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1
Non-invasive diagnosis of arterial patency after thrombolytic treatment and its relation to prognosis.溶栓治疗后动脉通畅性的无创诊断及其与预后的关系。
Br Heart J. 1993 Jun;69(6):485-91. doi: 10.1136/hrt.69.6.485.
2
Use of creatine kinase isoforms for diagnosis of infarct artery patency after thrombolytic therapy with streptokinase.
Coron Artery Dis. 1993 Feb;4(2):201-5. doi: 10.1097/00019501-199302000-00011.
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Aspirin does not improve early arterial patency after streptokinase treatment for acute myocardial infarction.对于急性心肌梗死,阿司匹林在链激酶治疗后并不能改善早期动脉通畅情况。
Br Heart J. 1993 Jun;69(6):492-5. doi: 10.1136/hrt.69.6.492.
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Non-invasive diagnosis of infarct artery patency after acute myocardial infarction by use of serial plasma troponin T concentrations: importance of measurement of peak levels.通过连续检测血浆肌钙蛋白T浓度对急性心肌梗死后梗死动脉通畅情况进行无创诊断:峰值水平测量的重要性。
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The effects of early coronary patency on the evolution of myocardial infarction: a prospective arteriographic study.早期冠状动脉通畅对心肌梗死演变的影响:一项前瞻性血管造影研究。
Br Heart J. 1987 Oct;58(4):345-51. doi: 10.1136/hrt.58.4.345.
6
Independent impact of thrombolytic therapy and vessel patency on left ventricular dilation after myocardial infarction. Serial echocardiographic follow-up.溶栓治疗和血管通畅对心肌梗死后左心室扩张的独立影响。系列超声心动图随访。
Circulation. 1994 Aug;90(2):800-7. doi: 10.1161/01.cir.90.2.800.
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Long-term prognostic importance of patency of the infarct-related coronary artery after thrombolytic therapy for acute myocardial infarction.急性心肌梗死溶栓治疗后梗死相关冠状动脉通畅的长期预后重要性。
Circulation. 1994 Jan;89(1):61-7. doi: 10.1161/01.cir.89.1.61.
8
Early detection of coronary artery patency after thrombolysis by determination of the MM creatine kinase isoforms in patients with acute myocardial infarction. PRIMI Study Group.通过测定急性心肌梗死患者的MM肌酸激酶同工酶来早期检测溶栓后冠状动脉通畅情况。PRIMI研究组。
Am Heart J. 1992 Apr;123(4 Pt 1):846-53. doi: 10.1016/0002-8703(92)90686-p.
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High dose intravenous streptokinase in acute myocardial infarction--short and long term prognosis.急性心肌梗死大剂量静脉注射链激酶——短期和长期预后
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10
Angiographic frame counts 90 minutes after streptokinase predict left ventricular function at 48 hours following myocardial infarction.链激酶治疗90分钟后的血管造影帧数可预测心肌梗死后48小时的左心室功能。
Heart. 1999 Feb;81(2):128-33.

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The Open-Artery Hypothesis: An Overview.开放动脉假说:概述
J Thromb Thrombolysis. 1997;4(2):227-237. doi: 10.1023/a:1008842917403.
2
Non-invasive diagnosis of infarct artery patency after acute myocardial infarction by use of serial plasma troponin T concentrations: importance of measurement of peak levels.通过连续检测血浆肌钙蛋白T浓度对急性心肌梗死后梗死动脉通畅情况进行无创诊断:峰值水平测量的重要性。
Heart. 1996 May;75(5):481-5. doi: 10.1136/hrt.75.5.481.
3
Aspirin does not improve early arterial patency after streptokinase treatment for acute myocardial infarction.对于急性心肌梗死,阿司匹林在链激酶治疗后并不能改善早期动脉通畅情况。
Br Heart J. 1993 Jun;69(6):492-5. doi: 10.1136/hrt.69.6.492.
4
Comparison of five cardiac markers in the detection of reperfusion after thrombolysis in acute myocardial infarction.急性心肌梗死溶栓治疗后五种心脏标志物在再灌注检测中的比较。
Br Heart J. 1995 May;73(5):422-7. doi: 10.1136/hrt.73.5.422.

