Association between basilar artery configuration and Vessel Wall features: a prospective high-resolution magnetic resonance imaging study

Basilar artery (BA) atherosclerotic occlusive disease is the most common cause for posterior circulation strokes, with potentially disastrous patient outcome and a high risk of recurrent stroke [1, 2]. Anatomically, BA arises from the junction of the bilateral vertebral arteries (VAs) and then divides into the bilateral posterior cerebral arteries (PCAs) and branches out into two pairs of cerebellar arteries. VA diameter may vary within the same individual, with only 6–26% of cases exhibiting equal size bilaterally in angiographic studies [3]. Previous studies identified VA hypoplasia as a predisposing factor for posterior circulation stroke [4, 5]. Conversely, VA dominance was shown to often cause BA curvature and the subsequent development of peri-vertebrobasilar junction infarcts [4, 5]. In other studies, fetal type PCA (fPCA) was shown to be a predisposing factor to ischemic events in the posterior circulation [6, 7].

The grade of intracranial artery stenosis and vulnerability of plaques are used as indications to guide the clinical management of patients [8]. One study demonstrated that symptomatic stenosis of the vertebrobasilar arteries was associated with a greatly increased risk of recurrent stroke [9]. Other studies demonstrated that vulnerability of intracranial artery plaque and cerebral hypoperfusion at the distal stenotic site were highly associated with stroke events and recurrence [10, 11]. Furthermore, an anterior circulation acute ischemic stroke study revealed associations between collateral circulation and thrombus characteristics, with patients displaying higher collateral scores having a lower thrombus burden and larger number of previous thrombi [12, 13].

However, the relationship between intracranial vessel configuration and wall features remains poorly investigated. BA configuration plays a role in posterior circulation hemodynamics and may influence the vessel wall features of BA. To test this hypothesis, we investigated the demographics, variants of VA and PCA, and BA vessel wall features. We compared the relationship between different BA configurations and vessel wall features using HRMRI.

This is a prospective registry study that has been approved by the ethics committee of our hospital. Written informed consent was obtained from the patients or their relatives.

When the BA becomes the site of an atherosclerotic lesion, whether cerebral vascular configuration is associated with the vessel features remains unclear. Hence, we aimed to explore the effects of varying anatomical configurations on culprit plaque characteristics in BA. To our knowledge, this is the first study to explore the correlation of posterior circulation artery configuration with culprit plaque features in BA using 3D HRMRI.

The present study found no statistical differences in vessel wall features between the complete and incomplete configuration of BA. Conversely, variations of configuration BA tree had no relationship with the vessel wall features of BA. The fPCA and VA lumen size difference are common variations of posterior circulation. fPCA is a common anatomical variant of the circle of Willis and can be accompanied by hypoplastic BA [22]. In our study, 23.5% of patients had fPCA, consistent with previous reports [22]. Lochner et al. found that fPCA accompanied by hypoplastic BA may predispose individuals to ischemic events in the posterior circulation [6]. Another study found that unequal VA diameter may cause BA curvature and the subsequent development of peri-vertebrobasilar junctional infarcts [5]. Ravensbergen et al. showed that the geometry of the vertebrobasilar junction correlated with occurrence of atherosclerotic plaque at the apex of the vertebrobasilar junction and lateral wall of BA [23]. In our study, there were 10 patients (29.4%) with non-dominant VA occlusion, and among them, 3 patients’ VA (8.8%) ended in a PICA. Overall, although variants of VA and PCA were associated with ischemic stroke, variations in the vertebrobasilar tree configuration had no relationship with BA vessel wall features. The results suggest that variants of artery configuration cannot trigger the formation of plaques.

Our study showed that the proximal configuration tree of BA was associated with strong plaque enhancement. In the present study, 64.2% of plaques showed enhancement. A previous study found that BA plaque enhancement and composition correlated with stroke events [24]. Plaque enhancement reflects the extent of vessel wall inflammation. The incomplete configuration of proximal VA may cause differences in long-term patient outcomes, but further studies are warranted to confirm this hypothesis.

Our study also showed that the proximal configuration tree of BA was associated with strong plaque enhancement and the distal configuration tree of BA was closely related with intraplaque hemorrhage. In the present study, 20.6% presented intraplaque hemorrhage on HRMRI. Plaque enhancement and intraplaque hemorrhage on HRMRI are markers of plaque destabilization and progression strongly associated with stroke events [24], which are also associated with endothelial dysfunction and neovascularization of the artery wall [25, 26]. The relationship between incomplete distal configuration of BA and intraplaque hemorrhage is difficult to explain given our present understanding. The incomplete distal configuration of BA indicated different hemodynamics and blood flow reserve on the top of BA. The fPCA indicated that most or all the blood flow of PCA was from the ipsilateral internal carotid artery. In a complete BA tree, the most common distribution pattern of blood flow at the top of the BA is as a parallel arrangement of vessels [27]. The fPCA changes this flow pattern, thereby affecting the regional vessel wall shear force. A study showed that blood flow shear stress acts on vessel walls, causing endothelial injury and plaque instability and presenting with plaque enhancement [28]. Poor collateral circulation and high grade of stenosis produced high-speed blood flow around the plaque, leading to erosion of the plaque’s fibrous cap or endothelium injury in the middle cerebral artery and carotid artery and subsequently causing plaque enhancement [29, 30]. The underlying mechanism of plaque enhancement correlated with distal incomplete configuration of BA needs to be further elucidated.

Unequal VA diameter was found to cause BA curvature and development of peri-vertebrobasilar junctional infarcts [5]. Dominant VA flow acted on the contralateral wall of BA to generate the tortuous geometry of BA, which strongly affected velocity and wall shear stress distribution [31], and finally, triggered the formation of BA plaque and affected intraplaque hemorrhage. The geometry of vertebrobasilar artery was shown to be correlated with occurrence of atherosclerotic plaques and plaque distribution [31]. Asymmetric VAs causing BA bending is a chronic process and is not only influenced by shear stress but also by vascular risk factors [31, 32]. The mechanism underlying the correlation between intraplaque hemorrhage and incomplete proximal configuration of BA also needs to be further elucidated.

This study has some limitations. First, the number of subjects is rather small and all patients come from a single stroke center, meaning that selection bias may be a concern. Second, our study population exclusively represented a high degree of stenosis, meaning that caution should be exerted when generalizing the findings.

We found that the complete configuration of BA was not associated with BA vessel features; the proximal configuration of BA was related to intraplaque hemorrhage and the distal configuration of BA was associated with strong plaque enhancement. Further studies are warranted to confirm the findings.