Thromb Haemost 1992; 68(03): 321-324
DOI: 10.1055/s-0038-1656373
Original Article
Schattauer GmbH Stuttgart

Tissue Plasminogen Activator Release in Chronic Venous Hypertension due to Heart Failure

Irena Keber
The University Medical Centre, Trnovo Hospital of Internal Medicine, Ljubljana, Slovenia
,
Dušan Keber
The University Medical Centre, Trnovo Hospital of Internal Medicine, Ljubljana, Slovenia
,
Mojca Stegnar
The University Medical Centre, Trnovo Hospital of Internal Medicine, Ljubljana, Slovenia
,
Nina Vene
The University Medical Centre, Trnovo Hospital of Internal Medicine, Ljubljana, Slovenia
› Author Affiliations
Further Information

Publication History

Received 10 February 1992

Accepted after revision 06 April 1992

Publication Date:
04 July 2018 (online)

Preview

Summary

In order to study the effects of chronic venous hypertension due to heart failure on blood fibrinolytic activity, tissue plasminogen activator (t-PA) antigen, plasminogen activator inhibitor 1 (PAI-1) antigen, t-PA activity and PAI activity were measured before and after venous occlusion of the arm for 20 min in 15 patients with right-sided heart failure, 15 patients with left-sided heart failure, and 30 control healthy subjects. Central venous pressure, measured by observing the jugular veins, was above 15 cm of the blood column in all patients with right-sided heart failure, and normal (below 8 cm) in all patients with left-sided heart failure and control subjects. There was no difference in the basal concentrations of t-PA (11.0, 10.2 and 10.8 ng/ml; all values medians) and PAI-1 antigens and their activities between right and left-sided heart failure and the control subjects. After the occlusion, t-PA antigen increased significantly less in right-sided heart failure (28.6 ng/ml) than in left-sided heart failure and the control subjects (54.5 and 45.9 ng/ml, respectively). It was concluded that the poor increase in fibrinolytic activity that had already been reported in patients with heart failure, was due to low t-PA release during occlusion and not to a high basal PAI level. It was limited to the patients with right-sided heart failure and was probably the consequence of chronic systemic venous hypertension.