Introduction
: Vein of Galen Aneurysmal Malformation (VGAM) is an arteriovenous malformation that accounts for 30% of all pediatric vascular malformations. VGAMs undergo significant remodeling of hemodynamic and structural anatomy due to angiogenesis. These changes not only affect the malformation on a molecular and morphological basis, but may also lead to alterations in planned surgical procedures. It is imperative to better understand the dynamic, angiogenic environment of the cerebrovasculature in order to more effectively treat this disease.
Methods
: We present 36 cases of secondary angiogenesis in VGAM. We also present three case reports of angiogenesis secondary to VGAM.
Results
: Pre‐interventional angiogenesis was identified in 16 patients (44.4%) and post‐interventional angiogenesis in 20 patients (55.6%) following a stage of embolization therapy. The cohort of patients with pre‐interventional secondary angiogenesis was significantly older than patients with post‐interventional angiogenesis at initial angiogram (12 months ± 40.1 months vs. 4.0 months ± 5.4 months; p<0.05). Choroidal VGAMs presented with angiogenesis more frequently than Mural VGAMs (4/14 Mural vs 32/42 Choroidal; p<0.01). Angiogenesis was localized to either the left, right, or bilateral thalamus in 2 cases, to the cisternal space surrounding the VOG in 16 cases, and both in 18 cases.
Conclusions
: Upon identification of secondary angiogenesis, our team’s strategy is to embolize the venous component of the fistula. The ideal strategy in our practice is cannulation of the primary feeder of the malformation, as close to the fistula as possible, and injection of highly concentrated n‐BCA glue (70%‐90%) in a transarterial approach. After multiple rounds of embolization, feeders become less dilated and may be difficult to distinguish from angiogenesis. In this pattern, we use low‐concentrate nBCA (40%‐50%) from an identifiable, proximal feeder and occlude the venous component of the fistula. We identified two patterns of secondary angiogenesis: 1) pre‐interventional angiogenesis identified at the initial diagnostic angiogram, 2) de‐novo, post‐interventional angiogenesis during the staged‐embolization treatment‐course. Occasionally, we noted random bursts of angiogenesis. A combination of the hypoxic environment, inflammation, and hemodynamic alterations to the VGAM caused by liquid embolic/coiling may lead to a burst of angiogenesis that subsides after repeated treatment. We hypothesize that the immature sinuses typically associated with VGAM patients, which experience a decrease in blood flow and subsequently narrow after embolization, may contribute to turbulent blood flow. Development of parenchymal and subarachnoid angiogenesis is common during the multi‐session treatment of VGAM. It represents the response to the angiogenic stimuli released from the draining vein. This angiogenesis can be observed to regress spontaneously or mature as we continue to treat the VGAM. It is unnecessary to embolize secondary angiogenesis outright and it is our recommendation to chiefly target primary feeders of the VGAM as close to the venous component as possible.
P.205 Association Between Vein of Galen Aneurysmal Malformation and
Hirayama Disease: A Clue into Pathophysiology?
