Ogata N, Ogawa H, Ogata Y, Numata Y, Morigami Y, Suefuji H, Soejima H, Sakamoto T, Yasue H
Department of Cardiology, Japanese Red Cross Kumamoto Hospital, Kumamoto University School of Medicine, Honjo, Japan.
Jpn Circ J. 1998 Nov;62(11):801-6. doi: 10.1253/jcj.62.801.
The fibrinolytic capacity of patients with acute myocardial infarction (AMI) is known to be impaired. The primary regulatory element of the fibrinolytic system is plasminogen activator inhibitor (PAI). It has been previously observed that there are 2 peaks in the plasma PAI level of AMI patients at 4h and 16h after thrombolytic therapy with recombinant tissue plasminogen activator (rtPA). Lanoteplase/SUN9216 is a mutant tPA with a biological half-life longer than that of rtPA. Thrombolytic therapy with mutant tPA or rtPA was carried out consecutively in 21 patients with AMI (8 patients as the mutant tPA group, and 13 patients as the rtPA group). The recanalization time of the mutant tPA group was significantly faster than that of the rtPA group (16.1 +/- 3.9 min vs 39.6 +/- 4.8 min, p<0.01). The PAI activity at 4h after the initiation of thrombolysis was significantly lower in the mutant tPA group than in the rtPA group (8.74 +/- 5.46IU/L vs 26.74 +/- 3.35 IU/L, p<0.01). There was a one mild peak in serial plasma PAI activity levels 24h after the initiation of thrombolysis. The results suggest that thrombolytic therapy with mutant tPA reduced the impairment of fibrinolytic capacity. The mutant tPA gives faster recanalization and lower PAI activity after successful thrombolysis, compared with rtPA.
已知急性心肌梗死（AMI）患者的纤溶能力受损。纤溶系统的主要调节因子是纤溶酶原激活物抑制剂（PAI）。此前观察到，在使用重组组织纤溶酶原激活剂（rtPA）进行溶栓治疗后4小时和16小时，AMI患者血浆PAI水平出现两个峰值。拉诺替普酶/SUN9216是一种突变型tPA，其生物学半衰期比rtPA长。对21例AMI患者连续进行了突变型tPA或rtPA溶栓治疗（8例为突变型tPA组，13例为rtPA组）。突变型tPA组的再通时间明显快于rtPA组（16.1±3.9分钟对39.6±4.8分钟，p<0.01）。溶栓开始后4小时，突变型tPA组的PAI活性明显低于rtPA组（8.74±5.46IU/L对26.74±3.35IU/L，p<0.01）。溶栓开始后24小时，连续血浆PAI活性水平出现一个轻度峰值。结果表明，突变型tPA溶栓治疗减少了纤溶能力的损害。与rtPA相比，突变型tPA在成功溶栓后再通更快，PAI活性更低。
