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.
Cardiovascular Biomechanics Laboratory, Department of Mechanical Engineering, The University of Texas at San Antonio, San Antonio, TX, USA; Biomedical Engineering Program, UTSA-UTHSCSA, San Antonio, TX, USA.
Comput Biol Med. 2015 Jan;56:182-91. doi: 10.1016/j.compbiomed.2014.11.006. Epub 2014 Nov 15.
Coronary stenting is one of the most commonly used approaches to open coronary arteries blocked due to atherosclerosis. However, stent struts can induce stent thrombosis due to altered hemodynamics and endothelial dysfunction, and the microscopic process is poorly understood. The objective of this study was to determine the microscale processes during the initiation of stent thrombosis.
We utilized a discrete element computational model to simulate the transport, collision, adhesion, and activation of thousands of individual platelets and red blood cells in thrombus formation around struts and dysfunctional endothelium.
As strut height increased, the area of endothelium activated by low shear stress increased, which increased the number of platelets in mural thrombi. These thrombi were generally outside regions of recirculation for shorter struts. For the tallest strut, wall shear stress was sufficiently low to activate the entire endothelium. With the entire endothelium activated by injury or denudation, the number of platelets in mural thrombi was largest for the shortest strut. The type of platelet activation (by high shear stress or contact with activated endothelium) did not greatly affect results.
During the initiation of stent thrombosis, platelets do not necessarily enter recirculation regions or deposit on endothelium near struts, as suggested by previous computational fluid dynamics simulations. Rather, platelets are more likely to deposit on activated endothelium outside recirculation regions and deposit directly on struts. Our study elucidated the effects of different mechanical factors on the roles of platelets and endothelium in stent thrombosis.
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。然而，支架撑条可因血流动力学改变和内皮功能障碍而诱发支架内血栓形成，其微观过程尚不清楚。本研究的目的是确定支架内血栓形成起始阶段的微观过程。
我们利用离散元计算模型模拟数千个单个血小板和红细胞在支架撑条周围及功能失调内皮处血栓形成过程中的运输、碰撞、黏附和活化。
随着撑条高度增加，低剪切应力激活的内皮面积增加，这增加了壁内血栓中的血小板数量。对于较短的撑条，这些血栓通常位于再循环区域之外。对于最高的撑条，壁面剪切应力足够低，可激活整个内皮。由于损伤或剥脱导致整个内皮被激活，壁内血栓中血小板数量在最短撑条时最多。血小板激活类型（高剪切应力或与活化内皮接触）对结果影响不大。
在支架内血栓形成起始阶段，血小板不一定如先前计算流体动力学模拟所提示的那样进入再循环区域或沉积在撑条附近的内皮上。相反，血小板更可能沉积在再循环区域之外的活化内皮上，并直接沉积在撑条上。我们的研究阐明了不同力学因素对血小板和内皮在支架内血栓形成中作用的影响。
