ESTIMATION OF WALL SHEAR STRESS DYNAMIC FLUCTUATIONS IN INTRACRANIAL ATHEROSCLEROTIC LESIONS USING COMPUTATIONAL FLUID DYNAMICS

医学 血管成形术 剪应力 狭窄 心脏周期 经皮 血流动力学 血流 心脏病学 机械 放射科 物理
作者
Clemens M. Schirmer,Adel M. Malek
出处
期刊:Neurosurgery [Lippincott Williams & Wilkins]
卷期号:63 (2): 326-335 被引量:21
标识
DOI:10.1227/01.neu.0000313119.73941.9e
摘要

OBJECTIVE Intracranial stenosis (IS) is associated with significant morbidity and mortality from hypoperfusion and thromboembolism. We used computational fluid dynamic methods to analyze luminal patterns of wall shear stress (WSS), a known critical modulator of endothelial function, within patient-based IS lesions undergoing percutaneous angioplasty and stenting. METHODS High-resolution three-dimensional rotational angiographic data sets were reconstructed to yield a fine-resolution computational mesh allowing application of pulsatile computational fluid dynamic analysis with a non-Newtonian realistic model of blood. WSS and its gradient were analyzed spatiotemporally in five IS lesions before and after percutaneous angioplasty and stenting. RESULTS WSS within the stenosis reached average shear magnitudes of 1870 ± 783 dyn/cm2 with rapidly reversing direction to oscillating low values in the recirculation zone. WSS vectors revealed complex dynamic directional and amplitude oscillations not seen in healthy segments with time-dependent convergence and divergence strips sweeping back and forth across the lesion during the cardiac cycle. These areas also underwent extreme temporal WSS oscillation of 2052 ± 909 dyn/cm2 over a short time interval. The endothelial mechanotransductive response to such extreme WSS magnitudes and gradients, which were normalized by percutaneous angioplasty and stenting in the current study, remains undefined. CONCLUSION Computational fluid dynamic analysis of IS has uncovered a complex and hostile microhemodynamic environment characterized by wide and rapid shear variations in time and space. Characterization of the mechanical forces acting on the wall can help in determining the molecular transduction response of the luminal endothelium to these extreme stresses and may lead to better understanding of the hemodynamic contribution to stenosis pathophysiology.
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