Stimulation of endogenous fibrinolytic activity occurs after IPC, both in normal subjects and postthrombotic patients; however, baseline and overall fibrinolytic response in postthrombotic patients is reduced. The mechanism of increased fibrinolytic activity is likely because of a reduction in PAI-1, with a resulting increase of tPA activity.

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Abstract-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 (PϽ0.001 for all groups). FVII antigen levels were unchanged. Plasma TFPI (PϽ0.001) 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 (PϽ0.001 for all groups). Plasma prothrombin fragment F1.2 levels showed minimal changes. There was an inverse relationship between TFPI and FVIIa in normal subjects (rϭϪ0.31, Pϭ0.001) and patients (rϭϪ0.37, PϽ0.001). 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. Key Words: intermittent pneumatic compression Ⅲ tissue factor pathway Ⅲ factor VIIa Ⅲ tissue factor pathway inhibitor Ⅲ factor VII I ntermittent pneumatic compression (IPC) is an established nonpharmacological method of prophylaxis against deep vein thrombosis. 1 The mechanisms for the antithrombotic effects of IPC are unclear and generally considered to be due to reduction of venous stasis in the lower extremities and stimulation of endogenous fibrinolytic mechanisms. 1-4 However, the effects of IPC on the early events of blood coagulation are unknown. The initiating mechanism of blood coagulation is the tissue factor (TF)-dependent pathway, which is regulated primarily by the tissue factor pathway inhibitor (TFPI), a Kunitz type inhibitor circulating in plasma. [5][6][7] This pathway is initiated when factor VIIa (FVIIa, the activated form of FVII) is exposed to its cofactor, tissue factor (TF), leading to formation of TFFVIIa complex, which proteolytically activates factor X (FX) and factor IX (FIX). 5-7 TFPI inhibits FXa directly and the TF-FVIIa complex in the presence of FXa. 5-8 Thus TFPI is a key natural anticoagulant that functions at the initial steps of blood coagulation. 5-7 Although a thromboembolic disease secondary to an inherited TFPI deficiency is yet to be recognized, there is evidence in rabbits suggesting that TFPI protects against thrombosis after exposure of blood to TF 9,10 and decreases mortality in Escherichia coli-induced shock in baboons. 11 Plasma TFPI levels are elevated after ...

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A VFI greater than 7 showed a 73% sensitivity and 100% positive predictive value of identifying "critical venous reflux." The VFI may underestimate the degree of reflux in patients with proximal venous obstruction. Improvement of venous hemodynamics with tourniquet application suggests that venous reflux might be improved in some patients by correcting superficial venous insufficiency.