Chouhan VD, Comerota AJ, Sun L, Harada R, Gaughan JP, Rao AK.
Inhibition of tissue factor pathway during intermittent pneumatic compression: A
possible mechanism for antithrombotic effect.
Arterioscler Thromb Vasc Biol 1999 Nov;19(11):2812-7

Department of Medicine, The Sol Sherry Thrombosis Research Center, Temple
University School of Medicine, Philadelphia, PA 19140, USA.

Intermittent pneumatic compression (IPC) devices are an effective prophylaxis
against lower extremity deep vein thrombosis. Their antithrombotic effect has
been attributed to a reduction in venous stasis and enhanced fibrinolysis. The
initiating mechanism for blood coagulation is the tissue factor (TF) dependent
pathway, which is inhibited by tissue factor pathway inhibitor (TFPI). We have
investigated the effect of IPC on the TF pathway in 6 normal subjects and 6
patients with postthrombotic venous disease undergoing IPC for 120 minutes; all
subjects were studied with each of 5 IPC devices. In normal subjects and
patients, plasma factor VIIa (FVIIa) activity (the activated form of factor VII
[FVII]) declined from mean values ranging 51 to 65 and 50 to 53 mU/mL before IPC
with different devices to 10 to 13 and 20 to 22 mU/mL at 180 minutes,
respectively (P<0.001 for all groups). FVII antigen levels were unchanged. Plasma
TFPI (P<0.001) rose from mean baseline values ranging 69 to 79 and 57 to 61 ng/mL
to 76 to 123 and 71 to 79 ng/mL at 180 minutes in normal subjects and patients,
respectively (P<0. 001 for all groups). Plasma prothrombin fragment F1.2 levels
showed minimal changes. There was an inverse relationship between TFPI and FVIIa
in normal subjects (r=-0.31, P=0.001) and patients (r=-0.37, P<0.001). IPC
results in an increase in plasma TFPI and decline in FVIIa. Inhibition of TF
pathway, the initiating mechanism of blood coagulation, is a possible mechanism
for the antithrombotic effect of IPC.