Vertebrobasilar artery dissection is an uncommon cause of acute ischaemic stroke (AIS). Optimal endovascular management has not been established. This study aimed to share our experience with endovascular reperfusion therapy for vertebrobasilar artery occlusion due to vertebral artery dissection (VAD). We retrospectively reviewed 134 consecutive patients with AIS who received urgent endovascular reperfusion therapy between November 2017 and November 2019. Three patients diagnosed with VAD were investigated. The evaluation included mechanisms of vertebrobasilar artery occlusion due to VAD, variations in endovascular procedures, and functional outcomes. Dissections at the V3, V4 and extension of V3 to V4 segments were seen in one patient each. The mechanism of AIS was different in each patient: occlusion of the distal non-dissected artery due to an embolus from the dissection site (
distal occlusion
), haemodynamic collapse of the entire vertebrobasilar artery system due to the arterial dissection itself (
local occlusion
), or coexistence of
distal occlusion
and
local occlusion
(
tandem occlusion
). The endovascular reperfusion therapy was performed corresponding to the abovementioned mechanisms: mechanical thrombectomy for
distal occlusion
, stenting for
local occlusion
, and a combination of thrombectomy and stenting for
tandem occlusion
. In all three patients, effective recanalization and functional independence (modified Rankin Scale scores of 0–2 at 90 days after the onset) were achieved. Endovascular treatment corresponding to the individual mechanism of AIS may improve patient outcomes.
A 72-year-old man was admitted to our hospital because of right upper limb monoplegia 8 hours after the initial intravitreal injection of aflibercept, which is an inhibitor of vascular endothelial growth factor. Magnetic resonance diffusion-weighted images showed recent ischemic lesions in the left corona radiata and the right superior frontal gyrus. Laboratory findings showed mild hyperfibrinolysis. A patent foramen ovale was diagnosed on transesophageal echocardiography; however, lower-extremity ultrasonography did not detect deep vein thrombosis. The source of embolism remained unknown. A possible mechanism of cerebral emboli in the present case was a rapidly induced hypercoagulative state due to transfer of aflibercept from the vitreous body to the systemic circulation.
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