摘要
目的 :探讨福辛普利对早期急性心肌梗塞 (AMI)患者纤溶活性的影响。 方法 :49例发病 2 4小时内的 AMI患者随机分福辛普利组 2 6例和常规治疗组 2 3例。常规治疗组静脉滴注硝酸甘油 ,口服肠溶阿司匹林等 ,福辛普利组在常规治疗基础上口服福辛普利 ,每次 10 mg,每日 1次。检测治疗前和治疗后 2周时血浆组织纤溶酶原激活剂 (t PA)活性、含量及其抑制物 (PAI- 1)活性。 结果 :治疗前福辛普利组和常规治疗组 t PA活性、t PA含量、PAI- 1活性无显著性差异 (P分别 >0 .0 5 )。治疗后 2周时福辛普利组 t PA活性显著高于常规治疗组 (P<0 .0 1) ,t PA含量、PAI- 1活性显著低于常规治疗组 (P分别 <0 .0 1)。 结论 :福辛普利能提高 AMI患者内源性纤溶活性 ,可能是血管紧张素转换酶抑制剂减少 AMI后再梗塞事件和早期病死率的机制之一 。
Objective:To explore the effects of fosinopril on fibrinolytic activity in the patients with early acute myocardial infarction(AMI). Methods:Forty nine patients with AMI within 24h after the onset of chest pain were randomized into fosinopril group ( n=26) and routine treatment group ( n= 23).The routine treatment group received nitroglycerin,asprin and so on.The fosinopril group received fosinopril (10 mg/d,po) basing on routine treatment.Before and after 2 weeks of therapy,plasma activity and mass concentrations of tissue plasminogen activator (tPA),activity of plasminogen activator inhibitor 1(PAI 1) were measured in all patients. Results:There were no difference in tPA activity,tPA mass concentrations,PAI 1 activity between the two groups before treatment ( p >0 05,respectively).After 2 weeks therapy,plasma tPA activity were significantly higher,tPA mass concentrations and PAI 1 activity were significantly lower in the fosinopril group than in the routine group ( p <0 01,respectively). Conclusion:Fosinopril can improve endogenous firbinolytic activity in patients with AMI,this may be one of the mechanisms that angiotensin converting enzyme (ACE) inhibitors reduce recurrent myocardial infarction and early mortality in patients after AMI.
出处
《中国循环杂志》
CSCD
北大核心
2000年第6期335-337,共3页
Chinese Circulation Journal
