Cerebral hyperperfusion syndrome after percutaneous transluminal stenting of the craniocervical arteries

被引:189
作者
Meyers, PM
Higashida, RT
Phatouros, CC
Malek, AM
Lempert, TE
Dowd, CF
Halbach, VV
机构
[1] Univ Calif San Francisco, Med Ctr, Neurovasc Med Grp, Dept Radiol,Neurointervent Sect, San Francisco, CA 94123 USA
[2] Univ Calif San Francisco, Dept Neurosurg, San Francisco, CA 94143 USA
关键词
carotid stent; cerebral revascularization; hyperperfusion syndrome; interventional neuroradiology;
D O I
10.1097/00006123-200008000-00013
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
OBJECTIVE: Cerebral hyperperfusion syndrome is a recognized complication of carotid endarterectomy, with a reported incidence of 0.3 to 1.2%. The incidence of cerebral hyperperfusion after endovascular revascularization procedures of the craniocervical arteries remains unknown. We evaluated the incidence of cerebral hyperperfusion syndrome in our endovascular revascularization series. To our knowledge, there are no previous studies evaluating the incidence of hyperperfusion syndrome after percutaneous transluminal angioplasty/stenting. METHODS: Between March 1996 and February 2000, 140 patients underwent percutaneous transluminal angioplasty/stenting of the craniocervical arteries at our institution. In all patients, selective bilateral arteriography of the carotid and vertebral arteries was performed to document the sites of craniocervical stenosis and collateral blood flow and the results of the endovascular revascularization procedure. We then reviewed all pertinent medical records, arteriographic films, and sectional imaging studies to determine the incidence of cerebral hyperperfusion in this series. RESULTS: Seven patients (5.0%) developed clinical or radiological manifestations of cerebral hyperperfusion. In the target group, percutaneous transluminal stenting achieved a 90 to 100% reduction in stenotic lesions (mean stenosis, 91%) of the carotid (n = 5) and vertebral (n = 2) arteries. All seven patients remained neurologically stable immediately after treatment. There was delayed development of clinical and radiographic findings, suggestive of cerebral hyperperfusion. Six patients showed evidence of ipsilateral hemispheric edema, including two patients who developed intracranial hemorrhage (one parenchymal, one parenchymal and subarachnoid) documented by computed tomographic brain scans. Symptoms resolved within 72 hours in the four patients without hemorrhage. The two patients with hemorrhage recovered during a more protracted period (range, 3 wk to 6 mo). There were no long-term sequelae or deaths during a cumulative follow-up of 84 months (mean follow-up, 12 mo). CONCLUSION: Hyperperfusion syndrome is an uncommon but potentially serious complication of extracranial and intracranial angioplasty and stenting procedures. The clinical manifestations ave similar to hyperperfusion syndrome after carotid endarterectomy; however, the prevalence may be greater in the high-risk cohort commonly referred for endovascular treatment. Our findings suggest that patients undergoing endovascular stenting procedures should be closely monitored for evidence of hyperperfusion, with careful monitoring of blood pressure, heart rate, and anticoagulation. Further research is needed to confirm that cerebral hyperperfusion is the pathogenesis of this condition.
引用
收藏
页码:335 / 343
页数:9
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