Aznar J, Estellés A, Tormo G, Sapena P, Tormo V, Blanch S, España F
Department of Clinical Pathology, Hospital La Fe, Valencia, Spain.
Br Heart J. 1988 May;59(5):535-41. doi: 10.1136/hrt.59.5.535.
Several fibrinolytic variables, including plasminogen activator inhibitor activity, were studied before and after exercise in 67 normolipidaemic patients with coronary artery disease and in 25 hyperlipidaemic patients with coronary artery disease. Before exercise plasminogen activator inhibitor activity was higher in the patient groups than in a group of 10 healthy volunteers. For those who were normolipidaemic plasminogen activator inhibitor activity was greater in patients with angina pectoris who had had a myocardial infarction. The concentration of antigenic tissue-type plasminogen activator was similar in all the patients with coronary artery disease and higher than in the control group. After the exercise test fibrinolytic capacity was lower in the patients with angina pectoris and a previous history of myocardial infarction. After exercise both the released immunological tissue-type plasminogen activator and fibrinolytic capacity were lower in the hyperlipidaemic patients than in the normolipidaemic patients. The concentration of plasminogen activator inhibitor was also higher in the hyperlipidaemic patients. Patients with hyperlipidaemia IV had the highest plasminogen activator inhibitor activity. The increase in plasminogen activator inhibitor activity found in the patients was partially inhibited by antiserum against plasminogen activator inhibitor-1 in vitro. The formation of a complex of about 115,000 daltons between plasminogen activator inhibitor and purified tissue-type plasminogen activator was detected by a zymographic fibrin technique. These findings show that in patients with coronary artery disease fibrinolytic activity is impaired by an increase in plasminogen activator inhibitor. Impaired fibrinolysis may be related to the clinical evolution of coronary artery disease in these patients.
在67例血脂正常的冠心病患者和25例血脂异常的冠心病患者中,研究了运动前后包括纤溶酶原激活物抑制剂活性在内的几个纤溶变量。运动前,患者组的纤溶酶原激活物抑制剂活性高于10名健康志愿者组成的对照组。对于血脂正常的患者,曾发生过心肌梗死的心绞痛患者的纤溶酶原激活物抑制剂活性更高。所有冠心病患者的抗原性组织型纤溶酶原激活物浓度相似,且高于对照组。运动试验后,有心绞痛且有心肌梗死病史的患者纤溶能力较低。运动后,血脂异常患者释放的免疫组织型纤溶酶原激活物和纤溶能力均低于血脂正常的患者。血脂异常患者的纤溶酶原激活物抑制剂浓度也更高。IV型高脂血症患者的纤溶酶原激活物抑制剂活性最高。患者中发现的纤溶酶原激活物抑制剂活性增加在体外被抗纤溶酶原激活物抑制剂-1抗血清部分抑制。通过酶谱纤维蛋白技术检测到纤溶酶原激活物抑制剂与纯化的组织型纤溶酶原激活物之间形成了约115,000道尔顿的复合物。这些发现表明,在冠心病患者中,纤溶酶原激活物抑制剂增加会损害纤溶活性。纤溶功能受损可能与这些患者冠心病的临床进展有关。