doi: 10.1161/hc0302.103591
(Circulation. 2002;105:279.)
© 2002 American Heart Association, Inc.
Brief Rapid Communications |
Proteolysis of Tissue Factor Pathway Inhibitor-1 by Thrombolysis in Acute Myocardial Infarction
From Medizinische Klinik und Deutsches Herzzentrum der Technischen Universität München, Germany.
Correspondence to Dr. I. Ott, Deutsches Herzzentrum, Lazarettstr. 36, 80636 München, Germany. E-mail ott{at}dhm.mhn.de
Background— In acute myocardial infarction (AMI), surface-bound tissue factor pathway inhibitor-1 (TFPI-1) inhibits an increased monocyte procoagulant activity. In addition, TFPI-1 is released from microvascular endothelial cells after treatment with heparin and thereby contributes to its antithrombotic properties.
Methods and Results— We examined 19 patients in a randomized study comparing intravenous fibrinolysis with alteplase (n=9) and revascularization by stent placement with additional abciximab treatment (n=10). We obtained blood samples for analysis of monocytic TFPI-1 surface expression by flow cytometry and plasma TFPI-1 concentrations by immunoassay before and after therapy. We found a significant decrease in surface TFPI-1 on circulating monocytes 24 hours after thrombolysis (P=0.006) that was not observed after stenting. Systemic plasma TFPI-1 concentrations increased immediately after stenting by 71±14% (P=0.008), whereas after thrombolysis, a decrease in TFPI-1 plasma concentrations of 21±11% was observed (P=0.075). In vitro experiments confirmed that plasmin decreased TFPI-1 surface expression dose-dependently.
Conclusions— Activation of the fibrinolytic system by alteplase in AMI decreases surface-associated TFPI-1 on circulating monocytes and plasma TFPI-1. Reduced TFPI-1 may contribute to thrombotic complications after fibrinolysis in AMI.
Key Words: myocardial infarction • thrombolysis • leukocytes
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