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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 ,但有待进一步研究
Objective: To investigate the effect of fosinopril on fibrinolytic activity in patients with early acute myocardial infarction (AMI). Methods: A total of 49 patients with AMI within 24 hours of onset were randomized to receive 26 cases of fosinopril and 23 cases of conventional treatment. Conventional treatment group intravenous nitroglycerin, oral enteric-coated aspirin, fosinopril group on the basis of routine treatment of oral fosinopril, each 10 mg, 1 day. The activity, content and inhibitor of plasminogen activator (t PA) in plasma were measured before treatment and 2 weeks after treatment. Results: There was no significant difference in t PA activity, t PA content and PAI-1 activity between the fosinopril group and the conventional treatment group before treatment (P> 0.05). At 2 weeks after treatment, t PA activity in fosinopril group was significantly higher than that in conventional treatment group (P <0.01). T PA content and PAI-1 activity in fosinopril group were significantly lower than those in the conventional treatment group (P <0.01, respectively). CONCLUSIONS: Fosinopril can increase endogenous fibrinolytic activity in patients with AMI and may be one of the mechanisms by which angiotensin-converting enzyme inhibitors reduce the rate of reinfarction and early mortality after AMI. However, further study is needed