急性心肌梗死患者早期纤溶活性和血管紧张素Ⅱ水平的变化及福辛普利的干预研究

Changes of Plasma Fibrinolytic Activity and Level of Angiotensin Ⅱ and Effects of Fosinopril on Them in the Early Phase in Patients with Acute Myocardial Infarction

目的探讨急性心肌梗死(AMI)患者早期纤溶活性和血管紧张素Ⅱ水平的变化及福辛普利的干预作用。方法将39例发病24 h内的AMI患者随机分为福辛普利组(21例)和常规治疗组(18例),福辛普利组在常规治疗基础上口服福辛普利(10 mg/d),检测治疗前和治疗后2周纤溶酶原激活剂抑制物-1(PAI-1)含量与活性、组织纤溶酶原激活剂(t-PA)活性及血管紧张素Ⅱ(AngⅡ)浓度,并取20名正常人作为正常对照组。结果AMI患者PAI-1含量和活性、AngⅡ水平明显高于正常对照组(P<0.01);t-PA活性明显低于正常对照组(P<0.01)。AMI患者血浆AngⅡ浓度与PAI-1含量和活性成显著正相关(r分别为0.78和0.61,均P<0.01),与t-PA活性无关(r=0.24,P>0.05)。治疗后2周福辛普利组较常规治疗组PAI-1含量和活性、AngⅡ浓度显著降低(P<0.01),t-PA活性明显升高(P<0.01)。结论AMI患者早期纤溶活性降低并与肾素-血管紧张素系统(RAS)激活有关,福辛普利通过降低AngⅡ水平可以提高AMI患者内源性纤溶活性,可能是血管紧张素转换酶(ACE)抑制剂减少AMI后再梗死事件和早期病死率的重要机制之一。

Objective To investigate the changes of plasma fibrinolytic activity and the level of angiotensin Ⅱ （Ang Ⅱ ） and the effects of fosinopril on them in the early phase in patients with acute myocardial infarction（AMI）. Methods Thirty nine patients with AMI were randomized into the fosinopril group （n = 21） and routine treatment group （n - 18）. Fosinopril group received fosinopril （10 mg/d, po） basing on routine treatment . Plasma mass concentration and activity of plasminogen activitor inhibitor type-1（PAI-1）, activity of tissue plasminogen activator （t-PA） and level of Ang Ⅱ were measured before and 2 weeks after treatment. Twenty heahhy subjects as controls. Results Compared with controls, plasma mass concentration and activity of PAI-1, level of Ang Ⅱ, was higher （P〈0.01）, activity of t PA was lower （P〈0.01） in patients with AMI. There was a positive correlation between level of Ang Ⅱ and mass concentration or activity of PAI-1（ r = 0.78, 0.61 respectively, P 〈 0.01 ）, there was no correlation between level of Ang Ⅱ and activity of t-PA（ r = 0.24, P 〉 0.05）. After 2 weeks therapy, plasma mass concentration and activity of PAI-1, level of Ang Ⅱ were significantly decreased, activity of t-PA was significantly increased in the fosinopril group than in the routine treatment group（ P 〈0.01, respectively）. Conclusion These data suggest that the activation of RAS is associated with the endogenous fibrinolytic balance in AMI. Angiotensin converting enzyme （ACE） inhibitors can improve the fibrinolytic activity by inhibiting the products of Ang Ⅱ , it may be one of the important mechanisms that ACE inhibitors reduce recurrent myocardial infarction and early mortality in patients after AMI.