Parekh N, Venkatesh B, Cross D, Leditschke A, Atherton J, Miles W, Winning A, Clague A, Rickard C
Royal Brisbane Hospital, Herston, Australia.
J Am Coll Cardiol. 2000 Oct;36(4):1328-35. doi: 10.1016/s0735-1097(00)00857-3.
We studied the incidence of myocardial injury in aneurysmal subarachnoid hemorrhage (SAH) using the more sensitive cardiac troponin I (cTnI) assay, correlated changes in cTnI with creatine kinase, MB fraction (CK-MB), myoglobin, and catecholamine metabolite assays, and examined the predictive value of changes in cTnI for myocardial dysfunction.
Myocardial injury in aneurysmal SAH as evidenced by elevated CK-MB fraction has been reported. Little published data exist on the value of cTnI measurements in aneurysmal SAH.
Thirty-nine patients were studied for seven days. Clinical cardiovascular assessment, electrocardiographic (ECG), echocardiography, cTnI, CK, CK-MB and CK-MB index, myoglobin and 24-h urinary catecholamine assays were performed in all patients. The ECG abnormalities were defined by the presence of ST-T changes, prolonged QT intervals, and arrhythmias. An abnormal echocardiogram was defined by the presence of wall-motion abnormalities and a reduced ejection fraction. The severity of SAH was graded clinically and radiologically.
Eight patients demonstrated elevations in cTnI (upper limit of normal is 0.1 microg/liter with the immunoenzymatic assay and 0.4 microg/liter with the sandwich immunoassay), while five had abnormal CK-MB levels (upper limit of normal is 8 microg/liter). Patients with more severe grades of SAH were more likely to develop a cTnI leak (p < 0.05). Patients with cTnI elevations were more likely to demonstrate ECG abnormalities (p < 0.01) and manifest clinical myocardial dysfunction (p < 0.01) as evidenced by the presence of a gallop rhythm on auscultation and clinical or radiological evidence of pulmonary edema as compared to those with CK-MB elevations. The sensitivity and specificity of cTnI to predict myocardial dysfunction were 100% and 91%, respectively, whereas the corresponding figures for CK-MB were 60% and 94%, respectively. Elevations in myoglobin levels (upper limit of normal <70 microg/liter) and urinary catecholamine metabolites (urinary vanilmandelate/creatinine ratio upper limit of normal, 2.6) are a nonspecific finding.
Measurements of cTnI reveal a higher incidence of myocardial injury than predicted by CK-MB in aneurysmal SAH, and elevations of cTnI are associated with a higher incidence of myocardial dysfunction. Thus, cTnI is a highly sensitive and specific indicator of myocardial dysfunction in aneurysmal SAH.
我们使用更敏感的心肌肌钙蛋白I（cTnI）检测方法研究了动脉瘤性蛛网膜下腔出血（SAH）中心肌损伤的发生率，将cTnI的变化与肌酸激酶、肌酸激酶同工酶MB（CK-MB）、肌红蛋白以及儿茶酚胺代谢产物检测结果进行关联，并探讨cTnI变化对心肌功能障碍的预测价值。
已有报道称动脉瘤性SAH中存在CK-MB升高所证实的心肌损伤。关于cTnI检测在动脉瘤性SAH中的价值，公开数据较少。
对39例患者进行了为期7天的研究。对所有患者进行了临床心血管评估、心电图（ECG）、超声心动图、cTnI、CK、CK-MB及CK-MB指数、肌红蛋白和24小时尿儿茶酚胺检测。ECG异常定义为存在ST-T改变、QT间期延长和心律失常。超声心动图异常定义为存在室壁运动异常和射血分数降低。SAH的严重程度通过临床和影像学进行分级。
8例患者cTnI升高（免疫酶法正常上限为0.1μg/升，夹心免疫法正常上限为0.4μg/升），而5例患者CK-MB水平异常（正常上限为8μg/升）。SAH分级更严重的患者更易发生cTnI泄漏（p<0.05）。与CK-MB升高的患者相比，cTnI升高的患者更易出现ECG异常（p<0.01）并表现出临床心肌功能障碍（p<0.01），听诊可闻及奔马律以及有临床或影像学肺水肿证据。cTnI预测心肌功能障碍的敏感性和特异性分别为100%和91%，而CK-MB的相应数值分别为60%和94%。肌红蛋白水平升高（正常上限<70μg/升）和尿儿茶酚胺代谢产物（尿香草扁桃酸/肌酐比值正常上限为2.6）是一项非特异性发现。
在动脉瘤性SAH中，cTnI检测显示的心肌损伤发生率高于CK-MB预测的发生率，且cTnI升高与心肌功能障碍的较高发生率相关。因此，cTnI是动脉瘤性SAH中心肌功能障碍的一种高度敏感且特异的指标。
