Prediction of complex flow patterns in intracranial atherosclerotic disease using computational fluid dynamics
Prediction of complex flow patterns in intracranial atherosclerotic disease using computational fluid dynamics
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DOI：
10.1227/01.neu.0000280081.68618.22
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发表时间：
2007-10-01
期刊：
影响因子：
4.8
通讯作者：
Malek, Adel M.
中科院分区：
文献类型：
--
作者：
Clemens, M. Schirmer;Malek, Adel M.
目的：虽然颈动脉和椎动脉颅内动脉粥样硬化性疾病（ICAD）可导致血流动力学功能不全和血栓栓塞，但由于其复杂的特征和复杂的三维几何形状，其流体动力学特性仍然不确定。我们使用计算流体动力学（CFD）分析模拟有症状的ICAD病变的血流动力学。方法：9个ICAD病变（6个颈动脉，2个椎体，1个大脑中动脉）进行了高分辨率基于导管的数字旋转血管造影。对重建的靶病灶三维体积进行分割，并用于生成混合计算网格。动态脉动CFD分析进行使用非牛顿剪切依赖模型的血液的viscosity.RESULTS：CFD结果显示复杂的流动模式内ICAD病变与midstenotic剪切速率大于19000/s，足够高，以诱导高剪切血小板活化。狭窄内的涡度和螺旋度随后突然减速并形成涡核。压力梯度大多在狭窄大于75%时显著，平均时间平均下降27.2 +/- 17.8 mmHg。与颅内循环的三维解剖结构所赋予的平滑变化的螺旋度不同，ICAD病变的狭窄后区域显示出显著且快速波动的螺旋度和涡度模式，这可能有助于狭窄喉部内高剪切区域激活的血小板的传播。支架血管成形术恢复ICAD病变的血流动力学概况对侧controls.CONCLUSION：基于患者的症状性ICAD病变研究使用CFD分析似乎窝藏血液动力学病理环境，有利于血小板的活化，聚集和远端栓塞，并逆转血管内支架血管成形术。
OBJECTIVE: Although carotid and vertebral intracranial atherosclerotic disease (ICAD) can lead to both hemodynamic insufficiency and thromboembolism, its fluid dynamic properties remain undefined because of its intricate features and complex three-dimensional geometry. We used computational fluid dynamic (CFD) analysis to model the hemodynamics of symptomatic ICAD lesions.METHODS: Nine ICAD lesions (six carotid, two vertebral, one middle cerebral) underwent high-resolution catheter-based digital rotational angiography. The reconstructed three-dimensional volumes of the target lesions were segmented and used to generate hybrid computational meshes. Dynamic pulsatile CFD analysis was performed using a non-Newtonian shear-dependent model of blood's viscosity.RESULTS: CFD results revealed complex flow patterns within ICAD lesions with midstenotic shear rates of greater than 1 9,000/s, sufficiently high to induce high-shear platelet activation. Vorticity and helicity within the stenoses were followed by sudden deceleration with formation of vortex cores. Pressure gradients were significant mostly at greater than 75% stenosis with a mean time-averaged drop of 27.2 +/- 17.8 mmHg. Unlike the smoothly-varying helicity imparted by the three-dimensional anatomy of the intracranial circulation, poststenotic regions of ICAD lesions showed significant and rapidly fluctuating helicity and vorticity patterns, which may contribute to the propagation of platelets activated by the high shear region within the stenosis throat. Stent angioplasty restored the hemodynamic profile of ICAD lesions to within contralateral controls.CONCLUSION: Patient-based symptomatic ICAD lesions studied using CFD analysis appear to harbor a hemodynamically pathological environment that favors the activation, aggregation and distal embolization of platelets and is reversed by endovascular stent angioplasty.