Abstract
Objectives: Patients with symptomatic atherosclerotic vertebrobasilar disease are at high risk for recurrent stroke and we have demonstrated that distal flow status is independently associated with this risk. Our aim was to assess the mechanism of recurrent strokes in these patients related to their distal flow status. Methods: Patients with symptomatic atherosclerotic vertebrobasilar disease were enrolled in a prospective longitudinal cohort study (VERiTAS) with a median follow-up of 23 months. Large-vessel flow in the posterior circulation distal to the stenosis and/or occlusion was measured on quantitative MR angiography and dichotomized into normal or low flow. Three observers, who were blinded to the distal flow status, independently reviewed the imaging done at the time of the recurrent stroke to classify the most likely stroke mechanism. Results: Ten out of 72 enrolled patients had a recurrent stroke in the posterior circulation. Four patients were determined to have embolic infarcts, four patients had infarcts caused by plaques that occluded a branch or perforating artery (junctional plaques), and two patients had imaging that suggested hemodynamic infarction. Five of the ten patients with recurrent strokes had low distal flow. Of these, two patients had hemodynamic infarcts, one patient had an embolic infarct, and two patients had a junctional plaque. None of the five patients with normal flow had hemodynamic infarcts, three patients had embolic infarcts, and two patients had a junctional plaque. Conclusion: Despite the small numbers, there seems to be a higher risk of hemodynamic infarction in patients with low flow distal to symptomatic vertebrobasilar disease than in the presence of normal distal flow. This would confirm the hypothesis that in addition to embolic strokes and those related to junctional plaque, patients with low distal flow are at risk for hemodynamic infarction. Further studies are required to determine whether flow measurements could be used to select patients who may benefit from endovascular treatment of atherosclerotic vertebrobasilar disease.
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