Fifty-four patients with Q-wave acute
myocardial infarction (AMI) were treated with
heparin combined with intravenous
single-chain urokinase-type plasminogen activator (prourokinase). To determine the optimal treatment regimen, prourokinase was applied in 3 different ways: group I received a bolus of 7.5 mg and a subsequent infusion of 40.5 mg over 60 minutes. Patency of the
infarct artery was observed in 7 patients (50%) at the end of the infusion time. One hour after the end of the infusion the
fibrinogen level had decreased to 87 +/- 12% of the preinfusion level; the
plasminogen and
alpha-2 antiplasmin levels to 61 +/- 13% and 59 +/- 34%, respectively. In group II prourokinase was administered as a 7.5 mg bolus followed by 66.5 mg over 60 minutes. Eleven patients (55%) had patent
infarct-related coronary arteries and
fibrinogen,
plasminogen and
alpha-2 antiplasmin levels had decreased to 58 +/- 29%, 38 +/- 18% and 21 +/- 14%, respectively. Group III was treated with a bolus of 3.7 mg prourokinase and 250,000 IU
urokinase followed by 44.3 mg prourokinase, resulting in a patency rate of 65% (13 patients).
Fibrinogen,
plasminogen and
alpha-2 antiplasmin levels decreased to 76 +/- 15%, 67 +/- 15% and 47 +/- 29%, respectively.
Fibrin-specific thrombolysis can be achieved with glycosylated prourokinase. At higher dosages considerable systemic activation of the fibrinolytic system with little enhancement of the observed
therapeutic effect occurred. The combination of prourokinase and
urokinase yielded a higher patency rate than either dosage of prourokinase alone, although the difference was not statistically significant in this pilot trial.