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

本研究的目的是确定的频率和可逆性， 冠心病患者纤溶活性异常， 非急性缺血性胸痛综合征。 组织纤溶酶原的测量 激活（t-PA），组织纤溶酶原激活抑制剂（IPA）和α 2-对10例顽固性心绞痛患者术前给予抗纤溶酶， 在使用Ancrod长期治疗后，Ancrod是一种蛇vemon衍生物， 具有脱纤维和间接tPA性质。 我们发现 大多数严重难治性心绞痛患者存在纤溶异常， 活动无论是在休息或运动，这些异常可以 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， 症状 这些初步观察表明，原发性或后天性 纤溶活性的缺陷可能在缺血性胸痛中起一定作用 症状，这种异常可以改善与特定的 具有血栓溶解性质的药物制剂。

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.