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大动脉粥样硬化性疾病继发缺血性卒中的机制。

Mechanisms of ischemic stroke secondary to large artery atherosclerotic disease.

作者信息

Derdeyn Colin P

机构信息

Washington University School of Medicine, Mallinckrodt Institute of Radiology, 510 South Kingshighway Boulevard, St Louis, MO 63110, USA.

出版信息

Neuroimaging Clin N Am. 2007 Aug;17(3):303-11, vii-viii. doi: 10.1016/j.nic.2007.03.001.

Abstract

Atherosclerotic occlusive disease of the cervical and intracranial arteries leads to ischemic stroke through two separate, but interrelated, mechanisms: local thrombosis or embolism from atherosclerotic plaque, and hemodynamic failure (low flow). In this article, the author discusses the evidence linking these two mechanisms with cerebral ischemia, and the evidence for the synergistic effects of thromboembolism and impaired hemodynamics. An understanding of these two mechanisms is important because these mechanisms provide the rationale for revascularization for patients who have atherosclerotic stenosis or occlusion. In addition, the biologic imaging of atherosclerotic plaques and hemodynamic assessment eventually will play an important role in stratifying patient risk and guiding physiologically based patient selection for intervention.

摘要

颈内和颅内动脉的动脉粥样硬化闭塞性疾病通过两种独立但相互关联的机制导致缺血性卒中

动脉粥样硬化斑块引起的局部血栓形成或栓塞,以及血流动力学衰竭(低流量)。在本文中,作者讨论了将这两种机制与脑缺血联系起来的证据,以及血栓栓塞和血流动力学受损协同作用的证据。了解这两种机制很重要,因为这些机制为患有动脉粥样硬化狭窄或闭塞的患者进行血管重建提供了理论依据。此外,动脉粥样硬化斑块的生物成像和血流动力学评估最终将在对患者风险进行分层以及指导基于生理学的患者干预选择方面发挥重要作用。

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