A sub-set of patients with nonacute vertebrobasilar artery occlusion (VBAO) suffers recurrent ischemic events and progressive disability despite intensive medical therapy. Optimal management in these patients is unknown, and there is little literature to guide therapy. Recently, revascularization with stenting has been tried [1, 2]. However, the efficacy is unsure.
We report on 27 patients (24 men, three women; age, 57 ± 10 years) with symptomatic intracranial VBAO beyond 24 h who received revascularization with stenting. The median time between onset of symptoms and revascularization was 1·5 months [interquartile range (IQR), 0·7–3·4], and that between imaging-documented occlusion and revascularization was 9·5 (IQR, 6–18) days.
Successful revascularization, which was defined as Thrombolysis in Myocardial Infarction  ≥2 of antegrade blood flow through the recanalized portion, was achieved in 26 of 27 patients. The median mRSs (modified Rankin Scale) were 4 (IQR, 2–5) 24 h before operation and 3 (IQR, 1–5) six-days after operation (T = 46, P = 0·0016). Five (19%) periprocedural complications occurred. Of them, one caused death, two caused NIHSS (National Institutes of Health Stroke Scale) increase with 3 and 5 scores, and two were solved without new symptoms and NIHSS increase.
The latest mean duration of clinical follow-up was 10·5 ± 6·6 months in 27 patients. The median mRS was 2 (IQR, 1–4). The proportion of patients with mRS ≤ 2 increased from 27·34% preventive to 61·54%. One transient ischemic attack, two strokes, and two deaths (both died of multiple organ failure) occurred postoperatively. The mean angiographic follow-up was 8·6 ± 3·5 months in nine patients. During this period, two patients developed in-stent restenosis and one reocclusion. Two of them were symptomatic.
Our results suggested that revascularization with stenting of nonacute VBAO is technically feasible and probably of benefit in appropriately selected patients. It can prevent from recurrent ischemic event and promote functional recovery, which may be due to the reperfusion of the hemodynamic compromise and neuroplasticity  in poststroke brain. However, the high risk of complication should prompt extreme caution.