Paul M Rady Department of Mechanical Engineering University of Colorado Boulder Bolder CO.
Department of Neurology University of Colorado Anschutz Medical Campus Aurora CO.
J Am Heart Assoc. 2023 Dec 5;12(23):e030792. doi: 10.1161/JAHA.123.030792. Epub 2023 Nov 28.
Disambiguation of embolus pathogenesis in embolic strokes is often a clinical challenge. One common source of embolic stroke is the carotid arteries, with emboli originating due to plaque buildup or perioperatively during revascularization procedures. Although it is commonly thought that thromboemboli from carotid sources travel to cerebral arteries ipsilaterally, there are existing reports of contralateral embolic events that complicate embolus source destination relationship for carotid sources. Here, we hypothesize that emboli from carotid sources can travel to contralateral hemispheres and that embolus interactions with collateral hemodynamics in the circle of Willis influence this process.
We use a patient-specific computational embolus-hemodynamics interaction model developed in prior works to conduct an in silico experiment spanning 4 patient vascular models, 6 circle of Willis anastomosis variants, and 3 different thromboembolus sizes released from left and right carotid artery sites. This led to a total of 144 different experiments, estimating trajectories and distribution of approximately 1.728 million embolus samples. Across all cases considered, emboli from left and right carotid sources showed nonzero contralateral transport ( value <-0.05). Contralateral movement revealed a size dependence, with smaller emboli traveling more contralaterally. Detailed analysis of embolus dynamics revealed that collateral flow routes in the circle of Willis played a role in routing emboli, and transhemispheric movement occurred through the anterior and posterior communicating arteries in the circle of Willis.
We generated quantitative data demonstrating the complex dynamics of finite size thromboembolus particles as they interact with pulsatile arterial hemodynamics and traverse the vascular network of the circle of Willis. This leads to a nonintuitive source-destination relationship for emboli originating from carotid artery sites, and emboli from carotid sources can potentially travel to cerebral arteries on contralateral hemispheres.
在栓塞性中风中，对栓子发病机制的鉴别常常是临床挑战。颈动脉是栓塞性中风的一个常见来源，栓子源于斑块形成或血管再通术期间的围手术期。尽管通常认为来自颈动脉源的血栓栓子会向同侧大脑动脉移动，但也有报道称存在对侧栓塞事件，这使颈动脉源的栓子源-靶关系复杂化。在这里，我们假设来自颈动脉源的栓子可以向对侧半球移动，并且栓子与Willis 环侧支循环血流动力学的相互作用会影响这一过程。
我们使用先前工作中开发的基于患者的计算栓子-血流动力学相互作用模型，对 4 个患者血管模型、6 个 Willis 环吻合变体和 3 种不同大小的血栓栓子从左、右颈动脉部位释放的情况进行了计算机模拟实验。这总共进行了 144 种不同的实验，估计了大约 172.8 万个栓子样本的轨迹和分布。在所有考虑的情况下，来自左、右颈动脉源的栓子均显示出非零的对侧输送（ value <-0.05）。对侧运动显示出大小依赖性，较小的栓子向对侧移动得更远。对栓子动力学的详细分析表明，Willis 环中的侧支血流路径在引导栓子方面发挥了作用，并且通过 Willis 环的前交通动脉和后交通动脉发生了跨半球运动。
我们生成了定量数据，证明了有限大小血栓栓子颗粒在与脉动动脉血流动力学相互作用并穿过 Willis 环血管网络时的复杂动力学。这导致了源自颈动脉源的栓子源-靶关系变得不直观，并且来自颈动脉源的栓子可能会向对侧半球的大脑动脉移动。
