RESUMO
BACKGROUND: Acute early carotid stent thrombosis (AcuteCST) is a rare complication after carotid artery stenting (CAS). The purpose of this retrospective study was to investigate the incidence, causes, and optimal management of AcuteCST. METHODS: Medical records of all patients undergoing CAS between 2008 and 2016 were retrospectively reviewed. The time of thrombosis, grade of stenosis, lesion side, preprocedural and postprocedural anticoagulants, causes, symptoms, treatment, recanalization, and outcome were reviewed. RESULTS: Overall, 674 patients were treated with CAS. Four cases of AcuteCST were identified (0.59%). In the first patient, the stent thrombosis was attributed to dissection caused by filter deployment within a distal internal carotid artery with 360° coiling. Notably, in 3 of the 4 cases of thrombosis a second overlapping stent had been deployed. In total, 41 patients of the cohort under investigation underwent overlapping stent deployment. The use of a second overlapping stent as a bail-out procedure due to dissection or malposition or due to long lesions was correlated with increased rate of thrombosis (3/41 [7.3%] vs. 1/633 [0.002%]). In 2 patients, carotid stents were thrombosed within 2 hr of the procedure. Endovascular thrombus aspiration and subsequent eversion carotid endarterectomy with stent explantation in the first patient and intrathrombus urokinase administration with thromboaspiration and additional stent placement in the second patient were followed. In the other 2 patients having their carotid stents thrombosed 3 and 4 days after the procedure, treatment with low weight molecular heparin and antiplatelet regimens was followed. CONCLUSIONS: The use of overlapping stents in the carotid artery is a predisposing factor for AcuteCST. Prognostic factors of this potentially devastating complication are the initial clinical presentation expressing the grade of ischemic brain damage, the accurate and timely recognition of the thrombosis, and the prompt restoration of oxygenated blood flow into the viable tissue at risk of infarction.