According to a previous study, the formation of FTP is not related to congenital genetic factors and acquired neck activity [10]. Instead, it is mainly related to the changes noted in cerebral hemodynamics [11]. The internal carotid artery in the FTP supports both PCA and MCA. The additional presence of the occlusion of the tentorium cerebellum affects the anterior and posterior circulation of the leptomeningeal collateral circulation [12, 13]. These hemodynamic changes play an important role in the development of atherosclerosis [14–17]. Hong et al. reported that the presence of the FTP could increase the compensatory blood flow of the internal carotid artery system and reduce the vertebrobasilar blood flow [18], resulting in vascular dilation and reduced blood flow rate in MCA. Lu et al. demonstrated that the low blood flow rate could decrease Wall Shear Stress (WSS). Low WSS was closely associated with the formation of atherosclerotic plaques [19]. Endothelial cell damage and lipid deposition are caused by high WSS due to the growth of the plaque. This promotes the development of atherosclerotic plaques and positive vessel remodeling. Positive remodeling is a crucial mechanism of atherosclerotic plaque formation and is more likely to cause acute ischemic stroke [20–22].
The present study demonstrated that the FTP group was more prone to exhibit positive remodeling and had a lower degree of stenosis than the control group in MCA, whereas no significant difference was noted in the VBA plaques between the two groups. The results of Lambert et al. were consistent with the results reported in the present study [23]. In contrast to this conclusion, certain inconsistencies were noted in the data presented in the current study and those of Yang’s study. The latter supported the conclusion that patients with severe vertebral basilar intracranial stenosis and poor collateral circulation were more likely to develop positive remodeling, diffuse plaque distribution, and plaque enhancement. The difference may be due to the fact that Yang et al. included patients with posterior circulation stroke or TIA with ≥ 70% vertebral basilar intracranial stenosis [5]. By contrast, the present study included all patients with a vertebral basilar plaque and did not examine the stenosis rates of the patients in detail.
In addition, the majority of the stroke patients in the present study demonstrated enhanced plaques in MCA and VBA, which also verified that plaque enhancement was a marker of plaque instability and acute stroke [24, 25]. The previous studies demonstrated that enhanced plaques were associated with vessel wall neovascularization and inflammation[26, 27]. Our finding was similar to the result of Wang et al. that enhanced plaques in the symptomatic group were more frequent than that in the asymptomatic group[28].
The present study is one of the first studies that focus on the difference between anterior and posterior cerebral circulating artery plaques caused by FTP. By contrast, the majority of the previous studies focused on ischemic stroke as a result of changes occurring in the intracranial collateral circulation caused by FTP. Despite its novelty, the present study exhibits several limitations. Firstly, the sample size used was small and a single-center study design was used. Certain patients could not be included due to incomplete clinical data. Secondly, data processing was performed by an independent investigator and not by software, which may be subject to selective bias. Thirdly, due to low image resolution, the components of the intracranial arterial plaques were not studied.