本文引用的文献

1
An improved procedure for serum creatine phosphokinase determination.一种改进的血清肌酸磷酸激酶测定方法。
J Lab Clin Med. 1967 Apr;69(4):696-705.
2
Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction.左心室收缩末期容积是心肌梗死后恢复过程中生存的主要决定因素。
Circulation. 1987 Jul;76(1):44-51. doi: 10.1161/01.cir.76.1.44.
3
Usefulness of a rapid initial increase in plasma creatine kinase activity as a marker of reperfusion during thrombolytic therapy for acute myocardial infarction.
Am J Cardiol. 1988 Jul 1;62(1):20-4. doi: 10.1016/0002-9149(88)91358-6.
4
Detection of coronary artery reperfusion with creatine kinase-MB determinations during thrombolytic therapy: correlation with acute angiography.
J Am Coll Cardiol. 1988 Apr;11(4):729-34. doi: 10.1016/0735-1097(88)90204-5.
5
GISSI-2 and the heparin controversy.
Lancet. 1990 Aug 4;336(8710):297-8. doi: 10.1016/0140-6736(90)91818-u.
6
Streptokinase and recombinant tissue plasminogen activator (rt-PA) are equally effective in treating acute myocardial infarction.
Ann Intern Med. 1991 Mar 1;114(5):417-23. doi: 10.7326/0003-4819-114-5-417.
7
Does thrombolysis in myocardial infarction (TIMI) perfusion grade 2 represent a mostly patent artery or a mostly occluded artery? Enzymatic and electrocardiographic evidence from the TEAM-2 study. Second Multicenter Thrombolysis Trial of Eminase in Acute Myocardial Infarction.
J Am Coll Cardiol. 1992 Jan;19(1):1-10. doi: 10.1016/0735-1097(92)90043-m.
8
Early detection of coronary artery patency after thrombolysis by determination of the MM creatine kinase isoforms in patients with acute myocardial infarction. PRIMI Study Group.通过测定急性心肌梗死患者的MM肌酸激酶同工酶来早期检测溶栓后冠状动脉通畅情况。PRIMI研究组。
Am Heart J. 1992 Apr;123(4 Pt 1):846-53. doi: 10.1016/0002-8703(92)90686-p.
9
Are enzymatic tests good indicators of coronary reperfusion?酶学检测是冠状动脉再灌注的良好指标吗?
Br Heart J. 1992 Feb;67(2):150-4. doi: 10.1136/hrt.67.2.150.
10
Clinical measurement of myocardial infarct size. Modification of a method for the estimation of total creatine phosphokinase release after myocardial infarction.
Circulation. 1975 Apr;51(4):614-20. doi: 10.1161/01.cir.51.4.614.

溶栓治疗后动脉通畅性的无创诊断及其与预后的关系。

Non-invasive diagnosis of arterial patency after thrombolytic treatment and its relation to prognosis.

作者信息

Norris R M, White H D, Cross D B, Woo K S, Elliott J M, Twigden D, Williams B, Johnson R N

机构信息

Cardiology Department, Green Lane Hospital, Auckland, New Zealand.

出版信息

Br Heart J. 1993 Jun;69(6):485-91. doi: 10.1136/hrt.69.6.485.

DOI:10.1136/hrt.69.6.485
PMID:8343313
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1025157/
Abstract

OBJECTIVE

To validate a simple noninvasive method with serial creatine kinase measurements for diagnosis of early patency of the infarct related artery after thrombolytic treatment with streptokinase. To investigate the relation between early patency of the infarct related artery and prognosis.

DESIGN

Patients under 76 years of age and seen within six hours of the start of prolonged chest pain and ST segment elevation were treated with streptokinase (1.5 x 10(6) U) intravenously over 30-60 minutes. Blood for measurement of total creatine kinase activity was taken at baseline and at 1, 2, 3, 4, 8, 12, 16, 20, and 24 hours after starting treatment. The rise in enzyme activity at each time from baseline was expressed as a proportion of the total rise from baseline to peak.

