Abstract W P78: Gene Expression Comparison of Flow Diversion and Coiling in an Experimental Aneurysm Model
Backgound and Purpose: Mechanisms of both healing and complications, including spontaneous aneurysm rupture, remain unclear following flow diverter treatment. The aim of the current study was to compare the gene expression of various key molecules involved in the healing of aneurysms between aneurysms treated with microcoils and flow diverters.
Methods: Saccular aneurysms were created in rabbits (n=12). Aneurysms were either treated with coils (n=6) or with flow diverters (n=6). Aneurysm tissue was harvested at four weeks following treatment and used for gene expression and zymography experiments. Genes with a fold change of 1.2 or greater were considered up regulated, whereas those with a fold change of 0.8 or less were considered down regulated.
Results: All coil embolized aneurysms were completely occluded at follow up. Two aneurysms were occluded and the remaining four samples were incompletely occluded in the flow diverter treated group. The following genes were expressed at lower levels in the flow diverter group as compared to the coiled aneurysm group: genes encoding proteinases (matrix metalloproteinases -2 and -9), cellular markers (endothelial nitric oxide synthase and smooth muscle actin), and structural proteins (collagens and fibronectin). Genes related to inflammation (tumor necrosis factor-α and monocyte chemoattractant protein -1) were up regulated in flow diverter treated aneurysms compared to coil embolized aneurysms. Notably, the enzymatic activity of active MMP-9 was high in aneurysms treated with flow diverters.
Conclusion: As compared to coiled aneurysms, the molecular milieu surrounding aneurysms treated with flow diverters is characterized by higher levels of activated proteases, elevated expression of genes encoding inflammatory proteins, and diminished expression of genes encoding structural proteins. These data may provide improved understanding of rupture risk and healing following aneurysm treatment, and inform development of therapies aimed at lowering rupture risk and accelerating healing.
Author Disclosures: C. Puffer: None. Y. Ding: None. D. Dai: None. J. Cebral: Research Grant; Significant; NIH. D. Kallmes: Other Research Support; Significant; Sequent Medicals, Covidien Inc, Codman. R. Kadirvel: Research Grant; Significant; NIH.
- © 2015 by American Heart Association, Inc.