Roopnarinesingh Ricardo, Leppert Michelle, Mukherjee Debanjan
medRxiv. 2023 Aug 23:2023.04.20.23288892. doi: 10.1101/2023.04.20.23288892.
Disambiguation of embolus etiology in embolic strokes is often a clinical challenge. One common source of embolic stroke is the carotid arteries, with emboli originating due to plaque build up, or perioperatively during revascularization procedures. While it is commonly thought that thromboemboli from carotid sources travel to cerebral arteries ipsilaterally, there are existing reports of contralateral embolic events which 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 influences this process. We use a patient-specific computational embolus-hemodynamics interaction model developed in prior works to conduct an 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 non-zero contralateral transport (p 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 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 non-intuitive source-destination relationship for emboli originating from carotid artery sites, and emboli from carotid sources can potentially travel to cerebral arteries on contralateral hemispheres.
明确栓塞性中风的栓子病因往往是一项临床挑战。栓塞性中风的一个常见栓子来源是颈动脉,栓子的形成是由于斑块积聚,或在血管重建手术期间形成。虽然通常认为来自颈动脉的血栓栓子会同侧进入脑动脉,但已有对侧栓塞事件的报道,这使得颈动脉来源的栓子源-目的地关系变得复杂。在此,我们假设来自颈动脉的栓子可以进入对侧半球,并且栓子与 Willis 环中的侧支血流动力学相互作用会影响这一过程。我们使用先前研究中开发的针对特定患者的计算栓子-血流动力学相互作用模型,对 4 个患者血管模型、6 种 Willis 环吻合变体以及从左右颈动脉部位释放的 3 种不同大小的血栓栓子进行了一项实验。这总共产生了 144 个不同的实验,估计了大约 172.8 万个栓子样本的轨迹和分布。在所有考虑的病例中,来自左右颈动脉的栓子均显示出非零的对侧传输(p 值<0.05)。对侧移动显示出大小依赖性,较小的栓子向对侧移动得更多。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,并且跨半球移动是通过 Willis 环中的前交通动脉和后交通动脉发生的。我们生成了定量数据,证明了有限大小的血栓栓子颗粒与搏动性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部位的栓子的非直观源-目的地关系,并且来自颈动脉的栓子可能会进入对侧半球的脑动脉。