Augmented plasma protein C activity after coronary thrombolysis with urokinase in patients with acute myocardial infarction

Cardiology. 1992;80(3-4):252-6. doi: 10.1159/000175010.

Abstract

Coronary thrombolysis reduces morbidity and mortality in patients with acute myocardial infarction, however, the exact effects of thrombolytic agents on the status of intrinsic hemostases are not fully understood. In the present study, we examined serial changes in plasma thrombin and protein C activities of 6 patients with acute myocardial infarction treated with urokinase. Fibrinolysis occurred immediately after urokinase injection with an increase in the plasma thrombin-antithrombin III complex, suggesting a subsequent procoagulant state due to thrombin generation. Correspondent increases in plasma protein C activity were observed, however, protein S levels did not change at all. Our findings suggest that urokinase administration for coronary thrombolysis not only causes fibrinolysis, but also induces thrombin activity, which may be antagonized by augmented intrinsic protein C activity.

MeSH terms

  • Aged
  • Antithrombin III / metabolism
  • Blood Proteins / metabolism
  • Glycoproteins / metabolism
  • Humans
  • Male
  • Middle Aged
  • Myocardial Infarction / blood
  • Myocardial Infarction / drug therapy*
  • Peptide Hydrolases / metabolism
  • Protein C / metabolism*
  • Protein S
  • Thrombin / metabolism
  • Thrombolytic Therapy*
  • Urokinase-Type Plasminogen Activator / therapeutic use*

Substances

  • Blood Proteins
  • Glycoproteins
  • Protein C
  • Protein S
  • antithrombin III-protease complex
  • Antithrombin III
  • Peptide Hydrolases
  • Thrombin
  • Urokinase-Type Plasminogen Activator