脂肪颗粒在颈动脉中的运动及其对血液动力学的影响

很多研究表明, 动脉粥样硬化通常发生在具有复杂血液动力学的区域, 比如分叉动脉和弯曲动脉. 这些地方常伴随有低壁面剪切力或震荡壁面剪切力, 这是动脉粥样硬化形成的一大诱因. 使用计算流体力学软件对2D颈动脉分叉血管进行了模拟, 研究了脂肪颗粒在颈动脉中的运动及其对血液动力学的影响. 研究表明: 1)血管狭窄对于脂肪颗粒的运动有重要影响, 同时也影响栓塞的形成; 2)脂肪颗粒可能会黏附在血管壁面, 但由于血流的冲击作用, 脂肪颗粒会随后在壁面略微铺展; 3)颈动脉狭窄区域后方是下一个血栓的可能生长位点; 4)当栓塞形成时, 速度和壁面剪切力分布将变得复杂多变, 这对于血管是有害的.

Movement of fat particles in carotid artery and its influence on hemodynamics

It has been widely observed that atherosclerotic diseases occur in regions with complex hemodynamics, such as artery bifurcations and regions of high curvature. These regions usually have low or oscillatory wall shear stress, which is a main factor that results in thrombus formation. In addition, after the thrombosis, the stenosis will in turn affect the hemodynamics. In the blood circulation, the abnormal substances that do not dissolve in the blood can block the vascular cavity, which is called embolism. These substances such as fat particles are called embolus. Embolism results in high velocity and wall shear stress (WSS), which is harmful to the vessel wall. Embolism leads to stroke easily, resulting in the death of the patient. Here, the authors focus on the formation process of fat embolism and its influence on hemodynamics. In order to investigate the influence of various factors on the movement of a fat particle, we carry out the single factor simulation. Fat particles do not dissolve in the blood and easily adhere to the vessel wall. We use a virtual fluid that represents the fat particles. In the present work, a two-dimensional (2D) carotid bifurcation is established, and the simulation is carried out by the computational fluid dynamics software. The movement of the fat particles relies on the thrust and surface friction of the blood, and the values of thrust and surface friction are governed by the blood velocity, viscosity and the diameter of the fat particle, which has little relationship with the density, especially for a blood vessel that is not too long. The fat particles can smoothly pass through the carotid sinus when the vessel is 0 or 25% stenosed, which indicates that the embolism does not occur and the fat particle does not adhere to the vessel wall. Small deformation occurrs when the vessel is 25% stenosed for 0.6 s. When the degree of stenosis increases to 50%, the fat particles partially blocks the vascular cavity. We give an experiment about the influences of the stenosis on the movement of two fat particles and thrombus. When the carotid sinus is 0 or 25% stenosed, the two fat particles adhere to the vessel wall at the end of internal carotid artery (ICA), resulting in fat embolism. One fat article is on the upper wall of ICA and the other is on the lower wall. At the end of ICA, the vascular diameter becomes smaller and the two fat particles cannot pass through it. When the carotid sinus is 50% stenosed, the two fat particles merge into a larger one and partially block the narrow vascular cavity, impeding blood circulation. The findings in this paper may help hematological experts to check the spread of atherosclerotic disease. The main conclusions drawn from the present study are a) the vascular stenosis has an important influence on the movement of fat particles and the formation of embolism as well; b) the fat particles may adhere to the vessel wall, and due to the flow of blood, the fat particles spread slightly on the wall; c) the region behind the stenosis might be the next site of thrombosis; d) with the movement of fat particles, the maximum negative WSS increases slightly, and its coordinate position moves to the right; e) when embolism occurs, the velocity and WSS distribution become very complex, which is harmful to the vessel.