Division of Neurosurgery, St. Michael's Hospital, Labatt Family Centre of Excellence in Brain Injury and Trauma Research, Keenan Research Centre of the Li Ka Shing Knowledge Institute of St. Michael's Hospital and Department of Surgery, University of Toronto, Toronto, Ontario, Canada.
Stroke. 2012 Aug;43(8):2102-7. doi: 10.1161/STROKEAHA.112.658153. Epub 2012 Jun 7.
Early identification of patients at risk of angiographic vasospasm after aneurysmal subarachnoid hemorrhage (SAH) may mitigate its sequelae. One mechanism that may contribute to angiographic vasospasm is increased central sympathetic activity, which is also thought to cause electrocardiographic (ECG) changes after SAH. Here, we perform the first study to determine the association between ECG changes and angiographic vasospasm after SAH.
Exploratory analysis was performed on 413 patients from CONSCIOUS-1, a prospective randomized trial of clazosentan for the prevention of angiographic vasospasm. ECGs were obtained within 24 hours of aneurysm rupture and during the vasospasm risk period. Angiographic vasospasm was assessed using catheter angiography at baseline and 7 to 11 days after SAH. Multivariate logistic regression was used to identify significant associations.
The most prevalent finding on ECG both immediately following SAH and during the vasospasm risk period was QT prolongation (42% and 25%, respectively). A prolonged QT interval and tachycardia on the baseline ECG were associated with angiographic vasospasm (OR, 1.86; 95% CI, 1.00-3.45; and OR, 10.83; 95% CI, 1.17-100.50, respectively). QT prolongation on ECG during the vasospasm risk period was also associated with angiographic vasospasm (OR, 3.53; 95% CI, 1.67-7.39). No ECG findings were associated with delayed ischemic neurological deficit, but tachycardia and ST changes were associated with worse clinical outcome.
QT prolongation and tachycardia on ECG were independently associated with angiographic vasospasm after aneurysmal SAH on multivariate analysis.
URL: http://clinicaltrials.gov. Unique Identifier: NCT00111085.
早期识别动脉瘤性蛛网膜下腔出血(SAH)后发生血管痉挛的高危患者,可能减轻其继发损伤。一种可能导致血管痉挛的机制是中枢交感神经活性增加,这也被认为是 SAH 后心电图(ECG)改变的原因。在此,我们进行了第一项研究,以确定 SAH 后 ECG 改变与血管痉挛之间的关联。
对 CONSCIOUS-1 前瞻性随机氯苯唑沙宗预防血管痉挛试验中的 413 例患者进行探索性分析。在动脉瘤破裂后 24 小时内和血管痉挛风险期内获取 ECG。在 SAH 后 7 至 11 天使用导管血管造影术评估血管造影性血管痉挛。采用多元逻辑回归识别有意义的关联。
SAH 后即刻和血管痉挛风险期内 ECG 最常见的发现是 QT 间期延长(分别为 42%和 25%)。基线 ECG 上的 QT 间期延长和心动过速与血管造影性血管痉挛相关(OR,1.86;95%CI,1.00-3.45;OR,10.83;95%CI,1.17-100.50)。血管痉挛风险期内 ECG 上的 QT 间期延长也与血管造影性血管痉挛相关(OR,3.53;95%CI,1.67-7.39)。没有 ECG 发现与迟发性缺血性神经功能缺损相关,但心动过速和 ST 改变与更差的临床结局相关。
多元分析显示,SAH 后心电图上的 QT 间期延长和心动过速与血管造影性血管痉挛独立相关。