抄録
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 4 h and 16 h 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 4 h after the initiation of thrombolysis was significantly lower in the mutant tPA group than in the rtPA group (8.74±5.46 IU/L vs 26.74±3.35 IU/L, p<0.01). There was a one mild peak in serial plasma PAI activity levels 24 h 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. (Jpn Circ J 1998; 62: 801 - 806)
