COMPARISON OF ENZYMATIC AND ANATOMIC ESTIMATES OF MYOCARDIAL INFARCT SIZE IN MAN
COMPARISON OF ENZYMATIC AND ANATOMIC ESTIMATES OF MYOCARDIAL INFARCT SIZE IN MAN
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DOI：
10.1161/01.cir.70.5.824
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发表时间：
1984-01-01
期刊：
影响因子：
37.8
通讯作者：
ROBERTS, R
中科院分区：
文献类型：
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作者：
HACKEL, DB;REIMER, KA;ROBERTS, R
基于血浆MB肌酸激酶（MB- ck）水平的心肌梗死大小的酶促估计与尸检获得的49颗人类心脏的解剖梗死大小进行了比较。研究的患者被纳入急性梗死发作后18小时内梗死面积限制的多中心调查（MILIs）研究项目，并在5家参与医院中的1家接受治疗。梗死面积是通过在核心实验室进行CK分析的一系列血浆MB-CK测量来估计的。在尸检中获得的心脏由核心病理实验室独立研究，不知道MB-CK水平或临床结果。在数据协调中心对两个实验室的数据进行比较。在49个心脏中，12个被排除在外，要么是因为解剖梗死大小无法确定，要么是因为在MILIS研究入组时发生的梗死无法与其他梗死明确区分。在剩下的37个心脏中，36个有峰值MB-CK水平，但只有25个样本足以估计梗死面积。这25颗心脏的总体相关系数（Spearman）为0.87，表明酶对梗死面积的估计与解剖测量密切相关。在治疗组和对照组患者中，心肌梗死面积的CK估计显然是评估心肌梗死面积及其治疗效果的有效临床终点。
Enzymatic estimates of myocardial infarct size based on plasma levels of MB creatine kinase (MB-CK) were compared with anatomic infarct size in 49 human hearts obtained at autopsy. The patients studied were enrolled in the Multicenter Investigation of Limitation of Infarct Size (MILIs) study program within 18 h of the onset of acute infarction and were treated at 1 of 5 participating hospitals. Infarct size was estimated from serial measurements of plasma MB-CK made at the core laboratory for CK analysis. Hearts obtained at autopsy were studied independently by the core pathology laboratory without knowledge of the MB-CK levels or clinical results. Data from the 2 laboratories were compared at the data coordinating center. Of 49 hearts, 12 were excluded either because anatomic infarct size could not be established or because the infarct occurring at the time of enrollment in the MILIS study could not be distinguished with certainty from other infarcts. Of the remaining 37 hearts, peak MB-CK level was available in 36, but samples sufficient for estimation of infarct size were available only 25. The overall correlation coefficient (Spearman) was 0.87 for these 25 hearts, indicating the enzymatic estimates of infarct size correlate closely with anatomic measurements. CK estimates of myocardial infarct size evidently represent a valid clinical end point for assessing myocardial infarct size, and the effect of therapy thereon, in groups of treated and control patients.