Department of Neurology, Washington University School of Medicine, Campus Box 8111, 660 S Euclid Avenue, S Louis, MO 63110, USA.
Stroke. 2012 Jul;43(7):1788-94. doi: 10.1161/STROKEAHA.111.646836. Epub 2012 Apr 5.
Angiographic vasospasm frequently complicates subarachnoid hemorrhage and has been implicated in the development of delayed cerebral ischemia. Whether large-vessel narrowing adequately accounts for the critical reductions in regional cerebral blood flow underlying ischemia is unclear. We sought to clarify the relationship between angiographic vasospasm and regional hypoperfusion.
Twenty-five patients with aneurysmal subarachnoid hemorrhage underwent cerebral catheter angiography and 15O-positron emission tomographic imaging within 1 day of each other (median of 7 days after subarachnoid hemorrhage). Severity of vasospasm was assessed in each intracranial artery, whereas cerebral blood flow and oxygen extraction fraction were measured in 28 brain regions distributed across these vascular territories. We analyzed the association between vasospasm and perfusion and compared frequency of hypoperfusion (cerebral blood flow<25 mL/100 g/min) and oligemia (low oxygen delivery with oxygen extraction fraction≥0.5) in territories with versus without significant vasospasm.
Twenty-four percent of 652 brain regions were supplied by vessels with significant vasospasm. Cerebral blood flow was lower in such regions (38.6±12 versus 48.7±16 mL/100 g/min), whereas oxygen extraction fraction was higher (0.48±0.19 versus 0.37±0.14, both P<0.001). Hypoperfusion was seen in 46 regions (7%), but 66% of these were supplied by vessels with no significant vasospasm; 24% occurred in patients without angiographic vasospasm. Similarly, oligemia occurred more frequently outside territories with vasospasm.
Angiographic vasospasm is associated with reductions in cerebral perfusion. However, regional hypoperfusion and oligemia frequently occurred in territories and patients without vasospasm. Other factors in addition to large-vessel narrowing must contribute to critical reductions in perfusion.
血管痉挛常并发于蛛网膜下腔出血，并与迟发性脑缺血的发生有关。目前尚不清楚大血管狭窄是否足以解释导致缺血的区域性脑血流的严重减少。我们旨在阐明血管痉挛与区域性灌注不足之间的关系。
25 例颅内动脉瘤性蛛网膜下腔出血患者在发病后 1 天内（蛛网膜下腔出血后中位数 7 天）分别进行了脑血管造影和 15O-正电子发射断层扫描成像。评估每支颅内动脉的血管痉挛严重程度，同时测量 28 个分布于这些血管区域的脑区的脑血流和氧摄取分数。我们分析了血管痉挛与灌注之间的关系，并比较了存在和不存在显著血管痉挛的区域的低灌注（脑血流<25 mL/100 g/min）和低氧血症（氧输送低伴氧摄取分数≥0.5）的频率。
652 个脑区中有 24%的区域由存在显著血管痉挛的血管供血。这些区域的脑血流较低（38.6±12 比 48.7±16 mL/100 g/min），而氧摄取分数较高（0.48±0.19 比 0.37±0.14，均 P<0.001）。有 46 个区域（7%）存在低灌注，但其中 66%的区域由没有显著血管痉挛的血管供血；24%的患者没有血管造影性血管痉挛。同样，低氧血症也更常发生在血管痉挛区域之外。
血管造影性血管痉挛与脑灌注减少有关。然而，区域性低灌注和低氧血症经常发生在没有血管痉挛的区域和患者中。除了大血管狭窄之外，其他因素也必须对灌注的严重减少起作用。
