Markers of fibrinolytic potency and clotting activation in stable angina pectoris: role of urokinase, assessment of atrioventricular differences and correlation with coronary patency
Ja. Paramo et al., Markers of fibrinolytic potency and clotting activation in stable angina pectoris: role of urokinase, assessment of atrioventricular differences and correlation with coronary patency, FIBRINOL PR, 13(3), 1999, pp. 133-138
To characterize the extent of activation of the hemostatic system and to de
tect local alterations which may favour thrombus formation we obtained samp
les from the right atrium (RA) and left ventricle (LV) of 60 stable angina
patients (mean age 59 years, M/F: 49/11) during the cardiac catheterization
procedure. None of the patients had a recent myocardial infarction or angi
oplasty. Plasma was prepared from citrated blood samples and the following
parameters were determined: thrombin-antithrombin (TAT) complexes, prothrom
bin fragment 1+2 (F1+2), plasmin-antiplasmin (PAP) complexes, tissue-type p
lasminogen activator (t-PA), plasminogen activator inhibitor (PAI-1) activi
ty and the levels of both u-PA activity (scu-PA) and antigen (u-PA Ag). Res
ults were correlated with the angiographic findings. The analysis of the di
fferent parameters analyzed between patients with coronary stenosis or occl
usion in one or more vessels (n=47) and without occlusion (n=13), showed no
differences for TAT, PAP, F1+2, and PAI-1 activity between groups. However
, a significant increase of t-PA antigen could be demonstrated in patients
with occlusion (10.5+/-4.9 ng/ml) as compared to those with angiographicall
y-verified coronary patency (7.5+/-3.2 ng/ml) (P<0.03), suggesting that t-P
A may be a good marker for occlusion in these patients. u-PA results showed
the lowest ratio in the more severe patients (59 vs 66%) (P<0.05). The scu
-PA/u-PA ratio was also significantly reduced in the sample taken from RA a
s compared with LV (P<0.001). Our results point to an enhanced local activa
tion of the fibrinolytic system in the more severe patients with stable ang
ina pectoris and to atrioventricular differences in the u-PA components.