卡托普利治疗对近期无并发症心肌梗死男性患者内源性纤维蛋白溶解的影响。

Effects of captopril therapy on endogenous fibrinolysis in men with recent, uncomplicated myocardial infarction.

作者信息

Wright R A, Flapan A D, Alberti K G, Ludlam C A, Fox K A

机构信息

Cardiovascular Research Unit, University of Edinburgh, United Kingdom.

出版信息

J Am Coll Cardiol. 1994 Jul;24(1):67-73. doi: 10.1016/0735-1097(94)90543-6.

DOI:10.1016/0735-1097(94)90543-6

PMID:8006284

Abstract

OBJECTIVES

This study investigated the effects of captopril therapy on endogenous fibrinolysis in men with recent, uncomplicated myocardial infarction.

BACKGROUND

Angiotensin-converting enzyme inhibitors reduce the incidence of acute coronary syndromes in patients with mild left ventricular dysfunction after myocardial infarction. Abnormal endogenous fibrinolysis, reflected in increased levels of endogenous tissue-type plasminogen activator (t-PA) antigen and plasminogen activator inhibitor type 1 activity, is associated with an increased risk of myocardial infarction in patients with ischemic heart disease.

METHODS

In a randomized, double-blind crossover study beginning 8 weeks after uncomplicated myocardial infarction, patients received 4 weeks of placebo and 4 weeks of captopril (75 mg daily) therapy. At the end of each treatment period, we measured t-PA antigen and plasminogen activator inhibitor type 1 antigen and activity.

RESULTS

Median values in the 15 patients after placebo and in 12 normal men matched for age and body mass index were, respectively, t-PA antigen 16.0 versus 9.5 ng/ml (p = 0.001), plasminogen activator inhibitor type 1 antigen 17.3 versus 8.6 ng/ml (p = 0.29) and plasminogen activator inhibitor type 1 activity 13.2 versus 6.3 AU/ml (p = 0.04). After 4 weeks of treatment with captopril in the 15 patients, the estimated (95% confidence interval) median reduction in t-PA antigen was 7.3 ng/ml (-4.6 to -10.3 ng/ml, p = 0.001), in plasminogen activator inhibitor type 1 antigen 3.1 ng/ml (+1.5 to -8.4 ng/ml, p = 0.17) and in plasminogen activator inhibitor type 1 activity -2.2 AU/ml (-1.0 to -4.3 AU/ml, p = 0.02).

CONCLUSIONS

Treatment with captopril after uncomplicated myocardial infarction is associated with a significant decrease in elevated levels of t-PA antigen and plasminogen activator inhibitor type 1 activity. This may help to explain the reduction in risk of coronary thrombosis associated with the use of angiotensin-converting enzyme inhibitors.

摘要

目的

本研究调查了卡托普利治疗对近期发生无并发症心肌梗死男性患者内源性纤维蛋白溶解的影响。

背景

血管紧张素转换酶抑制剂可降低心肌梗死后轻度左心室功能不全患者急性冠状动脉综合征的发生率。内源性组织型纤溶酶原激活物（t-PA）抗原水平升高和1型纤溶酶原激活物抑制剂活性增加所反映的内源性纤维蛋白溶解异常，与缺血性心脏病患者心肌梗死风险增加相关。

方法

在无并发症心肌梗死后8周开始的一项随机、双盲交叉研究中，患者接受4周安慰剂治疗和4周卡托普利（每日75毫克）治疗。在每个治疗期结束时，我们测量了t-PA抗原、1型纤溶酶原激活物抑制剂抗原和活性。

结果

15例接受安慰剂治疗的患者以及12例年龄和体重指数匹配的正常男性的中位数分别为：t-PA抗原16.0对9.5纳克/毫升（p = 0.001），1型纤溶酶原激活物抑制剂抗原17.3对8.6纳克/毫升（p = 0.29），1型纤溶酶原激活物抑制剂活性13.2对6.3 AU/毫升（p = 0.04）。15例患者接受卡托普利治疗4周后，估计（95%置信区间）t-PA抗原中位数降低7.3纳克/毫升（-4.6至-10.3纳克/毫升，p = 0.001），1型纤溶酶原激活物抑制剂抗原降低3.1纳克/毫升（+1.5至-8.4纳克/毫升，p = 0.17），1型纤溶酶原激活物抑制剂活性降低-2.2 AU/毫升（-1.0至-4.3 AU/毫升，p = 0.02）。