PATIENTS

Patients studied were in the following groups: (a) Sixty patients took part in a validation study with angiographic determination of patency of the infarct related coronary artery at 2.6 (0.3) hours (mean (SD)) after starting streptokinase. (b) A further 258 patients did not have early arteriography, but data were added to those from the 60 validation patients to find the relation between enzymatically determined early patency of the infarct related artery and 30 day mortality. (c) A further subset of 232 patients with first infarctions (including patients from groups (a) and (b) had angiocardiography at three weeks after infarction, and data were used to investigate the relation between early patency of the infarct related artery and left ventricular function.

MAIN OUTCOME MEASURES

Normalised rate of rise of creatine kinase activity at three hours after starting streptokinase in relation to angiographic patency of the infarct related coronary artery at 2.5 hours; 30 day cardiac mortality; and left ventricular function at three weeks in survivors of first infarction.

RESULTS

In the validation study, a rise in three hour creatine kinase activity of > 20% of peak occurred in 34/37 patients with initially patent infarct related coronary arteries (sensitivity 92%), and a rise to < 20% of peak occurred in 21/23 patients with initially occluded arteries (specificity 91%). In the prognostic study, 30 day mortality was 2.1% in the 191 patients with three hour creatine kinase > 20% of peak and 8.7% in the 127 patients with three hour creatine kinase < 20% of peak (p < 0.01). Angiocardiography in three week survivors of anterior infarction (n = 95) showed better left ventricular function when three hour creatine kinase was > or = 20% than when it was < 20% of peak (mean (SEM) end systolic volume 71 (5) v 96 (9) ml, p < 0.02; ejection fraction 56% (2%) v 51% (2%), NS).

CONCLUSION

Non-invasive determination of early patency of the infarct related artery by the normalised rate of rise of creatine kinase activity at three hours seems to be reliable, and may be prognostically important and of value for use in clinical trials.

摘要

目的

验证一种通过连续测定肌酸激酶来诊断链激酶溶栓治疗后梗死相关动脉早期开通情况的简单无创方法。研究梗死相关动脉早期开通与预后的关系。

设计

年龄在76岁以下、在长时间胸痛和ST段抬高开始后6小时内就诊的患者,在30 - 60分钟内静脉注射链激酶(1.5×10⁶U)。在开始治疗后的基线、1、2、3、4、8、12、16、20和24小时采集血样测定总肌酸激酶活性。每次相对于基线的酶活性升高表示为从基线到峰值总升高的比例。

患者

研究的患者分为以下几组:(a)60例患者参与了一项验证研究,在开始链激酶治疗后2.6(0.3)小时(均值(标准差))通过血管造影确定梗死相关冠状动脉的开通情况。(b)另外258例患者未进行早期血管造影,但将其数据与60例验证患者的数据相加,以寻找酶学测定的梗死相关动脉早期开通与30天死亡率之间的关系。(c)另外232例首次梗死患者的子集(包括(a)组和(b)组的患者)在梗死后3周进行了心血管造影,数据用于研究梗死相关动脉早期开通与左心室功能的关系。

主要观察指标

开始链激酶治疗后3小时肌酸激酶活性的标准化升高率与2.5小时梗死相关冠状动脉血管造影开通情况的关系;第30天的心脏死亡率;首次梗死幸存者3周时的左心室功能。

结果

在验证研究中,37例最初梗死相关冠状动脉开通的患者中有34例(敏感性92%)在3小时时肌酸激酶活性升高超过峰值的20%,2³例最初血管闭塞的患者中有21例(特异性91%)升高至峰值的20%以下。在预后研究中,191例3小时肌酸激酶超过峰值20%的患者第30天死亡率为2.1%,127例3小时肌酸激酶低于峰值20%的患者第30天死亡率为8.7%(p<0.01)。前壁梗死3周幸存者(n = 95)的心血管造影显示,3小时肌酸激酶≥峰值20%时左心室功能优于低于峰值20%时(平均(标准误)收缩末期容积71(5)对96(9)ml,p<0.02;射血分数56%(2%)对51%(2%),无显著性差异)。

结论

通过3小时时肌酸激酶活性的标准化升高率进行梗死相关动脉早期开通的无创测定似乎是可靠的,在预后方面可能很重要,并且对临床试验有价值。