INCREASED CIRCULATING PLASMINOGEN-ACTIVATOR INHIBITOR-1 IN PATIENTS WITH PATENT FEMORODISTAL VENOUS BYPASS

Citation
S. Peltonen et al., INCREASED CIRCULATING PLASMINOGEN-ACTIVATOR INHIBITOR-1 IN PATIENTS WITH PATENT FEMORODISTAL VENOUS BYPASS, Thrombosis research, 82(4), 1996, pp. 369-377
Citations number
32
Categorie Soggetti
Hematology,"Cardiac & Cardiovascular System","Peripheal Vascular Diseas
Journal title
ISSN journal
00493848
Volume
82
Issue
4
Year of publication
1996
Pages
369 - 377
Database
ISI
SICI code
0049-3848(1996)82:4<369:ICPIIP>2.0.ZU;2-Q
Abstract
Veins used for arterial bypass grafting undergo wall remodeling when e xposed to altered flow, which may affect fibrinolytic mechanisms and s ubsequently the fate of the graft. Our aim was to study the extent of blood coagulation and fibrinolysis activation in 27 patients with pate nt grafts two years after femoro-distal bypass surgery. The two matche d control groups included 10 and 19 conservatively treated patients ha ving similar degree of arterial insufficiency (mean ankle/brachial blo od pressure index) as the bypass group pre- and post-operatively, resp ectively. Plasma samples for coagulation and fibrinolysis activation w ere determined using ELISA and chromogenic assays. When compared with the control groups circulating tissue-type plasminogen activator antig en, and especially plasminogen activator inhibitor type-1, PAI-1 antig en and activity were significantly increased, the mean increase rangin g between 54% and 140% in the bypass group. Thrombin-antithrombin III complex, fibrinogen, and C-reactive protein, did not differ, while tri glycerides were elevated in the bypass group. Ten patients in the bypa ss group were insulin resistent, but this did not explain the differen ces in the fibrinolytic parameters between the bypassed and control pa tients. Patients with peripheral vein grafts had upregulation of PAI-I in their circulation implying reduced fibrinolytic capacity. Increase d PAI-1, a risk factor for venous thrombosis, might reflect developing intimal hyperplasia, and it remains to be studied whether upregulatio n of PAI-1 in venous grafts associates with graft failure.