Introduction: Histopathological changes in cerebral arteriovenous malformation (AVM) draining veins secondary to chronically high AVM inflow are unknown. We examine the relationship between draining vein wall thickness and AVM flow.
Methods: Records of patients with cerebral AVMs evaluated at our institution between 2007-2013 were retrospectively reviewed. Patients were included if a surgical specimen of the nidus was available and if flows were obtained before treatment using quantitative magnetic resonance angiography. Specimens were mounted on slides and stained with elastin special stain. Perinidal veins were identified and maximum wall thickness was measured from digitized images (Figure 1). Intranidal arteries were also identified and diameters measured. Total AVM flow was estimated as aggregate flow within primary arterial feeders or flow in single draining veins. Relationship between maximum vein wall thickness, total AVM flow, flow per draining vein, flow per unit volume of AVM, and mean intranidal artery diameter was assessed.
Results: 28 patients (20 male, 8 female) with mean age of 37 years (range 16-68 years) were included. Spearman’s correlation revealed a statistically significant relationship between maximum vein wall thickness and total AVM flow (rho=+0.51, P=0.006) (Figure 2) and AVM flow per draining vein (rho=+0.41, P=0.03). However, there was no statistically significant correlation between maximum vein wall thickness and flow per unit volume of AVM (rho=+0.27, P=0.17) or mean intranidal artery diameter (rho=+0.42, P=0.24). Mean vein wall thickness was significantly higher in presence of venous ectasia (562 µm vs. 300 µm, P=0.007). Presence of venous stenosis was not significantly associated with age, Spetzler-Martin grade, volume, number of draining veins, deep venous drainage, intranidal fistula, or maximum vein wall thickness.
Conclusions: Maximum vein wall thickness is significantly related to total AVM flow and AVM flow per draining vein. This finding implicates chronically high AVM inflow in venous intimal hyperplasia and possible subsequent development of venous outflow stenosis.
Patient Care: A better understanding of the pathophysiology of venous intimal hyperplasia as well as the impact of chronically high AVM inflow on the development of venous outflow stenosis can improve our management of patients with AVMs and lead to treatments to circumvent stenosis formation and to mitigate hemorrhage risk.
Learning Objectives: By the conclusion of this session, participants should be able to:
1) Describe the relationship between draining vein wall thickness and AVM flow.
2) Understand the pathophysiology of venous intimal hyperplasia.
3) Discuss the impact of chronically high AVM inflow on the development of venous outflow stenosis.