Effect of Age on Cerebral Arteriovenous Malformation Draining Vein Stenosis

Brunozzi, Denise; Ismail, Rahim; Pandey, Dilip K.; Charbel, Fady T.; Alaraj, Ali

doi:10.1016/j.wneu.2018.02.116

Cited by 8 publications

(2 citation statements)

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“…2 That prevalence and degree of outflow stenosis of cerebral AVMs is associated with older age suggests that the stenosis is a progressive disease process. 31 In a 26 year (1990-2016) retrospective chart review, we also demonstrated a statistically significant association between intimal hyperplagia risk factors and AVM venous outflow stenosis. 32 Intimal hyperplagia risk factors included age >50 years, sex, race, hypertension, type 2 diabetes mellitus, hyperlipidemia, coronary artery disease, chronic kidney disease stage III, and cigarette smoking.…”

Section: Hypothesissupporting

confidence: 53%

“…28,29,30 In another recently published study, we demonstrated a statistically significant association between age and the prevalence of AVM venous outflow stenosis. 31 Venous stenosis was present in a significantly higher proportion of patients ≥50 years versus patients <50 years of age (P = 0.03). Additionally, the mean percentage stenosis was significantly higher in patients ≥50 years (32%) versus patients <50 years of age (22%, P = 0.001).…”

Section: Hypothesismentioning

confidence: 93%

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

et al. 2019

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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

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Section: Hypothesissupporting

confidence: 53%