Previous studies have shown that for one in five patients, cerebral infarction is caused by occlusion of the posterior circulation artery and the V4 segment of the VA is one of the most common locations of posterior circulation artery occlusion (13, 14). When occlusion occurred in the V4 segment of the VA, different hemodynamic changes were observed depending on occlusion sites. In occlusions that occurred distal to the PICA exit, the blood flow supplying the cerebellar hemisphere and brainstem was antegrade, as normal (15). However, if the occlusion occurred proximal to the PICA exit, in addition to the collateral circulation between the superior cerebellar artery (SCA) and the PICA (16), retrograde blood flow occurred in the segment of the ipsilateral VA distal to the PICA exit, coming from the contralateral VA. As this conforms to the characteristics of “intracerebral steal,” we name this phenomenon “V4 segment steal.”
Specifically, we define V4 segment steal as: when occlusion in the V4 segment occurs proximally to the PICA exit, the significant blood pressure gradient leads to retrograde blood flow from the contralateral VA through the junction of the vertebral basilar artery to the distal part of the ipsilateral VA. The V4 segment steal develops whenever: a) occlusion of the V4 segment of the VA occurs proximally to the PICA exit; b) the pathway from the contralateral VA to the ipsilateral PICA is patent; and c) a significant pressure gradient between the contralateral VA and the ipsilateral PICA is present. This retrograde blood flow in the distal part of the ipsilateral VA is visible on DSA.
It has been suggested that the term "vascular steal syndrome" be used only when diversion of flow is accompanied by symptoms of deficient circulation and that "steal phenomenon" or "steal effect" be used when the steal is asymptomatic (17). Common arterial steal syndromes include the subclavian artery steal (18), the vertebrobasilar artery steal and the carotid artery steal (19–21). In our study, two of five cases of new cerebral infarction were contralateral posterior circulation infarction. No obvious arterial stenosis was directly related to the infarction in one patient, and in the other, severe stenosis was present in the V1 segment of the contralateral VA. We hypothesize that the PICA of the ipsilateral VA occlusion stole blood flow from the contralateral VA, resulting in decreased blood flow in the stolen artery, thus leading to the occurrence of clinical ischemic events related to the stolen artery. We refer to this syndrome as blood steal syndrome of the V4 segment of VA. Only one case of acute infarction in the ipsilateral PICA occurred. We speculate that initiation of the V4 segment steal guarantees the blood supply source of the PICA, leading to fewer cerebral infarctions in the lower part of the cerebellar hemisphere of the medulla bulbar, the cerebellar tonsil and other important areas related to PICA (22, 23). Due to the small sample size and the use of retrospective analysis, the results of this study are inevitably limited and need to be confirmed through further research.
Our study indicates it is crucial for clinicians treating a patient with a VA occlusion to evaluate whether the occlusion site is located distal or proximal to the PICA exit, and whether the V4 segment steal is in place, since this may affect whether the patient needs further invasive treatment. This knowledge will be helpful when analyzing the clinical symptoms and prognosis of the patient and has important clinical significance.