction: The clinical significance of magnetic resonance vessel wall enhancement in intracranial aneurysms (IA) remains ill defined. In this report, we describe the histological analysis of resected human IAs which underwent MR-VWI. Methods: Consecutive IA patients undergoing microsurgical clipping were included. Patients received a 3T MRI T1 black blood sequence (Siemens Stryka, Munich, Germany) scan preoperatively. Three independent neuroradiologists reviewed the films. IAs were classified into an avidly enhancing category or no/mild enhancement category. IA wall tissue was harvested during microsurgical clipping. Tissue was fixed in paraffin and stained with hematoxylin/eosin and elastochrome for histological analysis. Immunohistochemical quantification of infiltrating macrophages was performed as previously described by Hasan et al. (2012, Stroke ). Results: 5 patients were classified as Avidly Enhancing (AE), whereas 5 patients were classified as “No or Mild Enhancement” (NME). Measurement of wall thickness from the operatively resected IA tissue revealed AE IA tissue had a higher average thickness than NME IA tissue (412.0 ± 78.6 µm vs 218.0 ± 67.6 µm. P =0.003).Semi-quantitative analysis for IA wall macrophage infiltration revealed a higher average level of infiltration within the resected AE IA tissue when compared with NME IA tissue (2.6 ± 0.5 vs 1.4 ± 0.5. P =0.048). Microscopic inspection of the histologically prepared IA tissue revealed NME IA tissue to be relatively hypocellular, whereas AE IA tissue was hypercellular. Both groups of resected IA tissue were deficient in elastin. Intra-operatively, AE IAs were thick and yellow walled while NME IAs were thin walled and transparent. Conclusion: Prior studies have associated macrophage infiltration and inflammatory degeneration with aneurysm rupture, yet it remains unclear whether thick enhancing (inflamed) walls or thin (acellular) walls are more prone to rupture. Future studies should prospectively investigate whether the presence or absence of IA-wall enhancement is associated with an increased risk of IA rupture.