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: 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.
Results: An increase in CD45+ cells was noted at 24hrs in all patients, however, 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.
Patient Care: A better understanding of the cellular mechanisms of vessel formation in EDAS revascularization will help guide research towards the development of new ways to facilitate the response to the surgery
Learning Objectives: By the conclusion of this session, participants should be able to: 1) Describe the importance of monocytes in new vessel growth 2) Discuss, in small groups, the implications of elevated CD11b/Gr1 positive cells in post-EDAS patients, and how we can apply this knowledge to improve our understanding of the mechanisms of EDAS revascularization