RESUMEN
Iatrogenic dissection (ID) is a well-known complication of neuroendovascular treatments. ID is predominantly attribute to endothelial injury by the manipulation of wires and/or catheters, and is generally detected in angiography during the procedure. We present a rare case with delayed ID due to deployment of a carotid stent. A 71-year-old man presented with transient motor weakness in the right extremity. Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) showed previous multiple cerebral infarctions without a diffusion sign, stenosis with vulnerable plaque in the left common carotid artery (CCA), and an extremely flexed internal carotid artery (ICA). On dual antiplatelet medication, carotid artery stenting (CAS) was completed with favorable dilation of the carotid lumen. Computed tomography angiography 4 days after the procedure revealed high-grade stenosis at the ICA adjacent to the distal edge of the deployed stent. ID with intramural hematoma was diagnosed on MRI. The ID was conservatively treated and remarkably diminished 4 months after the procedure. The patient was asymptomatic during the entire clinical course. This delayed ID was considered to be due to an endothelial injury caused by the distal edge and the constant radial force of the open-cell stent against the flexed vessel and exacerbated by dual antiplatelet therapy. Even in a patient with favorable arterial dilation in CAS procedure, the possibility of a delayed ID should always be considered.
RESUMEN
BACKGROUND: This study analyzes the incidence of microembolic infarctions (MIs) in the cerebellum after carotid artery stenting (CAS) to determine the risk factors. METHODS: From 2012 to 2019, 162 CASs in 155 patients were performed at our hospital. Fifty-seven patients (35.7%) showing new MIs on diffusion-weighted imaging after CAS were enrolled. Patients were assigned to either the cerebellar group (n = 14, 8.8%) if their MIs were in the cerebellum and/or cerebrum or the cerebral group (n = 43, 26.9%) if their MIs were only in the cerebrum. Patient characteristics, anatomic features, and clinical data were retrospectively compared between the 2 groups. RESULTS: Advanced age, right-sided carotid stenosis, severe calcification of aortic arch and brachiocephalic trunk, and vertebral artery narrowing with intraprocedural hemodynamic depression (IHD) significantly increased the development of cerebellar MIs. On multivariate analysis, advanced age, right-sided carotid stenosis, and vertebral artery narrowing with IHD were independent predictors of developing new cerebellar MIs. Cerebellar MIs after CAS were not uncommon. CONCLUSIONS: Catheter maneuvering in the aortic arch or the brachiocephalic trunk could be the main cause of thromboemboli in cerebellar MIs. Careful attention should be paid to catheter maneuvering, especially in older patients with right-sided carotid lesions. In addition, cerebellar hypoperfusion caused by vertebral artery narrowing with IHD might reduce washout of debris, a cause of cerebellar MIs.