Inhibition of tissue factor pathway during intermittent pneumatic compression - A possible mechanism for antithrombotic effect

Intermittent pneumatic compression (IPC) devices are an effective prophylax is against lower extremity deep vein thrombosis. Their antithrombotic effec t has been attributed to a reduction in venous stasis and enhanced fibrinol ysis. The initiating mechanism for blood coagulation is the tissue factor ( TF) dependent pathway, which is inhibited by tissue factor pathway inhibito r (TFPI). We have investigated the effect of IPC on the TF pathway in 6 nor mal subjects and 6 patients with postthrombotic venous disease undergoing I PC for 120 minutes; all subjects were studied with each of 5 IPC devices. I n normal subjects and patients, plasma factor VIIa (FVIIa) activity (the ac tivated form of factor VII [FVII) declined from mean values ranging 51 to 6 5 and 50 to 53 mU/mL before IPC with different devices to 10 to 13 and 20 t o 22 mU/mL at 180 minutes, respectively (P<0.001 for ail groups). FVII anti gen levels were unchanged. Plasma TFPI (P<0.001) rose from mean baseline va lues 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. T here 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, th e initiating mechanism of blood coagulation, is a possible mechanism for th e antithrombotic effect of IPC.