Abstract W P73: Inside Intramural Thrombus Formation with Inflammatory Reactions Is Relevant to the Rupture of Cerebral Aneurysms
Background and Purpose: Although recent researches on cerebral aneurysms (CAs) have been performed with the hydrodynamic or the molecular biological technique, the mechanisms of rupture are not fully understood. The aim of this study is to assess the mechanism by a comparison between ruptured and un-ruptured CAs with histopathological and electron-microscopic analysis.
Methods: We analyzed 33 CAs (24 ruptured, 9 un-ruptured) collected surgically after neck clipping. As for the ruptured CAs, we operated them within 24 hours from the onset. HE staining, Elastica Masson staining, PTAH staining, and CD68 immunohistochemical staining were performed with paraffin sections. Morphological analysis with Scanning Electron Microscopy (SEM) was performed with 6 CAs (3 ruptured, 3 un-ruptured).
Results: The common histopathological finding in both ruptured and un-ruptured CAs was that the aneurysmal wall consisted mostly of thick collagen layer without normal internal elastic lamina and media. The characteristic histopathological finding in ruptured CAs was inside intramural thrombus formation with infiltration of CD68 positive cells at the rupture point. The common SEM finding in both ruptured and un-ruptured CAs was the denudation of endothelial cells and the exposure of a subendothelial amorphous or a fibrous surface. The characteristic SEM finding in ruptured CAs was the cluster formation of thick fibrin fibers with incorporation of macrophages and platelets.
Conclusions: While the endothelial denudation, the disappearance of internal elastic lamina and media, and the predominance of collagen layer in the aneurysmal wall were common in both ruptured and un-ruptured CAs, inside intramural thrombus formation with inflammatory reactions was characteristic only in ruptured CAs. This result suggests that thrombo-inflammatory reactions in CAs may act as a trigger for ruptures.
Disclosure Block: Y. Shimoda: None. N. Nakayama: None. M. Hokari: None. T. Abumiya: None. H. Shichinohe: None. K. Kazumata: None. K. Houkin: None.
- © 2015 by American Heart Association, Inc.