(Circulation. 1995;92:3323-3330.)
© 1995 American Heart Association, Inc.
Articles |
Tissue Factor Mediates Prolonged Procoagulant Activity on the Luminal Surface of Balloon-Injured Aortas in Rabbits
From the Department of Medicine, Washington University School of Medicine, St Louis, Mo, and Scripps Research Institute, La Jolla, Calif (W.R., T.S.E.).
Correspondence to Dana R. Abendschein, PhD, Cardiovascular Division, Washington University School of Medicine, 660 S Euclid Ave, Campus Box 8086, St Louis, MO 63110.
Background Activation of coagulation has been implicated in both acute thrombotic occlusion and restenosis after balloon angioplasty. However, concomitant administration of antithrombotic agents has thus far failed to prevent these complications. Importantly, the factors contributing to procoagulant activity of balloon-injured arteries over time have not been defined. This study was designed to determine the duration of procoagulant activity on the luminal surface of balloon-injured arteries and the relative roles of tissue factor and thrombin in this response.
Methods and Results Abdominal aortas in rabbits were subjected to
repetitive balloon hyperinflations sufficient to disrupt the internal
elastic lamina. Aortas were excised at <1, 2, 4, 8, 16, 24, 48, and 72
hours and 1, 2, and 4 weeks after injury; divided into segments; and
perfused with recalcified human pooled plasma (n=58) or plasma depleted
of vitamin K–dependent coagulation factors (n=27) or first
incubated
with a monoclonal antibody to rabbit tissue factor (n=33) followed by
perfusion with human plasma. Samples of the effluent and plasma
perfusate were collected over 10 minutes and assayed for
fibrinopeptide A (FPA) as an index of the rate of
thrombin-induced fibrin formation. FPA in the effluent from
segments perfused with recalcified plasma, expressed as a percentage of
FPA in the perfusate, was elevated for 16 hours after
balloon-induced injury and exhibited two distinct increases
occurring <1 hour (1297±473%, mean±SD, n=5) and 8
hours
(1052±330%, n=6) after injury (P
.000001 versus
uninjured
vessels). Preincubation of segments at these intervals with an antibody
to tissue factor markedly attenuated the increases in FPA, as did
perfusion of segments with plasma depleted of vitamin K–dependent
coagulation factors, indicating that the observed increases in FPA in
whole plasma did not result from preformed thrombin bound to the
injured vessel wall.
Conclusions Tissue factor–mediated coagulation appears to be primarily responsible for prolonged procoagulant activity of balloon-injured arteries.
Key Words: thrombosis • coagulation • angioplasty
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