Introduction: We aimed to evaluate if prior oral anticoagulation (OAC) and its type determines a greater risk of symptomatic hemorrhagic transformation in patients with acute ischemic stroke (AIS) subjected to mechanical thrombectomy.Materials and Methods: Consecutive patients with AIS included in the prospective reperfusion registry NORDICTUS, a network of tertiary stroke centers in Northern Spain, from January 2017 to December 2019 were included. Prior use of oral anticoagulants, baseline variables, and international normalized ratio (INR) on admission were recorded. Symptomatic intracranial hemorrhage (sICH) was the primary outcome measure. Secondary outcome was the relation between INR and sICH, and we evaluated mortality and functional outcome at 3 months by modified Rankin scale. We compared patients with and without previous OAC and also considered the type of oral anticoagulants.Results: About 1.455 AIS patients were included, of whom 274 (19%) were on OAC, 193 (70%) on vitamin K antagonists (VKA), and 81 (30%) on direct oral anticoagulants (DOACs). Anticoagulated patients were older and had more comorbidities. Eighty-one (5.6%) developed sICH, which was more frequent in the VKA group, but not in DOAC group. OAC with VKA emerged as a predictor of sICH in a multivariate regression model (OR, 1.89 [95% CI, 1.01–3.51], p = 0.04) and was not related to INR level on admission. Prior VKA use was not associated with worse outcome in the multivariate regression model nor with mortality at 3 months.Conclusions: OAC with VKA, but not with DOACs, was an independent predictor of sICH after mechanical thrombectomy. This excess risk was associated neither with INR value by the time thrombectomy was performed, nor with a worse functional outcome or mortality at 3 months.

A 75-year-old woman was admitted to our neurology department with acute confusional syndrome. The patient was fully independent until the day before admission when she was cooking and suddenly fell to the ground. Past medical history was unremarkable and did not reveal previous symptoms of giant cell arteritis. MRI ( figure, A) showed multiple bilateral infarcts of posterior territory including both thalami. Thickening and pulse absence in both temporal arteries were observed. Giant cell arteritis was suspected (sedimentation rate 98 mm/h). Doppler study revealed the halo sign (smooth hypoechogenic mural thickening) in both vertebral arteries (figure, C) and right occipital artery (figure, B). Transcranial study detected microembolic signals in both vertebral arteries ( figure, D). The diagnosis of giant cell arteritis was confirmed by biopsy and steroid treatment was initiated. We believe that acute confusional syndrome in this patient was derived from the embolic process.1 A second Doppler study performed 10 days later showed no changes. The patient died of pneumonia on day 15.Ultrasonography is a usual test for giant cell arteritis diagnosis. The recognition of halo sign and microembolic detection in intracranial arteries allow prompt diagnosis and treatment.

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