ABNORMAL FIBRINOLYTIC ACTIVITY IN PATIENTS WITH CAD--IMPROVEMENT AFTER ANCROD

这项研究的目的是定义频率和可逆性 冠心病和冠心病患者纤溶活性异常 非急性缺血性胸痛综合征。组织型纤溶酶原检测 组织型纤溶酶原激活抑制物(t-PA)和α 10例顽固性心绞痛患者行2-抗纤溶酶治疗 在长期使用Ancrod治疗后，Ancrod是一种蛇毒的衍生品 具有去纤维蛋白原和间接tPA特性。我们发现 大多数重度顽固性心绞痛患者有异常的纤溶反应 休息或锻炼时的活动，这些异常可能 在Ancrod治疗期间得到改善或正常化。此外，Ancrod疗法 也延长了大多数患者的运动能力，减少了心绞痛 症状。这些初步观察表明，原始的或后天的 纤溶活性缺陷可能在缺血性胸痛中起一定作用 这种异常可以通过使用特定的药物来改善 具有溶栓特性的药剂。

The purpose of this study was to define the frequency and reversibility of abnormal fibrinolytic activity in patients with coronary artery disease and non-acute ischemic chest pain syndromes. Measurments of tissue plasminogen activate (t-PA), inhibitor of tissue plasminogen activation (IPA) and alpha 2-antiplasmin were made in 10 patients with refractory angina before and after long-term treatment using Ancrod, which is a snake vemon derivative possessing defibronogenating and indirect tPA properties. We found that most patients with severe refractory angina have abnormal fibronolytic activity either at rest or during exercise and that these abnormalities can be improved or normalized during Ancrod therapy. Moreover, Ancrod therapy also prolonged exercise capacity in most patients and reduced anginal symptoms. These preliminary observations suggest that primary or acquired deffects in fibrinolytic activity may play some role in ischemic chest pain syndromes and that such abnormalities can be improved with specific pharmaceutical agents having thrombolytic properties.