Intermittent pneumatic compression in chronic venous insufficiency favorably affects fibrinolytic potential and platelet activation.
Nineteen patients with symptoms of chronic venous insufficiency (CVI) were treated with 13-week cycles of intermittent pneumatic compression (IPC) during 2 h sessions twice weekly, with most treatments at home. At study completion, quantitative subjective scores for total symptomatology were improved in 16/19 patients (84%). Enhancement of fibrinolytic potential in vivo was detected in 86% of observations on specimens from CVI patients over 2 h of IPC, with accelerated euglobulin clot lysis times (ELT) noted within 15 min of initiating compression. The enhanced fibrinolytic potential was attributed to increased urokinase plasminogen activator (u-PA), probably released from perturbed endothelial cells by IPC. Significant decreases in total t-PA antigen (mass concentration) but not t-PA activity, were produced by IPC in CVI patients only (P = 0.0001), with greater effects noted in the non-anticoagulated versus the anticoagulated cohort. Plasminogen activator inhibitor type 1 (PAI-1) levels rose rapidly after IPC only in the controls and non-anticoagulated CVI patients. PAI-1 decreased in those receiving anticoagulation. No platelet perturbation was detected during IPC by measuring levels of beta-thromboglobulin or the thromboxane A2 metabolite, 11-dehydrothromboxane B2; however, significant (P < 0.003) decreases in plasma prostacyclin (PGI2) levels (measured as the stable 6-ketoprostaglandin F-1-alpha-metabolite) were observed after 15 min of IPC in non-anticoagulated CVI patients only. There was no evidence of increased thrombin generation by IPC, determined by urinary excretion of fibrinopeptide A and prothrombin fragment 1. Concurrent anticoagulation appears to mediate more favorable biochemical alterations in CVI, although subjective improvement did not correlate with anticoagulation. The mechanism(s) by which these physiologic changes compliment the mechanical effects of IPC remain to be elucidated and will require adequately controlled and powered studies.
Kessler
C M
CM
Department of Medicine of George Washington University Medical Center, Washington, DC 20037, USA.
Hirsch
D R
DR
Jacobs
H
H
MacDougall
R
R
Goldhaber
S Z
SZ
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000328:Adult; D000368:Aged; D002908:Chronic Disease; D005260:Female; D005342:Fibrinolysis; D006801:Humans; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation; D011312:Pressure; D013924:Thrombophlebitis / Q000150:complications / Q000188:drug therapy; D010959:Tissue Plasminogen Activator / Q000097:blood; D014689:Venous Insufficiency / Q000097:blood* / Q000209:etiology / Q000628:therapy*; D001620:beta-Thromboglobulin / Q000652:urine
D001620:beta-Thromboglobulin; D015121:6-Ketoprostaglandin F1 alpha; D010959:Tissue Plasminogen Activator