Setareh Salehi Omran, MD

Ferro JM, Coutinho JM, Jansen O, Bendszus M, Dentali F, Kobayashi A, van der Veen B, Miede C, Caria J, Huisman H, et al. Dural Arteriovenous Fistulae After Cerebral Venous Thrombosis. Stroke. 2020;51:3344–3347.

Intracranial dural arteriovenous fistulas (dAVF) are abnormal communications between the meningeal arteries and the dural venous sinuses or cerebral veins. dAVFs account for nearly 15% of intracranial vascular lesions and cause variable clinical symptoms depending on the location of the fistula and any associated edema resulting from venous congestion. Several risk factors have been associated with the development of dAVFs, including prior craniotomy, head trauma, thrombophilias, and cerebral venous thrombosis (CVT). Although the exact pathophysiology is unknown, progressive stenosis or occlusion of the dural venous sinuses may contribute to the development of dAVFs. Data is lacking on the frequency of dAVF formation after CVT.

Ferro et al. examined the frequency of dAVF development after CVT as part of a predefined substudy of the clinical trial RE-SPECT CVT. The trial was a prospective, randomized, multicenter, exploratory study of patients with acute CVT that were allocated to dabigatran 150mg twice daily or dose-adjusted warfarin for 24 weeks. All patients underwent MRI imaging at the end of treatment. Ferro et al. reviewed end-of-treatment MRIs (6 months after the acute CVT) for the presence of dAVF. If dAVF was found, the baseline images were evaluated to confirm whether this was a newly detected dAVF. Of the 112 patients included in this analysis, 57 were allocated to dabigatran and 55 to warfarin for treatment of their CVT. The mean age was 45.2 (SD 13.8 years), and more than half the patients were women (55%). The majority of patients had a dural venous sinus thrombosis. Three of the 112 patients had insufficient quality of follow-up imaging, which prevented meaningful evaluation for a dAVF. Among the remaining patients, there were no cases of dAVF 6 months following after CVT. Only one patient had an asymptomatic dAVF on their end-of-treatment imaging, and the dAVF was already present on baseline imaging.

One of the main strengths of this study is the systematic use of follow-up imaging for all of the prospectively enrolled patients, thereby allowing the detection of asymptomatic or minimally symptomatic dAVFs. Yet, these findings should be considered in light of several limitations. Most notably, the temporal relationship between CVT and dAVF development is unknown; the 6-month follow up period may have been too soon for dAVF development. Additionally, follow up surveillance for dAVF was done with MR imaging. Although MR imaging appears to be a reliable screening technique for dAVF, the current gold-standard is catheter angiography.

The study suggests that the frequency at which CVT leads to the development and formation of dAVFs is low. Based on these results, routine catheter angiography for dAVF detection within the first 6 months after CVT is likely to have low diagnostic yield. Future studies with long-term follow up of patients with CVT may help determine the overall frequency of dAVF formation.