Background: A small randomized controlled trial suggested that dabigatran may be as effective as warfarin in the treatment of cerebral venous thrombosis (CVT). We aimed to compare direct oral anticoagulants (DOACs) to warfarin in a real-world CVT cohort. Methods: This multicenter international retrospective study (United States, Europe, New Zealand) included consecutive patients with CVT treated with oral anticoagulation from January 2015 to December 2020. We abstracted demographics and CVT risk factors, hypercoagulable labs, baseline imaging data, and clinical and radiological outcomes from medical records. We used adjusted inverse probability of treatment weighted Cox-regression models to compare recurrent cerebral or systemic venous thrombosis, death, and major hemorrhage in patients treated with warfarin versus DOACs. We performed adjusted inverse probability of treatment weighted logistic regression to compare recanalization rates on follow-up imaging across the 2 treatments groups. Results: Among 1025 CVT patients across 27 centers, 845 patients met our inclusion criteria. Mean age was 44.8 years, 64.7% were women; 33.0% received DOAC only, 51.8% received warfarin only, and 15.1% received both treatments at different times. During a median follow-up of 345 (interquartile range, 140–720) days, there were 5.68 recurrent venous thrombosis, 3.77 major hemorrhages, and 1.84 deaths per 100 patient-years. Among 525 patients who met recanalization analysis inclusion criteria, 36.6% had complete, 48.2% had partial, and 15.2% had no recanalization. When compared with warfarin, DOAC treatment was associated with similar risk of recurrent venous thrombosis (aHR, 0.94 [95% CI, 0.51–1.73]; P =0.84), death (aHR, 0.78 [95% CI, 0.22–2.76]; P =0.70), and rate of partial/complete recanalization (aOR, 0.92 [95% CI, 0.48–1.73]; P =0.79), but a lower risk of major hemorrhage (aHR, 0.35 [95% CI, 0.15–0.82]; P =0.02). Conclusions: In patients with CVT, treatment with DOACs was associated with similar clinical and radiographic outcomes and favorable safety profile when compared with warfarin treatment. Our findings need confirmation by large prospective or randomized studies.

CHS was first described after carotid revascularization but is now also reported in patients with acute ischemic stroke. Proposed criteria involve a combination of new clinical symptoms, radiographic evidence of hyperperfusion, and/or presence of intracerebral hemorrhage occurring within 30 days after the carotid or intracranial vessel manipulation. Strongest risk factors include reduced cerebral vasoreactivity, contralateral stenosis of ≥ 70%, post-procedure hypertension, and recent ipsilateral stroke. Pathophysiology is incompletely understood but is likely due to increase in cerebral blood flow and impaired cerebral autoregulation, particularly in the areas of disrupted blood-brain barrier, as well as baroreceptor dysfunction during carotid surgery. Strict blood pressure control pre-, during, and post-procedure is recommended, depending on the recanalization status of the vessel. However, there is no randomized data regarding the goal blood pressure to prevent cerebral hyperperfusion syndrome. With technical advances, carotid or intracranial vessel manipulation is increasingly common. CHS is a likely under-recognized and serious complication of carotid revascularization and intracranial thrombectomy. Awareness of and surveillance for CHS is important to reduce morbidity and mortality. Future research should focus on validation of proposed diagnostic criteria and determining optimal post-procedure hemodynamic management to prevent CHS.

In a large, heterogeneous multistate cohort, probable misdiagnosis of CVT occurred in 1 of 30 patients but was not associated with the adverse clinical outcomes included in our study.