Naidech Andrew M, Kreiter Kurt T, Janjua Nazli, Ostapkovich Noeleen D, Parra Augusto, Commichau Christopher, Fitzsimmons Brian-Fred M, Connolly E Sander, Mayer Stephan A
Department of Neurology, Columbia University College of Physicians and Surgeons, New York, NY, USA.
Circulation. 2005 Nov 1;112(18):2851-6. doi: 10.1161/CIRCULATIONAHA.105.533620.
Cardiac troponin I (cTI) release occurs frequently after subarachnoid hemorrhage (SAH) and has been associated with a neurogenic form of myocardial injury. The prognostic significance and clinical impact of these elevations remain poorly defined.
We studied 253 SAH patients who underwent serial cTI measurements for clinical or ECG signs of potential cardiac injury. These patients were drawn from an inception cohort of 441 subjects enrolled in the Columbia University SAH Outcomes Project between November 1998 and August 2002. Peak cTI levels were divided into quartiles or classified as undetectable. Adverse in-hospital events were prospectively recorded, and outcome at 3 months was assessed with the modified Rankin Scale. Admission predictors of cTI elevation included poor clinical grade, intraventricular hemorrhage, loss of consciousness at ictus, global cerebral edema, and a composite score of physiological derangement (all P< or =0.01). Peak cTI level was associated with an increased risk of echocardiographic left ventricular dysfunction (odds ratio [OR], 1.3 per quintile; 95% CI, 1.0 to 1.7; P=0.03), pulmonary edema (OR, 2.1 per quintile; 95% CI, 1.6 to 2.7; P<0.001), hypotension requiring pressors (OR, 1.9 per quintile; 95% CI, 1.5 to 2.3; P<0.001), and delayed cerebral ischemia from vasospasm (OR, 1.3 per quintile; 95% CI, 1.07 to 1.7; P=0.01). Peak cTI levels were predictive of death or severe disability at discharge after controlling for age, clinical grade, and aneurysm size (adjusted OR, 1.4 per quintile; 95% CI, 1.1 to 1.9; P=0.02), but this association was no longer significant at 3 months.
cTI elevation after SAH is associated with an increased risk of cardiopulmonary complications, delayed cerebral ischemia, and death or poor functional outcome at discharge.
蛛网膜下腔出血（SAH）后经常出现心肌肌钙蛋白I（cTI）释放，并且与神经源性心肌损伤有关。这些升高的预后意义和临床影响仍不明确。
我们研究了253例SAH患者，这些患者因潜在心脏损伤的临床或心电图征象而接受了连续的cTI测量。这些患者来自1998年11月至2002年8月参加哥伦比亚大学SAH结局项目的441名受试者的初始队列。将cTI峰值水平分为四分位数或分类为不可检测。前瞻性记录住院期间的不良事件，并使用改良Rankin量表评估3个月时的结局。cTI升高的入院预测因素包括临床分级差、脑室内出血、发病时意识丧失、全脑水肿以及生理紊乱综合评分（所有P≤0.01）。cTI峰值水平与超声心动图左心室功能障碍风险增加相关（优势比[OR]，每五分位数为1.3；95%可信区间，1.0至1.7；P=0.03）、肺水肿（OR，每五分位数为2.1；95%可信区间，1.6至2.7；P<0.001）、需要使用升压药的低血压（OR，每五分位数为1.9；95%可信区间，1.5至2.3；P<0.001）以及血管痉挛导致的迟发性脑缺血（OR，每五分位数为1.3；95%可信区间，1.07至1.7；P=0.01）。在控制年龄、临床分级和动脉瘤大小后，cTI峰值水平可预测出院时的死亡或严重残疾（调整后的OR，每五分位数为1.4；95%可信区间，1.1至1.9；P=0.02），但这种关联在3个月时不再显著。
SAH后cTI升高与心肺并发症、迟发性脑缺血以及出院时死亡或功能结局不良的风险增加相关。
