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Plasminogen activator inhibitor type-1 determines plasmin formation in patients with ischaemic heart disease

O D Pedersen1, J Gram, J Jespersen

  • 1Department of Clinical Biochemistry, Ribe County Hospital in Esbjerg, Denmark.

Thrombosis and Haemostasis
|May 1, 1995
PubMed

Insights

This study investigated plasminogen activator inhibitor type-1 (PAI-1) in ischemic heart disease patients, finding PAI-1 activity decreases after stimulated tissue plasminogen activator (t-PA) release. These results suggest PAI-1 influences plasmin formation in this patient group.

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Biochemistry

Background:

  • Ischemic heart disease (IHD) involves complex hemostatic and fibrinolytic system alterations.
  • Plasminogen activator inhibitor type-1 (PAI-1) is a key regulator of the fibrinolytic system.
  • The precise role of PAI-1 in controlling plasmin formation in IHD patients requires further elucidation.

Purpose of the Study:

  • To determine if plasminogen activator inhibitor type-1 (PAI-1) regulates plasmin formation in patients with ischemic heart disease.
  • To assess changes in fibrinolytic markers following stimulated release of tissue plasminogen activator (t-PA).

Main Methods:

  • Sixty-two IHD patients were studied before and after infusion of 1-desamino-8-D-arginine vasopressin (DDAVP).
  • Measurements included PAI activity, PAI-1 antigen, t-PA activity, t-PA antigen, plasmin-alpha2-antiplasmin complex (PAP-complex), and D-dimer.
  • DDAVP was administered to stimulate t-PA release from the vascular endothelium.

Main Results:

  • Following DDAVP stimulation, median plasma t-PA activity and antigen significantly increased (P < 0.0001).
  • Concurrently, median plasma PAI activity and PAI-1 antigen levels significantly decreased (P < 0.0001).
  • Median PAP-complex levels increased significantly (P < 0.0001), while D-dimer showed a slight, significant decrease (P < 0.0008).

Conclusions:

  • The study indicates that PAI-1 levels decrease following stimulated t-PA release in IHD patients.
  • This suggests PAI-1 plays a role in modulating plasmin formation within the fibrinolytic system of these patients.
  • Further research is warranted to fully understand the implications of PAI-1 dynamics in ischemic heart disease.

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