Abstract：
UNASSIGNED: Carotid siphon calcification (CSC) serves as a marker of atherosclerosis and therefore may influence the outcome after subarachnoid hemorrhage (aSAH). We aimed to analyze the impact of CSC on neurological outcomes, ischemia, and vasospasm.
UNASSIGNED: A total of 716 patients with aSAH were treated between December 2004 and June 2016 in our central European tertiary neurovascular care center in Essen, Germany. CSC was recorded using the Woodcock scale (grades 0-3) on a computed tomography scan. Study end points included an unfavorable outcome at 6 months post-aSAH (modified Rankin Scale score ≥4), vasospasm, and early cerebral ischemia (72 hours) and delayed cerebral ischemia (delayed cerebral ischemia; >72 hours) in the follow-up computed tomography scans. The associations were adjusted for patients\' baseline characteristics and secondary complications. Finally, within a subgroup analysis, patients with and without daily aspirin intake after endovascular aneurysm occlusion were compared.
UNASSIGNED: Increasing grades of CSC were associated with lower rates of vasospasm in the anterior circulation. Severe CSC (grade 3) was independently related to the risk of an unfavorable outcome (adjusted odds ratio [aOR], 4.06 [95% CI, 1.98-8.33]; P<0.001) and early cerebral ischemia (aOR, 1.58 [95% CI, 1.03-2.43]; P=0.035) but not delayed cerebral ischemia (aOR, 1.08 [95% CI, 0.67-1.73]; P=0.763). In the aspirin subgroup analysis, the negative effect of severe CSC on functional outcome remained significant only in aSAH cases without aspirin (aOR, 5.47 [95% CI, 2.38-12.54]; P<0.001). In contrast, there was no association between severe CSC and unfavorable outcomes among individuals with daily aspirin intake (aOR, 0.84 [95% CI, 0.59-4.21]; P=0.603).
UNASSIGNED: Our data suggest CSC as a cerebrovascular risk factor resulting in higher rates of early cerebral ischemia and unfavorable outcomes after aSAH. However, by increasing arterial stiffness, CSC might lower the probability of vasospasm, which could explain the missing link between CSC and delayed cerebral ischemia. Additionally, aspirin intake seems to potentially mitigate the negative impact of CSC on aSAH outcome. Further investigations are needed to confirm the observations from the present study.
UNASSIGNED: A total of 716 patients with aSAH were treated between December 2004 and June 2016 in our central European tertiary neurovascular care center in Essen, Germany. CSC was recorded using the Woodcock scale (grades 0-3) on a computed tomography scan. Study end points included an unfavorable outcome at 6 months post-aSAH (modified Rankin Scale score ≥4), vasospasm, and early cerebral ischemia (72 hours) and delayed cerebral ischemia (delayed cerebral ischemia; >72 hours) in the follow-up computed tomography scans. The associations were adjusted for patients\' baseline characteristics and secondary complications. Finally, within a subgroup analysis, patients with and without daily aspirin intake after endovascular aneurysm occlusion were compared.
UNASSIGNED: Increasing grades of CSC were associated with lower rates of vasospasm in the anterior circulation. Severe CSC (grade 3) was independently related to the risk of an unfavorable outcome (adjusted odds ratio [aOR], 4.06 [95% CI, 1.98-8.33]; P<0.001) and early cerebral ischemia (aOR, 1.58 [95% CI, 1.03-2.43]; P=0.035) but not delayed cerebral ischemia (aOR, 1.08 [95% CI, 0.67-1.73]; P=0.763). In the aspirin subgroup analysis, the negative effect of severe CSC on functional outcome remained significant only in aSAH cases without aspirin (aOR, 5.47 [95% CI, 2.38-12.54]; P<0.001). In contrast, there was no association between severe CSC and unfavorable outcomes among individuals with daily aspirin intake (aOR, 0.84 [95% CI, 0.59-4.21]; P=0.603).
UNASSIGNED: Our data suggest CSC as a cerebrovascular risk factor resulting in higher rates of early cerebral ischemia and unfavorable outcomes after aSAH. However, by increasing arterial stiffness, CSC might lower the probability of vasospasm, which could explain the missing link between CSC and delayed cerebral ischemia. Additionally, aspirin intake seems to potentially mitigate the negative impact of CSC on aSAH outcome. Further investigations are needed to confirm the observations from the present study.
