Chesnutt Jennifer K W, Han Hai-Chao
Cardiovascular Biomechanics Laboratory, Department of Mechanical Engineering, The University of Texas at San Antonio, San Antonio, TX, USA.
Phys Biol. 2016 Jan 20;13(1):016001. doi: 10.1088/1478-3975/13/1/016001.
Coronary stenting is one of the most commonly used approaches to open coronary arteries blocked due to atherosclerosis. Stent malapposition can induce thrombosis but the microscopic process is poorly understood. The objective of this study was to determine the platelet-level process by which different extents of stent malapposition affect the initiation of stent thrombosis. We utilized a discrete element model to computationally simulate the transport, adhesion, and activation of thousands of individual platelets and red blood cells during thrombus initiation in stented coronary arteries. Simulated arteries contained a malapposed stent with a specified gap distance (0, 10, 25, 50, or 200 μm) between the struts and endothelium. Platelet-level details of thrombus formation near the proximal-most strut were measured during the simulations. The relationship between gap distance and amount of thrombus in the artery varied depending on different conditions (e.g., amount of dysfunctional endothelium, shear-induced activation of platelets, and thrombogenicity of the strut). Without considering shear-induced platelet activation, the largest gap distance (200 μm) produced no recirculation and less thrombus than the smallest two gap distances (0 and 10 μm) that created recirculation downstream of the strut. However, with the occurrence of shear-induced platelet activation, the largest gap distance produced more thrombus than the two smallest gap distances, but less thrombus than an intermediate gap distance (25 μm). A large gap distance was not necessarily the most thrombogenic, in contrast to implications of some computational fluid dynamics studies. The severity of stent malapposition affected initial stent thrombosis differently depending on various factors related to fluid recirculation, platelet trajectories, shear stress, and endothelial condition.
冠状动脉支架置入术是治疗因动脉粥样硬化导致冠状动脉阻塞最常用的方法之一。支架贴壁不良可诱发血栓形成，但微观过程尚不清楚。本研究的目的是确定不同程度的支架贴壁不良影响支架内血栓形成起始的血小板水平过程。我们利用离散元模型对冠状动脉支架置入术后血栓形成过程中数千个单个血小板和红细胞的运输、黏附和激活进行了计算模拟。模拟的动脉包含一个贴壁不良的支架，其支柱与内皮之间有特定的间隙距离（0、10、25、50或200μm）。在模拟过程中，测量了最近端支柱附近血栓形成的血小板水平细节。间隙距离与动脉内血栓量之间的关系因不同条件（如功能失调内皮的数量、剪切诱导的血小板激活以及支柱的血栓形成倾向）而异。在不考虑剪切诱导的血小板激活的情况下，最大间隙距离（200μm）不会产生再循环，且血栓形成比在支柱下游产生再循环的最小两个间隙距离（0和10μm）少。然而，在发生剪切诱导的血小板激活时，最大间隙距离产生的血栓比两个最小间隙距离多，但比中间间隙距离（25μm）少。与一些计算流体动力学研究的结论相反，大间隙距离不一定是血栓形成倾向最大的。支架贴壁不良的严重程度根据与流体再循环、血小板轨迹、剪切应力和内皮状况相关的各种因素，对初始支架内血栓形成的影响不同。
