Fibrinolytic parameters, lipid status and lipoprotein(a) in ischemic stroke patients.
BACKGROUND
Ischemic stroke is the third leading cause of mortality and morbidity in most countries in the world. Impaired fibrinolysis, as well as disordered lipid metabolism have been recognized as risk factors for this disease.


OBJECTIVE
To study some of fibrinolytic parameters, lipid status and lipoprotein(a) - Lp(a) in ischemic stroke patients in Serbia and to examine associations between Lp(a) and fibrinolytic parameters.


METHODS
Sixty ischemic stroke patients (case group, mean age 63.48 +/- 9.62 years) and 30 age and sex matched healthy controls (control group, mean age 60.2 +/- 7.96 years) were studied.


RESULTS
A significantly longer euglobulin clot lysis time (219.7 +/- 78,8 min. vs 183.5 +/- 58,22 min; p = 0.005) and higher levels of plasminogen activator inhibitor-1 (PAI-1) (48.5 +/- 17.1 ng/ml vs 27.1 +/- 10.1 ng/ml; p = 6.2 x 10(-11)), tissue-type plasminogen activator antigen (t-PA) (11.1 +/- 7.14 ng/ml vs 6.0 +/- 3.66 ng/ml; p = 5.2 x 10(-5)) and D-dimer (382.27 +/- 504.22 ng/ml vs 116.12 +/- 88.81 ng/ml; p = 0.0002) were found in cases compared to controls. There were no significant differences in fibrinogen levels (4.30 +/- 0.84 g/l vs 4.09 +/- 0.64 g/l; p = 0.23) or plasminogen activity (92.67 +/- 11.37% vs 96.87 +/- 9.48%; p = 0.085). There was no significant difference in Lp(a) concentration between cases and controls (0.15 +/- 0.11 g/l vs 0.12 +/- 0.11 g/l; p = 0.261). However, in the cases, but not in the controls, multivariate analysis of associations between fibrinolytic parameters and Lp(a) showed the highest correlation between t-PA and PAI-1, and the latent effect of Lp(a) on t-PA and PAI-1.


CONCLUSIONS
Our results show that there are important differences in the characteristics of the fibrinolytic mechanism in ischemic stroke patients compared to healthy population. The major differences are prolonged euglobulin clot lysis time and elevated PAI-1 and t-PA antigen in ischemic stroke patients. In addition, Lp(a) appears to be involved in the inhibition offibrinolysis in ischemic disease through a mechanism unrelated to its serum concentrations.
Vucković
Biljana A
BA
Department of Haemostasis, Thrombosis and Haematology Diagnostics, Centre for Laboratory Medicine, Clinical Centre of Vojvodina, Novi Sad, Serbia. vuckovic.b@sbb.rs
Djerić
Mirjana J
MJ
Ilić
Tatjana A
TA
Canak
Visnja B
VB
Kojić-Damjanov
Suncica Lj
SLj
Zarkov
Marija G
MG
Cabarkapa
Velibor S
VS
D000368:Aged; D000369:Aged, 80 and over; D000933:Antifibrinolytic Agents / Q000097:blood; D001780:Blood Coagulation Tests; D002545:Brain Ischemia / Q000097:blood* / Q000150:complications; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005342:Fibrinolysis; D006801:Humans; D008055:Lipids / Q000097:blood*; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D020521:Stroke / Q000097:blood* / Q000209:etiology; D010959:Tissue Plasminogen Activator / Q000097:blood
D000933:Antifibrinolytic Agents; D005338:Fibrin Fibrinogen Degradation Products; D008055:Lipids; D017270:Lipoprotein(a); D017395:Plasminogen Activator Inhibitor 1; C036309:fibrin fragment D; D010959:Tissue Plasminogen Activator