摘要：
■颈动脉虹吸钙化（CSC）是动脉粥样硬化的标志，因此可能会影响蛛网膜下腔出血（aSAH）后的预后。我们旨在分析CSC对神经系统预后的影响，缺血,还有血管痉挛.
■在2004年12月至2016年6月期间，共有716名aSAH患者在我们位于埃森的中欧三级神经血管护理中心接受了治疗，德国。在计算机断层扫描中使用Woodcock量表（0-3级）记录CSC。研究终点包括aSAH后6个月的不良结局（改良Rankin量表评分≥4），血管痉挛,和早期脑缺血（72小时）和迟发性脑缺血（迟发性脑缺血；>72小时）在后续的计算机断层扫描扫描。根据患者的基线特征和继发性并发症调整相关性。最后,在子组分析中，对血管内动脉瘤闭塞后每天服用阿司匹林和不服用阿司匹林的患者进行了比较.
■CSC分级增加与前循环血管痉挛发生率降低相关。严重CSC（3级）与不良结局的风险独立相关（调整后比值比[aOR]，4.06[95%CI，1.98-8.33]；P<0.001）和早期脑缺血（aOR，1.58[95%CI，1.03-2.43]；P=0.035)，但未延迟脑缺血(aOR，1.08[95%CI，0.67-1.73]；P=0.763）。在阿司匹林亚组分析中，严重CSC对功能结局的负面影响仅在无阿司匹林的aSAH病例中仍然显着（aOR，5.47[95%CI，2.38-12.54]；P<0.001）。相比之下,在每日服用阿司匹林的个体中，严重CSC与不良结局之间没有关联(aOR，0.84[95%CI，0.59-4.21]；P=0.603）。
■我们的数据表明，CSC是脑血管危险因素，导致aSAH后早期脑缺血的发生率更高，预后不良。然而,通过增加动脉僵硬度，CSC可能会降低血管痉挛的可能性，这可以解释CSC与迟发性脑缺血之间缺失的联系。此外,阿司匹林摄入似乎有可能减轻CSC对aSAH结局的负面影响.需要进一步的调查来证实本研究的观察结果。
■在2004年12月至2016年6月期间，共有716名aSAH患者在我们位于埃森的中欧三级神经血管护理中心接受了治疗，德国。在计算机断层扫描中使用Woodcock量表（0-3级）记录CSC。研究终点包括aSAH后6个月的不良结局（改良Rankin量表评分≥4），血管痉挛,和早期脑缺血（72小时）和迟发性脑缺血（迟发性脑缺血；>72小时）在后续的计算机断层扫描扫描。根据患者的基线特征和继发性并发症调整相关性。最后,在子组分析中，对血管内动脉瘤闭塞后每天服用阿司匹林和不服用阿司匹林的患者进行了比较.
■CSC分级增加与前循环血管痉挛发生率降低相关。严重CSC（3级）与不良结局的风险独立相关（调整后比值比[aOR]，4.06[95%CI，1.98-8.33]；P<0.001）和早期脑缺血（aOR，1.58[95%CI，1.03-2.43]；P=0.035)，但未延迟脑缺血(aOR，1.08[95%CI，0.67-1.73]；P=0.763）。在阿司匹林亚组分析中，严重CSC对功能结局的负面影响仅在无阿司匹林的aSAH病例中仍然显着（aOR，5.47[95%CI，2.38-12.54]；P<0.001）。相比之下,在每日服用阿司匹林的个体中，严重CSC与不良结局之间没有关联(aOR，0.84[95%CI，0.59-4.21]；P=0.603）。
■我们的数据表明，CSC是脑血管危险因素，导致aSAH后早期脑缺血的发生率更高，预后不良。然而,通过增加动脉僵硬度，CSC可能会降低血管痉挛的可能性，这可以解释CSC与迟发性脑缺血之间缺失的联系。此外,阿司匹林摄入似乎有可能减轻CSC对aSAH结局的负面影响.需要进一步的调查来证实本研究的观察结果。
