CAJ | 학술논문

目的：研究流固耦合作用下颈动脉内一个心动周期典型时刻血流动力学分布，探索颈动脉粥样斑块形成与发展机制。方法采用计算流体力学方法对一个心动周期颈动脉内血流特性进行数值分析，根据血流动力学特征参数分析心动收缩期和心动舒张期对血流分布特性的影响。结果获得一个心动周期典型时刻颈动脉内血流特性分布情况。与心动舒张期相比，心动收缩期颈外动脉入口处分布较大面积血流停滞区，该区域内血流速度低，壁面压力低，壁面切应力低，管壁形变量和von Mises等效应力较大。结论流固耦合作用下颈动脉血流速度低引起血液回流，脂质、纤维等大分子易沉积；壁面压力低形成“负压”效应，正常血流发生改变，流动速度变慢，脑部供血不足；壁面切应力低使近壁面血流流态被破坏，血小板活性增强，内膜过度增生；管壁形变量和von Mises等效应力较大易引起应力集中，增大血管破裂风险。
목적：연구류고우합작용하경동맥내일개심동주기전형시각혈류동역학분포，탐색경동맥죽양반괴형성여발전궤제。방법채용계산류체역학방법대일개심동주기경동맥내혈류특성진행수치분석，근거혈류동역학특정삼수분석심동수축기화심동서장기대혈류분포특성적영향。결과획득일개심동주기전형시각경동맥내혈류특성분포정황。여심동서장기상비，심동수축기경외동맥입구처분포교대면적혈류정체구，해구역내혈류속도저，벽면압력저，벽면절응력저，관벽형변량화von Mises등효응력교대。결론류고우합작용하경동맥혈류속도저인기혈액회류，지질、섬유등대분자역침적；벽면압력저형성“부압”효응，정상혈류발생개변，류동속도변만，뇌부공혈불족；벽면절응력저사근벽면혈류류태피파배，혈소판활성증강，내막과도증생；관벽형변량화von Mises등효응력교대역인기응력집중，증대혈관파렬풍험。
Objective To study the distribution of hemodynamics in carotid artery under the fluid-solid interaction at the typical point of time during a single cardiac cycle, and to explore the mechanism of the formation and development of carotid atherosclerotic plaque. Methods Numerical analysis the blood flow characteristics within a cardiac cycle in carotid artery was analyzed by using computational method of fluid dynamics. Based on the hemodynamic parameters, the influences of the cardiac systole and diastole on the blood flow distribution were analyzed. Results The distribution of blood flow in the carotid artery within a typical cardiac cycle was obtained. Compared with the findings in cardiac diastole, a larger area of blood stasis at the entrance of external carotid artery was observed. In this area, the flow velocity, the wall pressure and the wall shear stress were all lower, while the arterial wall deformation and von Mises equivalent stress were larger. Conclusion Under fluid-solid interaction, the low blood flow in carotid artery causes blood reflux, resulting in the deposition of lipid, fiber and other large molecular materials. The low wall pressure produced“negative pressure” effect, thus the normal blood flow is changed, the flow velocity becomes slow, and the blood supply of the brain becomes insufficient. The low wall shear stress destroys the blood flow near the wall, causing the increase of platelet activity and intimal hyperplasia. The larger arterial wall deformation variable and von Mises equivalent stress can cause stress concentration and increase vascular rupture risk.