The mechanism of ischemic stroke in patients with dolichoectatic basilar artery
The mechanism of ischemic stroke in patients with dolichoectatic basilar artery
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DOI：
10.1111/j.1468-1331.2005.00993.x
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发表时间：
2005-06-01
影响因子：
5.1
通讯作者：
Çalli, C
中科院分区：
文献类型：
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作者：
Kumral, E;Kisabay, A;Çalli, C
基底动脉延长（BD）可能通过多种机制引起脑干缺血，包括血栓形成、栓塞、深穿透动脉闭塞等。本研究的目的是确定和表征与BD相关的脑血管事件患者的临床、影像学表现和血流动力学机制，并将这些数据与未发生卒中的BD患者的数据进行比较。我们研究了29例连续卒中，2例短暂性脑缺血发作（TIA）伴BD的患者，这些患者已入住我们的卒中单元。我们通过经颅多普勒测量基底动脉（BA）扩张的直径、分叉的高度、侧向位移、形状变形和血流速度。将影像学和血流动力学结果与18例无卒中或TIA患者的结果进行比较。梗死部位以脑桥为主，局限性单发8例（28%），多发10例（32%），累及丘脑、中脑、大脑后动脉（PCA）区。与BA分支供血区的局限性梗死患者相比，BD患者更可能发生符合多发性梗死临床和影像学模式的卒中（60% vs. 40%）。高血压和后循环动脉粥样硬化改变在脑卒中患者中比无脑卒中患者更常见（分别为P = 0.004和P = 0.028），而其他血管危险因素的发生率在两组中无显著差异。与无脑血管事件的BD患者相比，卒中/TIA患者更常出现低血流速度，但在BA中不显著（71% vs. 39%; P = 0.1）。BA血流速度降低与涉及丘脑、中脑和PCA区域的远端病变显著相关，而与位于BA分支供血区域的病变显著相关（P = 0.02）。结论：BD可能通过多种机制引起椎基底动脉系统缺血，尤其是BA血流减少和椎基底动脉系统的动脉粥样硬化改变可能促进血栓栓塞性卒中。
Basilar artery dolichoectesia (BD) may cause brainstem ischemia by multiple mechanisms, including thrombosis, embolism, occlusion of deep penetrating arteries. The objective of this study was to determine and characterize clinical, imaging findings and hemodynamic mechanisms in patients with cerebrovascular event associated with BD and compare these data with those for patients with BD who did not have stroke. We studied 29 consecutive stroke, two transient ischemic attack (TIA) patients with BD who have been admitted to our stroke unit. We sought the diameter of ectasia, height of the bifurcation, lateral displacement, shape deformities, and blood flow velocity of the basilar artery (BA) by transcranial Doppler. Imaging and hemodynamic findings were compared with those found in a group of 18 patients without stroke or TIA. The main infarct localization was pons, eight (28%) with restricted single lesion, 10 (32%) with multiple lesions involving thalamus, midbrain, posterior cerebral artery (PCA) territory. Patients with BD were more probably to have had stroke fitting a clinical and imaging patterns of multiple infarcts than those with restricted infarct in territories supplied by branches of the BA (60% vs. 40%). Hypertension and atherosclerotic changes of the posterior circulation were more frequent in patients with stroke than those without (P = 0.004 and P = 0.028, respectively), whilst the incidence of other vascular risk factors were not significantly different in two groups. Patients with stroke/TIA had more often low blood flow velocity but not significant in the BA when compared with those for BD patients without cerebrovascular event (71% vs. 39%; P = 0.1). Reduced blood flow velocity in the BA was correlated significantly with distal lesions involving thalamus, midbrain and PCA territory rather than those located in the territory supplied by branches of the BA (P = 0.02). In conclusion, it seems probably that BD may cause vertebrobasilar system ischemia by multiple mechanisms, especially reduced blood flow in the BA and atheromatous changes in the vertebrobasilar system may precipitate thromboembolic stroke.