Resuscitation from out-of-hospital cardiac arrest: Implications for cardiac enzyme estimation
Resuscitation from out-of-hospital cardiac arrest: Implications for cardiac enzyme estimation
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DOI：
10.1016/s0300-9572(96)00971-9
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发表时间：
1996-11-01
期刊：
影响因子：
6.5
通讯作者：
Cawood, P
中科院分区：
文献类型：
--
作者：
Grubb, NR;Fox, KAA;Cawood, P
背景资料：由于调查和治疗是由根本原因决定的，因此，对突发性心肌梗塞的诊断对于院外心脏骤停受害者的管理是至关重要的。体外心脏按摩和除颤引起的骨骼肌和心肌损伤可能使心肌梗死的生化诊断复杂化。目的：（a）在无心肌梗死心电图证据的院外心脏骤停幸存者中，检查累积除颤能量与血清心肌肌钙蛋白T和MB肌酸激酶（MB-CK）质量水平之间的关系;（B）在这种情况下，使用MB-CK质量和肌钙蛋白T重新评估心肌梗死的诊断阈值。方法：对77例院外心脏骤停患者进行研究。在入院的前4天获得血清用于MB-CK质量、CK和肌钙蛋白T估计。根据心电图标准将患者分为三组：第1组，心肌梗死;第2组，无梗死证据;第3组，可疑心电图。计算记录的最高生化标记物水平与除颤能量的相关系数。受试者操作特征图用于确定第1组和第2组受试者的最佳生化诊断阈值。结果如下：使用预先确定的标准，27名患者有心肌梗死，34名没有心肌梗死，16名心电图可疑。在第2组中，除颤能量与肌钙蛋白T对数（r = 0.42，P < 0.05）、MB-CK质量对数（r = 0.51，P < 0.01）和总CK（r = 0.68，P < 0.001）显著相关。在第1组和第2组中，MB-CK质量和肌钙蛋白T比MB-CK分数提供了额外的诊断价值（P < 0.001）。通过调整冲击能量并不能提高诊断准确性。肌钙蛋白T的最佳阈值为4 ng/ml（敏感性88%，特异性95%），MB-CK质量的最佳阈值为60 ng/ml（敏感性88%，特异性88%），MB-CK分数的最佳阈值为总CK的8%（敏感性74%，特异性82%）。应谨慎解释这些值，因为本研究因排除心电图诊断不确定的患者而受到限制。结论：骨骼肌和心肌损伤发生在院外心脏骤停的幸存者中，并且与复苏的持续时间有关。这使潜在心肌梗死的生化诊断复杂化。需要MB-CK和肌钙蛋白T的特定高诊断阈值来优化诊断准确性。由于复苏后肌肉CK释放的变异性，使用MB-CK分数导致更大的诊断错误。
Background: diagnosis of precipitating myocardial infarction is essential for management of victims of out-of-hospital cardiac arrest, since investigations and treatment are determined by the underlying cause. Skeletal muscle and myocardial damage from external cardiac massage and defibrillation may complicate biochemical diagnosis of myocardial infarction. Objectives: (a) to examine the relationship between cumulative defibrillation energy and serum levels of cardiac troponin T and MB creatine kinase (MB-CK) mass in out-of-hospital cardiac arrest survivors without electrocardiographic evidence of myocardial infarction; (b) to reassess diagnostic thresholds for myocardial infarction using MB-CK mass and troponin T in this setting. Methods: 77 victims of out-of-hospital cardiac arrest were studied. Serum was obtained for MB-CK mass, CK and troponin T estimation on the first 4 days of admission. Patients were divided into three groups using electrocardiographic criteria: group 1, myocardial infarction, group 2, no evidence of infarction; and group 3, equivocal electrocardiograms. Correlation coefficients were calculated for highest recorded levels of the biochemical markers versus defibrillation energy. Receiver-operating characteristic plots were used to determine optimum biochemical diagnostic thresholds for subjects in groups 1 and 2. Results: using predefined criteria, 27 patients had myocardial infarction, 34 did not have myocardial infarction and 16 had equivocal electrocardiograms. Significant correlations were found for defibrillation energy versus log troponin T (r = 0.42, P < 0.05), log MB-CK mass (r = 0.51, P < 0.01) and total CK (r = 0.68, P < 0.001) in group 2. Within groups 1 and 2, MB-CK mass and troponin T provided additional diagnostic value over MB-CK fraction (P < 0.001). Diagnostic accuracy was not improved by adjusting for shock energy. The optimum threshold value was 4 ng/ml for troponin T (sensitivity 88%, specificity 95%), 60 ng/ml for MB-CK mass (sensitivity 88%, specificity 88%) and 8% of total CK for MB-CK fraction (sensitivity 74%, specificity 82%). These values should be interpreted with caution, since this study is limited by the exclusion of patients with uncertain electrocardiographic diagnoses into group 3. Conclusions: skeletal muscle and myocardial damage occurs in survivors of out-of-hospital cardiac arrest and is related to the duration of resuscitation. This complicates biochemical diagnosis of underlying myocardial infarction. Specific high diagnostic threshold values for MB-CK and troponin T are needed to optimise diagnostic accuracy. The use of MB-CK fraction leads to greater diagnostic error because of the variability of muscle CK release after resuscitation.