Taylor Joshua O, Meyer Richard S, Deutsch Steven, Manning Keefe B
Department of Biomedical Engineering, The Pennsylvania State University, 205 Hallowell Building, University Park, PA, 16802, USA.
Applied Research Laboratory, The Pennsylvania State University, State College, PA, USA.
Biomech Model Mechanobiol. 2016 Dec;15(6):1713-1731. doi: 10.1007/s10237-016-0793-2. Epub 2016 May 12.
While cardiovascular device-induced thrombosis is associated with negative patient outcomes, the convoluted nature of the processes resulting in a thrombus makes the full thrombotic network too computationally expensive to simulate in the complex geometries and flow fields associated with devices. A macroscopic, continuum computational model is developed based on a simplified network, which includes terms for platelet activation (chemical and mechanical) and thrombus deposition and growth in regions of low wall shear stress (WSS). Laminar simulations are performed in a two-dimensional asymmetric sudden expansion geometry and compared with in vitro thrombus size data collected using whole bovine blood. Additionally, the predictive power of the model is tested in a flow cell containing a series of symmetric sudden expansions and contractions. Thrombi form in the low WSS area downstream of the asymmetric expansion and grow into the nearby recirculation region, and thrombus height and length largely remain within 95 % confidence intervals calculated from the in vitro data for 30 min of blood flow. After 30 min, predicted thrombus height and length are 0.94 and 4.32 (normalized by the 2.5 mm step height). Importantly, the model also correctly predicts locations of thrombus deposition observed in the in vitro flow cell of expansions and contractions. As the simulation results, which rely on a greatly reduced model of the thrombotic network, are still able to capture the macroscopic behavior of the full network, the model shows promise for timely predictions of device-induced thrombosis toward optimizing and expediting the device development process.
虽然心血管装置引发的血栓形成与患者的不良预后相关，但导致血栓形成的过程错综复杂，使得在与装置相关的复杂几何形状和流场中模拟完整的血栓网络在计算上过于昂贵。基于一个简化的网络开发了一个宏观的连续介质计算模型，该模型包括血小板激活（化学和机械）以及在低壁面剪应力（WSS）区域血栓沉积和生长的项。在二维不对称突然扩张几何形状中进行层流模拟，并与使用全牛血收集的体外血栓大小数据进行比较。此外，在包含一系列对称突然扩张和收缩的流动池中测试该模型的预测能力。血栓在不对称扩张下游的低WSS区域形成，并生长到附近的再循环区域，血栓高度和长度在很大程度上保持在根据30分钟血流的体外数据计算的95%置信区间内。30分钟后，预测的血栓高度和长度分别为0.94和4.32（以2.5毫米的步高进行归一化）。重要的是，该模型还正确预测了在体外扩张和收缩流动池中观察到的血栓沉积位置。由于依赖大幅简化的血栓网络模型的模拟结果仍能捕捉完整网络的宏观行为，该模型有望及时预测装置引发的血栓形成，从而优化和加快装置开发过程。
