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Fibrinolytic parameters, lipid status and lipoprotein(a) in ischemic stroke patients

Biljana A Vucković1, Mirjana J Djerić, Tatjana A Ilić

  • 1Department of Haemostasis, Thrombosis and Haematology Diagnostics, Centre for Laboratory Medicine, Clinical Centre of Vojvodina, Novi Sad, Serbia. vuckovic.b@sbb.rs

Srpski Arhiv Za Celokupno Lekarstvo
|March 17, 2010
PubMed

Insights

Ischemic stroke patients exhibit impaired fibrinolysis, with longer clot lysis times and elevated levels of plasminogen activator inhibitor-1 (PAI-1) and tissue-type plasminogen activator (t-PA). Lipoprotein(a) (Lp(a)) may inhibit fibrinolysis through mechanisms independent of its concentration.

Area of Science:

  • Cardiovascular Research
  • Hematology
  • Biochemistry

Background:

  • Ischemic stroke is a leading cause of death and disability globally.
  • Impaired fibrinolysis and disordered lipid metabolism are recognized risk factors for ischemic stroke.

Purpose of the Study:

  • To investigate fibrinolytic parameters, lipid status, and lipoprotein(a) (Lp(a)) in Serbian ischemic stroke patients.
  • To explore associations between Lp(a) and fibrinolytic parameters in ischemic stroke.

Main Methods:

  • A study involving 60 ischemic stroke patients and 30 healthy controls.
  • Analysis of euglobulin clot lysis time, PAI-1, t-PA antigen, D-dimer, fibrinogen, plasminogen activity, and Lp(a) concentration.

Main Results:

  • Ischemic stroke patients showed significantly longer euglobulin clot lysis time and higher levels of PAI-1, t-PA antigen, and D-dimer compared to controls.
  • No significant differences were observed in fibrinogen levels or plasminogen activity between groups.
  • Lp(a) concentration did not differ between cases and controls, but multivariate analysis indicated a latent effect of Lp(a) on t-PA and PAI-1 in stroke patients.

Conclusions:

  • Ischemic stroke patients exhibit distinct fibrinolytic profiles, characterized by prolonged clot lysis and elevated PAI-1 and t-PA.
  • Lp(a) may play a role in inhibiting fibrinolysis in ischemic disease via mechanisms not directly related to its serum concentration.
Abstract

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