Reduced synthesis of tissue plasminogen activator by vascular endothelium during acute myocardial infarction

Aust N Z J Med. 1992 Jun;22(3):261-4. doi: 10.1111/j.1445-5994.1992.tb02122.x.

Abstract

We measured levels of tissue plasminogen activator (t-PA) antigen in 100 patients within six hours of the onset of acute myocardial infarction, in 34 patients with chronic angina but no recent infarction, and in 36 normal subjects. We also assayed von Willebrand factor in the acute patients and in the normal subjects. Measurements were repeated in 40 acute patients at three weeks after myocardial infarction. Although resting levels of t-PA antigen were not significantly different from normal during myocardial infarction, the capacity of the vascular endothelium to release t-PA after five minutes of venous occlusion was impaired (p less than 0.01). The acute phase vessel wall release of von Willebrand factor was increased during acute infarction (p less than 0.01). We conclude that impairment of t-PA production is associated with acute coronary thrombosis, although it is not possible to differentiate between a causative role or a secondary response due to exhaustion of the t-PA producing mechanism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Antigens / analysis
  • Coronary Artery Disease / enzymology
  • Coronary Thrombosis / enzymology
  • Endothelium, Vascular / enzymology*
  • Female
  • Humans
  • Male
  • Middle Aged
  • Myocardial Infarction / enzymology*
  • Time Factors
  • Tissue Plasminogen Activator / biosynthesis*
  • Tissue Plasminogen Activator / immunology
  • von Willebrand Factor / biosynthesis

Substances

  • Antigens
  • von Willebrand Factor
  • Tissue Plasminogen Activator