GWW School of Mechanical Engineering, Georgia Institute of Technology, Atlanta, GA 30332-0405, USA.
J Biomech. 2010 Nov 16;43(15):2970-7. doi: 10.1016/j.jbiomech.2010.07.011. Epub 2010 Aug 21.
Atherothrombosis can induce acute myocardial infarction and stroke by progressive stenosis of a blood vessel lumen to full occlusion. Since thrombus formation and embolization may be shear-dependent, we quantify the magnitude of shear rates in idealized severely stenotic coronary arteries (≥75% by diameter) using computational fluid dynamics to characterize the shear environment that may exist during atherothrombosis. Maximum shear rates in severe short stenoses were found to exceed 250,000s(-1) (9500dynes/cm(2)) and can reach a peak value of 425,000s(-1) for a 98% stenosis. These high shear rates exceed typical shear used for in vitro blood flow experiments by an order of magnitude, indicating the need to examine thrombosis at very high shear rates. Pulsatility and stenosis eccentricity were found to have minor effects on the maximum wall shear rates in severe stenoses. In contrast, increases in the stenosis length reduced the maximum shear to 107,000s(-1) (98% stenosis), while surface roughness could increase focal wall shear rates to a value reaching 610,000s(-1) (90% stenosis). The "shear histories" of circulating platelets in these stenoses are far below reported activation thresholds. Platelets may be required to form bonds in 5μs and resist shear forces reaching 8000pN per platelet. Arterial thrombosis occurs in the face of pathological high shear stress, creating rapid and strong bonds without prior activation of circulating platelets.
动脉粥样硬化血栓形成可通过血管管腔的进行性狭窄至完全闭塞导致急性心肌梗死和中风。由于血栓形成和栓塞可能依赖于切变率，因此我们使用计算流体动力学来量化理想化严重狭窄冠状动脉（直径狭窄≥75%）中的切变率大小，以描述动脉粥样硬化血栓形成过程中可能存在的切变环境。发现严重短狭窄处的最大切变率超过 250,000s(-1)（9500dynes/cm(2)），而 98%狭窄处的最大切变率可达到 425,000s(-1)。这些高切变率超过了典型的体外血流实验中使用的切变率，表明需要在非常高的切变率下检查血栓形成。脉动和狭窄偏心度对严重狭窄处的最大壁切变率的影响较小。相比之下，增加狭窄长度将最大切变率降低至 107,000s(-1)（98%狭窄），而表面粗糙度可将局部壁切变率增加到 610,000s(-1)（90%狭窄）。这些狭窄处循环血小板的“切变历史”远低于报道的激活阈值。血小板可能需要在 5μs 内形成键并抵抗达到每个血小板 8000pN 的切变力。动脉血栓形成发生在病理高切应力下，在没有循环血小板预先激活的情况下迅速形成强键。
