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

Abstract

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 outf low 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 hyperplagia risk factors and venous

Delayed Spontaneous Thrombosis of Neglected Direct Carotid-Cavernous Fistula: A Case Report

“…The exact cause of spontaneous thrombosis of the fistula is difficult to elucidate; however, a chronic high flow state can induce venous intimal hyperplasia and subsequently lead to venous stenosis and thrombosis. 11 Such a phenomenon might have been the cause of spontaneous thrombosis of venous outflow in our case. Besides, the nature of intermediate flow of the fistula might have been a contributing factor.…”

“…The baseline MRI had revealed direct CCF with significant ballooning of a right-sided CS secondary to long-standing high flow fistula. The exact cause of spontaneous thrombosis of the fistula is difficult to elucidate; however, a chronic high flow state can induce venous intimal hyperplasia and subsequently lead to venous stenosis and thrombosis [ 11 ]. Such a phenomenon might have been the cause of spontaneous thrombosis of venous outflow in our case.…”

State of the Art in the Role of Endovascular Embolization in the Management of Brain Arteriovenous Malformations—A Systematic Review

“…For this reason, the overexpression of HIF-1alpha in human bAVMS led researchers to suggest the potential role of a hypoxic incident in the pathogenesis of bAVMs [ 29 ]. Likewise, intracranial venous hypertension has been hypothesized as a causative agent of bAVMS because it also induces the expression of HIF-1 and therefore stimulates the expression of VEGF [ 4 , 9 , 30 ]. Molecular and histological examinations of human bAVM specimens demonstrated inflammatory cell infiltrations, increased levels of angiogenic factors, and inflammatory cells [ 4 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 ].…”

Angioarchitectural features amongst patients with unruptured brain arteriovenous malformations presenting with headache: findings from a single center retrospective review of 76 patients

“…Despite AVM-induced venous stenosis being associated with an increased risk of intracerebral hemorrhage in several studies, the best prospective longitudinal studies on AVM natural history do not report the incidence of venous stenosis. [ 13 – 16 ] The underreporting is likely explained by the fact that most vascular stenoses are described as a relative value to what the normal or expected caliber of the vessel should be. This is uniquely difficult with venous structures as they are more variable compared to their arterial counterparts thus making the denominator in the equation difficult to determine.…”