Objective: This is a case report of delayed distal coil migration after coil embolization of the ruptured cerebral aneurysm. Case presentation: A 68-year-old man became unconscious suddenly and was transferred to our hospital. Glasgow Coma Scale (GCS) score was E1V1M5. Head CT revealed subarachnoid hemorrhage (SAH). Digital subtraction angiography (DSA) revealed an anterior communicating artery (Acom) aneurysm. Endovascular coiling of the Acom aneurysm was performed to prevent re-bleeding. under general anesthesia. Acute cardiac infarction developed on day 16, and the patient was treated in the cardiovascular department. Follow-up CT on day 38 revealed a high-density sign at the distal part of the anterior cerebral artery. No further treatment was performed since the patient was asymptomatic. Conclusions: Delayed distal coil migration may occur after coil embolization of cerebral aneurysm. X-ray examinations (CT and craniogram) were helpful for diagnosis of delayed distal coil migration after endovascular treatment of cerebral aneurysm.

Objective: To evaluate risk in relation to plaque characteristics for estimating thromboembolic events during carotid artery stenting (CAS). Methods: MR imaging of 64 carotid artery stenotic lesions were reviewed retrospectively in patients for CAS with a balloon protection device (Guardwire) and filter (Angioguard XP). Magnetization-prepared rapid acquisition with gradient echo (MPRAGE) was used for MR plaque imaging. Lesions were classified into three types according to the intensities on MPRAGE: high-intensity, intermediate-intensity and isointensity groups. If the plaque displayed signal intensity of 200% compared to sternocleidomastoid muscle intensity, it was categorized as "high signal intensity." Results: Periprocedural adverse events occurred in 10 of 64 procedures (15.6%). Persistent neurological deficit was related to 3 procedures (5.1%). Transient neurological ischemic events occurred in 4 procedures (6.3%). Thromboembolic events of CAS for high-and intermediateintensity plaques on MPRAGE were 21.1% and 16.7%, respectively. Incidence of thromboembolic events for high-intensity plaques (21.1%) was significantly higher than that for iso-intensity plaque (0%) (P=0.013). Incidence of thromboembolic events for high-intensity plaques with use of a filter device (21.1%) was significantly higher than that with a balloon protection device (7%) (P=0.013). Although incidence of neurological ischemic event in CAS with a filter device (26.7%) was significantly higher than that with a balloon protection device (6.1%) (P=0.026), the morbidity rate was not significantly different between the two groups (0% vs 6.1%). Conclusions: High-intensity plaque on MPRAGE is related to a high rate of thromboembolic events during CAS. To avoid thromboembolic complications during CAS, an individual approach is needed for each case.

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