Abstract T P90: Characterization of Inflammatory Cells after EDAS Surgery in Patients with Intracranial Arterial Stenosis
Introduction: Indirect revascularization via encephaloduroarteriosynangiosis (EDAS) establishes collateral flow through new vessels formed from external carotid branches in patients with moyamoya disease and intracranial arterial stenosis (IAS) of non-moyamoya origin. A better understanding of the process of neovascularization is key to improve the potential therapeutic effects of these techniques. To gain a more in-depth understanding on the mechanisms behind the pro-angiogenic effects, we performed detailed evaluation of cellular changes in circulating monocytes.
Methods and Results: Dynamics in inflammatory cell were assessed by cell surface marker analysis by flow cytometry of blood from patients at 24, 48 and 72 hours and compared to baseline control (pre-operative) levels from the same patient. While increase in CD45+ cells was noted at 24hrs in all patients, a particularly impressive elevation in the percentage of CD11b/Gr1 positive cells was found in patients at 48 and 72hrs post-surgery. Although CD11b suggested a monocytic population, these cells were F480 low/negative indicating a shift in the differentiation of monocytes or exit of a different population of inflammatory cells from the bone marrow.
Conclusions: Our findings are in accordance with recent publications suggesting a pro-angiogenic role of macrophages during vascular expansion and repair. The findings are consistent with the concept that CD11b/Gr1 cells might constitute an important subset of monocyte/macrophages poised to mediate vascular repair upon stroke and could represent a clinically valuable tool.
Author Disclosures: N.R. Gonzalez: Research Grant; Significant; AHA 12PILT12760011 . L. Iruela-Arispe: None.
This research has received full or partial funding support from the American Heart Association, Western States - Alaska, Arizona, California, Hawaii, Idaho, Montana, Nevada, Oregon, Utah, Washington.
- © 2014 by American Heart Association, Inc.