Department of Neurosurgery, University of Illinois at Chicago, United States.
Department of Neurosurgery, University of Illinois at Chicago, United States.
Med Hypotheses. 2019 Feb;123:86-88. doi: 10.1016/j.mehy.2019.01.003. Epub 2019 Jan 7.
Cerebral arteriovenous malformations (AVMs) are an uncommon vascular anomaly that carry the risk of rupture and hemorrhage. Several factors have been implicated in the propensity of an AVM to bleed. One such factor is stenosis of AVM draining veins, as impairment of the AVM venous drainage system is associated with increased risk of intracranial hemorrhage. Currently, our understanding of the pathogenesis of AVM venous outflow stenosis is limited, as there is insufficient data on the blood flow patterns and local hemodynamic parameters of these draining veins. The angioarchitecture of AVMs features a nidus lacking a high resistance capillary network. Accordingly, our previous studies on AVM arterial feeders have demonstrated an abnormally high flow volume rate along with low pulsatility and resistance indices on quantitative magnetic resonance angiography. As such, AVM vessels endure high, non-physiologic levels of flow that may partially contribute to ectasia or stenosis depending on whether wall shear stress (WSS) is high or low, respectively. We hypothesize that AVM venous outflow stenosis occurs most commonly near the junction of the draining vein and the dural venous sinus. Increased flow volume rate through the AVM circuit coupled with the variation in compliance and rigidity between the walls of the draining vein and the dural venous sinus likely create turbulence of blood flow. The resulting flow separation, low WSS, and departure from axially aligned, unidirectional flow may create atherogenic conditions that can be implicated in venous intimal hyperplasia and outflow stenosis. We have previously found there to be a significant association between intimal hyperplasia risk factors and venous outflow stenosis. Additionally, we have found a significant association between age and likelihood as well as degree of stenosis, suggesting a progressive disease process. Similar conditions have been demonstrated in the pathophysiology of stenosis of the carotid artery and dialysis arteriovenous fistulas. In both of these conditions, the use of computational fluid dynamics (CFD) has been employed to characterize the local hemodynamic features that contribute to the pathogenesis of intimal hyperplasia and stenosis. We recommend the utilization of CFD to characterize the anatomic and hemodynamic features of AVM venous outflow stenosis. An improved understanding of the possible causative features of venous outflow stenosis may impact how clinicians choose to manage the treatment of patients with AVMs.
脑动静脉畸形（AVM）是一种不常见的血管畸形，存在破裂和出血的风险。有几个因素与 AVM 出血倾向有关。其中一个因素是 AVM 引流静脉狭窄，因为 AVM 静脉引流系统受损与颅内出血风险增加相关。目前，我们对 AVM 静脉流出道狭窄的发病机制了解有限，因为关于这些引流静脉的血流模式和局部血流动力学参数的数据不足。AVM 的血管结构特征为没有高阻力毛细血管网络的病灶。因此，我们之前对 AVM 动脉供血动脉的研究表明，在定量磁共振血管造影上，血流量异常高，搏动指数和阻力指数低。因此，AVM 血管承受着高、非生理水平的血流，这可能部分导致血管扩张或狭窄，具体取决于壁切应力（WSS）是高还是低。我们假设 AVM 静脉流出道狭窄最常见于引流静脉与硬脑膜窦交界处附近。通过 AVM 循环的血流量增加，加上引流静脉壁和硬脑膜窦壁之间顺应性和刚性的变化，可能会导致血流湍流。由此产生的血流分离、低壁切应力以及偏离轴向对齐、单向流动可能会导致动脉粥样硬化条件，这可能与静脉内膜增生和流出道狭窄有关。我们之前发现内膜增生危险因素与静脉流出道狭窄之间存在显著相关性。此外，我们发现年龄与狭窄的可能性和程度之间存在显著相关性，表明这是一种进行性疾病过程。在颈动脉狭窄和透析动静脉瘘的病理生理学中也发现了类似的情况。在这两种情况下，都使用了计算流体动力学（CFD）来描述导致内膜增生和狭窄的局部血流动力学特征。我们建议使用 CFD 来描述 AVM 静脉流出道狭窄的解剖和血流动力学特征。对静脉流出道狭窄可能的致病特征的更好理解可能会影响临床医生如何选择治疗 AVM 患者的方法。
