Letter by Kvernland et al Regarding Article, "Stroke Mechanisms in Symptomatic Intracranial Atherosclerotic Disease: Classification and Clinical Implications".
Letter by Kvernland et al Regarding Article, "Stroke Mechanisms in Symptomatic Intracranial Atherosclerotic Disease: Classification and Clinical Implications".
复制标题
DOI:
10.1161/strokeaha.119.027673
复制
发表时间:
2019-11
期刊:
影响因子:
8.3
通讯作者:
Alexandra Kvernland;S. Yaghi;A. D. de Havenon
中科院分区:
文献类型:
--
作者:
Alexandra Kvernland;S. Yaghi;A. D. de Havenon
The recent article by Feng et al, 1 “Stroke Mechanisms in Symptomatic Intracranial Atherosclerotic Disease: Classification and Clinical Implications,” is an interesting analysis of stroke mechanisms in symptomatic intracranial atherosclerosis (ICAS), which is crucial for identifying the most effective secondary prevention therapies. The authors report good-to-excellent intrarater and interrater agreement classifying the probable mechanism of the index stroke event. Patients were followed for 1 year to determine the rate of recurrent stroke or transient ischemic attack in the index stroke parent artery’s vascular distribution. The authors found a higher risk of recurrence in patients with a mix of arteryto-artery embolism and hypoperfusion. This study has several major limitations. First, only 17 patients had recurrent stroke in 1 year. The low number of outcome events prevented several crucial analyses, the most important of which is analyzing which of the infarct patterns is associated with the high risk of recurrence. In addition, due to the small number of outcomes, the authors could not adjust for important potential confounders, such as stenosis severity of the qualifying symptomatic ICAS, collateral status, or differences in medical management. Second, hypoperfusion was present in at least 91 patients (59.4%; 46 with isolated hypoperfusion and 45 with artery-toartery embolism and hypoperfusion). On the contrary, 50%(61 of 122) of patients had< 70% stenosis of the affected artery. Therefore, some patients with luminal stenosis< 70% were coded as border-zone infarcts, which contradicts prior studies showing that impaired cerebral blood flow is unlikely when the luminal stenosis is< 75%. 2Third, this study does not differentiate between cortical and internal border-zone infarcts, which may not portend a similar risk of recurrence. 3 In fact, one study suggests that while internal border-zone infarcts are likely related to impaired distal perfusion, cortical border-zone infarcts are more likely related to reduced clearance of emboli in the cortical border-zone territory and less likely related to severe stenosis, occlusion, or impaired distal perfusion. 4