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Blood, 15 June 2001, Vol. 97, No. 12, pp. 3721-3726
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Regulation of monocyte procoagulant activity in acute myocardial
infarction: role of tissue factor and tissue factor
pathway inhibitor-1
Ilka Ott,
Martin Andrassy,
Dominik Zieglgänsberger,
Stefanie Geith,
Albert Schömig, and
Franz-Josef Neumann
From Deutsches Herzzentrum der Technischen
Universität Munich, Germany.
In acute myocardial infarction (AMI), monocyte procoagulant
activity is increased and may contribute to the risk for recurrence and
other thrombotic events. This study sought to investigate the role
tissue factor (TF) and tissue factor pathway inhibitor-1 (TFPI-1) in
the regulation of monocyte procoagulant activity in AMI. Serial venous
blood samples were obtained from 40 patients with AMI undergoing
revascularization by stent placement. Twenty patients with elective
stenting for stable angina served as control subjects. TF proteolytic
activity was measured with spectrozyme factor Xa (FXa), TF and TFPI-1
surface expression on monocytes by flow cytometry, RNA expression in
whole blood by reverse transcription-polymerase chain reaction, and
concentrations of plasma prothrombin fragments F1 + 2 by
immunoassay. Forty-eight hours after AMI, an increase was found in TF
RNA, followed by an increase in TF surface expression by 24% ± 4%
and in plasma concentration of F1 + 2 by 103% ± 17%
(P < .05). These changes could not be attributed to the
intervention because they did not occur in the control group. TFPI-1
RNA and binding to the monocyte surface remained unchanged. FXa
generation by monocytes of patients with AMI increased 53.6% ± 9%
in the presence of polyclonal antibodies to TFPI-1, indicating that
cell-associated TFPI-1 inhibits monocyte TF activity. The increased
monocyte procoagulant activity in AMI was caused by an up-regulation of
TF that was partially inhibited by surface-bound TFPI-1. Anticoagulant
therapy by direct inhibition of TF activity may, thus, be particularly
effective in AMI.
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