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Thromb Haemost 1987; 58(01): 237
DOI: 10.1055/s-0038-1643676
Abstracts
ANTITHROMBIN III
Schattauer GmbH Stuttgart

Increase of Thrombin-Antithrombin III (TAT) Complex Plasma Levels in Thromboembolic Diseases during Thrombolysis

Authors

  • R Seitz

    1   Div. of Internal Medicine, University of D-3550 Marburg, F.R.G

  • G Pratorius

    1   Div. of Internal Medicine, University of D-3550 Marburg, F.R.G

  • R Blanke

    1   Div. of Internal Medicine, University of D-3550 Marburg, F.R.G

  • B B Strauer

    1   Div. of Internal Medicine, University of D-3550 Marburg, F.R.G
Further Information

Publication History

Publication Date:
23 August 2018 (online)

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Recently an enzyme immuno assay of thrombin-antithrombinlll complex (TAT) plasma levels was developed by PELZER et al. (Thromb. Haemost. 54:24,1985). This test appears to be useful in the detection of intravasal thrombin generation, since all of 17 patients (pts.) with pulmonary embolism and 15 of 16 pts. with deep vein thrombosis (DVT) showed elevated values above 3 ng/ml.

In 9 pts. with acute myocardial infarction (AMI) the TAT levels increased significantly (p 0.001) 3 to 6 hours after thrombolytic therapy with 1.5 million units streptokinase (SK) over 30 minutes. A concomitant increase of fibrinopeptide A (FPA) levels (p=0.048) was observed. In contrast, 8 AMI pts. treated with heparin showed an insignificant increase of TAT and FPA. In 7 DVT pts. the TAT levels rose significantly (p 0.001) within 6 hours after start of urokinase (UK) infusion, while the FPA levels were enhanced prior to treatment and showed no further increase.

In order to assess the in vitro effects of SK and UK on TAT levels, clots obtained by recalcification of citrated plasma were incubated in heparin (2 units/ml) plasma. An increase of TAT occurred after addition of SK or UK, which was less pronounced when the clots were rinsed extensivly or squeezed before incubation. When SK or UK were added to plasma in the absence of a clot, still a small increase of TAT occurred which was absent in saline controls.

The data suggest that SK and UK action is associated with the generation of TAT complexes. In vivo, thrombin or thromboplastic material might be released by enhanced "wash out" from the recanalized coronary artery or from the reperfused in-farcted myocardium. Thrombin might also be released from binding sites on fibrin clots or fibrinogen. It is conceivable that these findings contribute to the understanding of reocclusion of infarct vessels after thrombolytic therapy. This points to the importance of careful anticoagulation in patients receiving thrombolytic therapy.