Cerebral arteriovenous malformation venous stenosis is associated with hemodynamic changes at the draining vein-venous sinus junction.

Cerebral arteriovenous malformations (AVMs) are an uncommon vascular anomaly that carry the risk of rupture and hemorrhage. Several factors have been implicated in the propensity of an AVM to bleed. One such factor is stenosis of AVM draining veins, as impairment of the AVM venous drainage system is associated with increased risk of intracranial hemorrhage. Currently, our understanding of the pathogenesis of AVM venous outflow stenosis is limited, as there is insufficient data on the blood flow patterns and local hemodynamic parameters of these draining veins. The angioarchitecture of AVMs features a nidus lacking a high resistance capillary network. Accordingly, our previous studies on AVM arterial feeders have demonstrated an abnormally high flow volume rate along with low pulsatility and resistance indices on quantitative magnetic resonance angiography. As such, AVM vessels endure high, non-physiologic levels of flow that may partially contribute to ectasia or stenosis depending on whether wall shear stress (WSS) is high or low, respectively. We hypothesize that AVM venous outflow stenosis occurs most commonly near the junction of the draining vein and the dural venous sinus. Increased flow volume rate through the AVM circuit coupled with the variation in compliance and rigidity between the walls of the draining vein and the dural venous sinus likely create turbulence of blood flow. The resulting flow separation, low WSS, and departure from axially aligned, unidirectional flow may create atherogenic conditions that can be implicated in venous intimal hyperplasia and outflow stenosis. We have previously found there to be a significant association between intimal hyperplasia risk factors and venous outflow stenosis. Additionally, we have found a significant association between age and likelihood as well as degree of stenosis, suggesting a progressive disease process. Similar conditions have been demonstrated in the pathophysiology of stenosis of the carotid artery and dialysis arteriovenous fistulas. In both of these conditions, the use of computational fluid dynamics (CFD) has been employed to characterize the local hemodynamic features that contribute to the pathogenesis of intimal hyperplasia and stenosis. We recommend the utilization of CFD to characterize the anatomic and hemodynamic features of AVM venous outflow stenosis. An improved understanding of the possible causative features of venous outflow stenosis may impact how clinicians choose to manage the treatment of patients with AVMs.