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Letter by Cao et al Regarding Article, "Intracranial Extension of Extracranial Vertebral Dissection Is Associated With an Increased Risk of Ischemic Events".

To the Editor: The study by Meglio et al revealed that in a large cohort of patients with vertebral artery dissection (VAD), extracranial VAD with intracranial extension (e+iVAD) appears associated with an increased risk of ischemic stroke. Extracranial VAD is an important cause of stroke, particularly in younger individuals. It has been associated with a high risk of ischemic stroke as initial symptom, but the risk of recurrent stroke is relatively low. The CADISS (Cervical Artery Dissection in Stroke Study) demonstrated that not only was the early risk of stroke recurrence lower than that reported in some previous studies, but the later risk of stroke recurrence between 3 and 12 months was also very low. This study showed that ischemic events at admission accounted for 55%, and the mean modified Rankin Scale was 0.6 (±0.8) at 3 months. However, the incidence of stroke recurrence was not given due to the retrospective clinical data, which needs to be further confirmed by prospective studies. Little is known about the pathophysiology underlying VAD and VAD-related stroke. This study suggested that despite similar baseline characteristics, lumen stenosis or occlusion was more frequent in patients with e+iVAD. However, the exact location of infarction was not available on the prospectively collected imaging data. As the author said, this study was not able to discriminate occlusions consecutive to an embolus from occlusions related to the dissection extension itself. The intracranial extension of extracranial VAD plus vessel abnormalities might be responsible for the increased risk of initial ischemic events through embolization, hemodynamic mechanism as well as the occlusion of V4 branches by the vascular wall hematoma. Transcranial Doppler was once proved useful in helping determine the possible mechanism of VAD-related stroke and evaluating the efficacy of treatment in reducing microemboli and subsequent stroke. Combining transcranial Doppler emboli with the imaging features of infarct location and VAD might help to accurately determine the pathogenesis of ischemic events caused by VAD and guide further treatment. Additionally, the optimal strategy (antiplatelets or anticoagulants) for the prevention of ischemic stroke in patients with extracranial arterial dissection is controversial. Systematic review and meta-analysis of observational studies did not show any significant difference in the occurrence of ischemic events or deaths between patients treated with antiplatelets versus anticoagulants. CADISS also found no difference in efficacy of antiplatelets and anticoagulants at preventing stroke and death. For one thing, the rarity of stroke events meant that the study could not answer the question of which strategy was superior overall. For another, any reduction in ischemic stroke was counterbalanced by an increase in hemorrhages—1 patient developed major bleeding, and 2 had minor bleeds in the anticoagulation group, but none in the antiplatelet group. Because of the high risk of bleeding in patients with intracranial VAD, the efficacy of antithrombotic therapy has been poorly studied, empirically in favor of antiplatelets but against anticoagulants in the case of excluding bleeding. Patients with intracranial dissection in CADISS were also excluded because of contraindications to the use of antiplatelets or anticoagulants. Moreover, immediate anticoagulation is also not recommended in patients with e+iVAD. In this study, 11 (up to 38%) patients in the e+iVAD group received initial anticoagulation therapy. However, the authors did not give any specific indications for the use of anticoagulants, which should be clarified.