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SAMMPRIS 试验中颅内血管成形术和支架置入后中风的机制。

Mechanisms of stroke after intracranial angioplasty and stenting in the SAMMPRIS trial.

机构信息

Mallinckrodt Institute of Radiology, Department of Neurology, Washington University School of Medicine, St Louis, Missouri, USA.

出版信息

Neurosurgery. 2013 May;72(5):777-95; discussion 795. doi: 10.1227/NEU.0b013e318286fdc8.

DOI:10.1227/NEU.0b013e318286fdc8
PMID:23328689
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3696348/
Abstract

BACKGROUND

Enrollment in the stenting and aggressive medical management for the prevention of stroke in intracranial stenosis (SAMMPRIS) trial was halted owing to higher-than-expected 30-day stroke rates in the stenting arm. Improvement in periprocedural stroke rates from angioplasty and stenting for intracranial atherosclerotic disease (ICAD) requires an understanding of the mechanisms of these events.

OBJECTIVE

To identify the types and mechanisms of periprocedural stroke after angioplasty and stenting for ICAD.

METHODS

Patients who experienced a hemorrhagic or ischemic stroke or a cerebral infarct with temporary signs within 30 days of attempted angioplasty and stenting in SAMMPRIS were identified. Study records, including case report forms, procedure notes, and imaging were reviewed. Strokes were categorized as ischemic or hemorrhagic. Ischemic strokes were categorized as perforator territory, distal embolic, or delayed stent thrombosis. Hemorrhagic strokes were categorized as subarachnoid or intraparenchymal. Causes of hemorrhage (wire perforation, vessel rupture) were recorded.

RESULTS

Three patients had an ischemic stroke after diagnostic angiography. Two of these strokes were unrelated to the procedure. Twenty-one patients had an ischemic stroke (n = 19) or cerebral infarct with temporary signs (n = 2) within 30 days of angioplasty and stenting. Most (n = 15) were perforator territory and many of these occurred after angiographically successful angioplasty and stenting of the basilar artery (n = 8). Six patients experienced a subarachnoid hemorrhage (3 from wire perforation) and 7 had a delayed intraparenchymal hemorrhage.

CONCLUSION

Efforts at reducing complications from angioplasty and stenting for ICAD must focus on reducing the risks of regional perforator infarction, delayed intraparenchymal hemorrhage, and wire perforation.

摘要

背景

由于支架置入组 30 天内卒中发生率高于预期,颅内狭窄(SAMMPRIS)试验的入组被停止。为了降低颅内动脉粥样硬化性疾病(ICAD)血管成形术和支架置入术围手术期卒中发生率,需要了解这些事件的发生机制。

目的

确定血管成形术和支架置入治疗 ICAD 后围手术期卒中的类型和机制。

方法

SAMMPRIS 中,在尝试血管成形术和支架置入后 30 天内发生出血性或缺血性卒中和短暂性脑梗死的患者被识别。研究记录,包括病例报告表、手术记录和影像学资料,都进行了审查。卒中分为缺血性或出血性。缺血性卒中分为穿支血管区、远端栓塞或支架内血栓形成后延迟。出血性卒中分为蛛网膜下腔或脑实质内出血。记录出血原因(导丝穿孔、血管破裂)。

结果

3 例患者在血管造影诊断后发生缺血性卒中,其中 2 例与操作无关。21 例患者在血管成形术和支架置入后 30 天内发生缺血性卒中(n=19)或短暂性脑梗死(n=2)。大多数(n=15)为穿支血管区,其中许多发生在基底动脉血管造影成功的血管成形术和支架置入术后(n=8)。6 例患者发生蛛网膜下腔出血(3 例来自导丝穿孔),7 例发生迟发性脑实质内出血。

结论

降低 ICAD 血管成形术和支架置入并发症的努力必须集中于降低区域性穿支血管梗死、迟发性脑实质内出血和导丝穿孔的风险。

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