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颅内侧支循环决定颈动脉斑块破裂的血流动力。

Intracranial collateralization determines hemodynamic forces for carotid plaque disruption.

机构信息

Center for Vascular Diagnostics, Department of Vascular Surgery, University of Maryland, Baltimore, MD 21201, USA.

出版信息

J Vasc Surg. 2011 Nov;54(5):1461-71. doi: 10.1016/j.jvs.2011.05.001. Epub 2011 Aug 6.

DOI:10.1016/j.jvs.2011.05.001
PMID:21820834
Abstract

INTRODUCTION

Percent diameter reduction provides an imperfect assessment of the risk for stroke from carotid atheroembolism. Stroke associated with atherosclerotic carotid stenosis commonly results from plaque disruption brought about by hemodynamic shear stress and Bernoulli forces. The aim of the present study was to predict the effect of incomplete intracranial collateralization through the circle of Willis (COW) on disruptive hemodynamic forces acting on carotid plaques.

METHODS

A simple circuit model of the major pathways and collaterals that form and supply the COW was developed. We modeled the intra- and extracranial arterial circuits from standard anatomic references, and the pressure-flow relationships within these conduits from standard fluid mechanics. The pressure drop caused by (laminar and turbulent) flow along the internal carotid artery path was then computed. Carotid circulation to the brain was classified as being with or without collateral connections through the COW, and the extracranial carotid circuit as being with or without severe stenosis. The pressure drop was computed for each scenario. Finally, a linear circuit model was used to compute brain blood flow in the presence/absence of a disconnected COW.

RESULTS

Pressure drop across a carotid artery stenosis increased as the flow rate within the carotid conduit increased. Poststenotic turbulence from a sudden expansion distal to the stenosis resulted in an additional pressure drop. Despite the stenosis, mean brain blood flow was sustained at 4.15 mL/s bilaterally. In the presence of an intact (collateralized) COW, this was achieved by enhanced flow in the contralateral (normal) carotid artery. However, in a disconnected COW, this was achieved by sustained systolic and enhanced diastolic flow through the stenosed artery. For a similar degree of stenosis, flow and velocity across the plaque was much higher when the COW was disconnected compared with an intact COW. Furthermore, the pressure drop across a similar stenosis was significantly higher with a disconnected COW compared with an intact COW.

CONCLUSIONS

Incomplete intracranial collateralization through the COW results in increased flow rates and velocities, and therefore large pressure drops across a carotid artery stenosis. This exerts large disruptive shear stress on the plaque compared with patients with an intact COW. Percent diameter reduction provides an inaccurate assessment of risk for atheroembolic stroke. An assessment of carotid flow rates, flow velocities, and the intracranial collateral circulation may add independent information to refine the estimation of stroke risk in patients with asymptomatic carotid atherosclerosis.

摘要

简介

颈动脉粥样硬化性狭窄患者发生的与动脉粥样硬化相关的卒中,通常是由血流切应力和伯努利力引起的斑块破裂导致的。本研究的目的是通过Willis 环(COW)预测不完全颅内侧支循环对作用于颈动脉斑块的破坏性血流动力学力的影响。

方法

开发了一个简单的 COW 主要通路和侧支的电路模型。我们以标准解剖参考为模型,构建了颅内和颅外动脉回路,以标准流体力学为模型,构建了这些导管内的压力-流量关系。然后计算了沿颈内动脉路径流动时(层流和湍流)引起的压降。通过 COW 将大脑的颈动脉循环分为有或无侧支连接,将颅外颈动脉回路分为有或无严重狭窄。为每个场景计算压降。最后,使用线性电路模型计算在没有连接的 COW 存在/不存在的情况下大脑的血流。

结果

随着颈动脉导管内的流速增加,颈动脉狭窄处的压降增加。狭窄下游突然扩张引起的后狭窄湍流导致额外的压降。尽管存在狭窄,但双侧平均脑血流仍维持在 4.15 mL/s。在完整(侧支化)COW 的情况下,通过对侧(正常)颈动脉的增强流量来实现。然而,在断开的 COW 中,通过狭窄动脉的持续收缩期和增强的舒张期流量来实现。对于类似程度的狭窄,当 COW 断开时,斑块上的流量和速度要高得多,而当 COW 完整时,情况则相反。此外,与完整的 COW 相比,当 COW 断开时,类似狭窄处的压降明显更高。

结论

COW 的不完全颅内侧支循环导致颈动脉狭窄处的流速和流量增加,从而导致较大的压降。这与完整 COW 的患者相比,对斑块施加了较大的破坏性切应力。颈动脉狭窄的粥样硬化性狭窄程度百分比降低提供了对动脉粥样硬化性血栓栓塞性卒中风险的不准确评估。评估颈动脉流量、流速和颅内侧支循环可能会提供独立信息,以细化对无症状颈动脉粥样硬化患者卒中风险的估计。

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