Background and Purpose—The role of abnormal angiogenesis in the formation and progression of cerebral arteriovenous malformations (AVMs) is unclear. Previous studies have demonstrated increased local expression of vascular endothelial growth factor (VEGF) in AVM tissue and increased circulating levels of VEGF in AVM patients. We sought to further investigate the role of VEGF in AVM pathophysiology by examining changes in plasma VEGF levels in patients undergoing treatment for AVMs.

Methods—Three serial blood samples were obtained from 13 AVM patients undergoing treatment: (1) before any treatment, (2) 24 hours postresection, and (3) 30 days postresection. Plasma VEGF concentrations were measured via commercially available enzyme-linked immunosorbent assay (ELISA). For controls, blood samples were obtained from 29 lumbar laminectomy patients.

Results—The mean plasma VEGF level in AVM patients at baseline was 36.08±13.02 pg/mL, significantly lower than that of the control group (80.52±14.02 pg/mL, P=0.028). Twenty-four hours postresection, plasma VEGF levels dropped to 20.09±4.54 pg/mL, then increased to 66.81±26.45 pg/mL 30 days later (P=0.048). The mean plasma VEGF concentration 30 days after resection was no longer significantly different from the control group (P=0.33).

Conclusions—Plasma VEGF levels in 13 AVM patients were unexpectedly lower than controls, dropped early after AVM resection, then significantly increased 30 days later. These results support the key role of abnormal angiogenesis in AVM pathophysiology and suggest that a disruption in systemic VEGF expression may contribute to the natural history of these lesions.