Background:Segmental arterial mediolysis (SAM) is an uncommon vascular disease, which manifests as catastrophic intraabdominal hemorrhage caused by rupture of visceral dissecting aneurysms in most cases. The etiology of SAM is still unclear, but SAM may be a vasospastic disorder and the responsible pressor agent is norepinephrine. Recently, abdominal SAM coexisting with intracranial dissecting aneurysms has been reported, but the relationship between intraabdominal and intracranial aneurysms in SAM remains unclear, as no cases of concomitant abdominal SAM and ruptured intracranial saccular aneurysm have been reported.Case Description:A 49-year-old woman underwent emergent clipping for a ruptured saccular aneurysm at the left C1 portion of the internal carotid artery. Intraoperatively, norepinephrine was continuously administered intravenously under general anesthesia. Four days after the subarachnoid hemorrhage (SAH), the patient suddenly developed shock due to massive hematoma in the abdominal cavity. Imaging showed multiple aneurysms involving the splenic artery, gastroduodenal artery, common hepatic artery, and superior mesenteric artery. Coil embolization of the splenic artery was performed immediately to prevent bleeding. Subsequent treatment for cerebral vasospasm following SAH was performed with prevention of hypertension, and the patient recovered with left temporal lobe infarction. The diagnosis was abdominal SAM based on the clinical, imaging, and laboratory findings.Conclusion:Norepinephrine release induced by SAH and/or iatrogenic administration of norepinephrine may have promoted abdominal SAM in this case. Abdominal SAM may occur subsequent to rupture of ordinary saccular aneurysm, and may provoke catastrophic abdominal hemorrhage in the spasm stage after SAH.

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Summary:Background: Restenosis is an important complication after carotid endarterectomy (CEA), occurring in up to 30% of patients undergoing CEA. Sporadic cases of restenosis have been reported. This study aimed to reveal the natural course of restenosis after CEA and its regression after treatment.Methods: Between January 2004 and August 2013, CEA was performed in 176 patients (190 vessels) at our hospital. Only those patients with a follow-up period of ≥6 months were included in this study. The mean postoperative follow-up period was 39.1 months (range, 6-117 months). A shunt was used in all cases, along with a patch and tacking suture in some cases (5% and 70%, respectively). All patients received antiplatelet drug therapy until the day of surgery. Restenosis was defined as >50% stenosis measured by three-dimensional computed tomography angiography or magnetic resonance angiography according to the North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria. Duplex ultrasound was used to record peak systolic velocity (PSV) in the surgically treated carotid artery.A PSV of >150 cm/s was considered to indicate a stenosis of >50%, according to the NASCET criteria.Findings: Restenosis developed in 14 out of 190 vessels (8%) and occlusion in 2 (1.1%). Age was the only risk factor significantly associated with restenosis. Restenosis occurred with a significantly higher incidence in younger patients (p = 0.035). Restenosis occurred within 12 months (mean 5.3 months) in all cases. Stenosis progressed 24 months after CEA in some cases, but progression of stenosis >24 months was noted in any case. Of the 14 cases of restenosis, carotid stenting was performed in 4 cases (29%), and medications were prescribed in the remaining 10 cases (71%). In 5 cases (36%), regression was noted after a postoperative period of 30 months. The factors for regression are uncertain; however, the rate of regression increased with time.