Comerota AJ, Chouhan V, Harada RN, Sun L, Hosking J,
Veermansunemi R, Comerota AJ Jr, Schlappy D, Rao AK.
The fibrinolytic effects of intermittent pneumatic compression: mechanism of
enhanced fibrinolysis.

Ann Surg 1997;226(3):306-13; disscussion 313-4

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

BACKGROUND AND OBJECTIVES: Intermittent pneumatic compression (IPC) is an
effective form of deep vein thrombosis prophylaxis for general surgery patients.
The antithrombotic effect of IPC is thought to be the result of increased venous
velocity and stimulation of endogenous fibrinolysis. However, the mechanism of
enhanced fibrinolytic activity and the relative effects on normal and
postthrombotic veins have not been defined. The purposes of this study are 1) to
quantify changes in fibrinolytic activity with IPC; 2) to study the mechanism of
fibrinolytic enhancement with IPC; and 3) to evaluate whether postthrombotic
patients have the same capacity for fibrinolytic enhancement with IPC as do
normal subjects. METHODS: Twelve volunteers (6 normal and 6 postthrombotic) had 5
IPC devices applied for 120 minutes in random fashion, 1 per week x 5 weeks. The
devices included single-chamber, sequential, foot, calf, and long-leg
compression. Subjects had an indwelling antecubital venous cannula placed for
blood drawn at baseline, 60, 120, and 180 minutes after IPC devices were applied.
Global fibrinolytic activity (euglobulin fraction, fibrin plate assay), tissue
plasminogen activator (tPA) antigen (Ag) and activity (Act), plasminogen
activator inhibitor-1 (PAI-1) Ag and Act, alpha-2-antiplasmin-plasmin complexes,
and von Willebrand factor (vWF) antigen were assayed. RESULTS: A striking
elevation in fibrinolytic activity was noted at 180 minutes with all devices in
normal subjects and postthrombotic patients (p = 0.01-0.0001); however, baseline
and stimulated fibrinolytic activity was attenuated in postthrombotic patients
(<0.03). The tPA-Act increased only in normal subjects (3.8 +/- 1.9%) (p =
0.057), despite a decrease in plasma tPA-Ag, which was observed in both normal
subjects (-12.4 +/- 3.8%) (p = 0.009) and patients (-17.2 +/- 3.1%) (p = 0.001).
PAI-1-Ag decreased in both normal subjects (-13.4 +/- 3.8%) (p = 0.007) and
patients (-12.0 +/- 3.1%) (p = 0.013) with a marked reduction in PAI-1-Act in
both normal subjects (p = 0.003) and patients (p = 0.004). There were no changes
in vWF, and alpha-2-antiplasmin-plasmin complexes increased only in
postthrombotic patients (p = 0.021). CONCLUSIONS: 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.