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Thromb Haemost 2001; 86(02): 557-562
DOI: 10.1055/s-0037-1616086
Review Article
Schattauer GmbH

Impairment of the Plasmin Activation System in Primary Pulmonary Hypertension: Evidence for Gender Differences

Günter Christ
1   Department of Cardiology, Department of Vascular Biology and Thrombosis Research
,
Senta Graf
1   Department of Cardiology, Department of Vascular Biology and Thrombosis Research
,
Renate Huber-Beckmann
1   Department of Cardiology, Department of Vascular Biology and Thrombosis Research
,
Gerlinde Zorn
1   Department of Cardiology, Department of Vascular Biology and Thrombosis Research
,
Irene Lang
1   Department of Cardiology, Department of Vascular Biology and Thrombosis Research
,
Meinhard Kneussl
2   Department of Pulmonary Medicine, University of Vienna, Austria
,
Bernd R. Binder
1   Department of Cardiology, Department of Vascular Biology and Thrombosis Research
,
Kurt Huber
1   Department of Cardiology, Department of Vascular Biology and Thrombosis Research
› Author Affiliations
Further Information

Publication History

Received 18 September 2000

Accepted after resubmission 15 February 2001

Publication Date:
12 December 2017 (online)

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Summary

Primary pulmonary hypertension (PPH) is a rare disorder, with marked in-situ thrombosis of small pulmonary vessels occurring primarily in adult women. We investigated whether differences in the plasmin- and thrombin activation system are associated with the predominate affection of females. Plasma levels of plasminogen activator inhibitor type 1 (PAI-1), tissue-type plasminogen activator (t-PA), fibrinogen, thrombin-antithrombin (TAT) complexes, and prothrombin fragments (F1.2) were measured at baseline and after standardized venous occlusion (VO) in patients with PPH (24 female, 9 male). At baseline, females showed significant higher TAT levels (p = 0.05), higher t-PA antigen levels (p = 0.01) and higher fibrinogen levels (p = 0.03) with positive correlation to mean pulmonary artery pressure (mPAP), as well as nonsignificant lower t-PA activity, higher PAI-1 antigen and activity and F1.2 levels. After VO, females showed a significantly blunted increase in t-PA antigen (p = 0.01) and t-PA activity (p = 0.001), correlating with mPAP, as well as increased PAI-1 activity (p = 0.05). We hypothesize, that the observed presence of gender differences in the plasmin- and thrombin activation system in PPH leading to an antifibrinolytic/prothrombotic state might, in part, explain the female predominant incidence of this disease.

Keywords

Primary pulmonary hypertension - fibrinolysis - blood coagulation - gender
 

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