title: Coagulation, fibrinolysis, and recanalization after acute deep venous thrombosis.
abstract: OBJECTIVE
  Recanalization is common after acute deep venous thrombosis, but the factors that contribute to its variable extent are unknown. The purpose of this study was to examine the relationship between recanalization and plasma markers of coagulation and fibrinolysis.
  
  
  METHODS
  Subjects with an ultrasound-confirmed deep venous thrombosis had prothrombin fragment 1+2 (F 1+2), tissue plasminogen activator (t-PA) activity, plasminogen activator inhibitor (PAI-1) activity, and t-PA antigen levels determined before anticoagulation therapy. Ultrasound and plasma studies were repeated at 14 days, 1 month, and every 3 months for 1 year.
  
  
  RESULTS
  Among 71 enrolled subjects, F 1+2 levels normalized within 14 days. The mean t-PA activity was within the normal range at all follow-up intervals. However, the mean t-PA antigen (10.7 plus minus 10.5 to 13.6 plus minus 13.5 ng/mL; P =.04) and PAI-1 (9.0 plus minus 8.1 to 13.2 plus minus 17.3 U/mL; P =.05) levels increased between the time of presentation and day 14. The mean reduction in thrombus score among 44 patients who completed 9 months of follow-up was 60.9% (plus minus 42.1%). Percent recanalization was directly associated with initial t-PA activity levels (R =.4; P =.006) and inversely related to F 1+2 (R = minus sign. 5; P =.004), t-PA antigen (R = minus sign.5, P =.002), and PAI-1 (r = minus sign. 5, P =.001) levels. However, only initial F 1+2 (P =.0009) and t-PA antigen (P =.004) levels were independent predictors of the degree of recanalization.
  
  
  CONCLUSIONS
  Although the mechanisms by which the venous lumen is restored are still being elucidated, recanalization is inversely related to levels of activated coagulation (F 1+2) and fibrinolytic inhibition (t-PA antigen) at the time of presentation.
authors.affiliation: Department of Surgery, University of Washington School of Medicine, Seattle, USA. meissner@u.washington.edu
authors.forename: Mark H
authors.initials: MH
authors.lastname: Meissner
authors.forename: Brenda K
authors.initials: BK
authors.lastname: Zierler
authors.forename: Robert O
authors.initials: RO
authors.lastname: Bergelin
authors.forename: Wayne L
authors.initials: WL
authors.lastname: Chandler
authors.forename: D Eugene
authors.initials: DE
authors.lastname: Strandness
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000502:physiology*; D005342:Fibrinolysis / Q000502:physiology*; D005500:Follow-Up Studies; D006801:Humans; D007866:Leg / Q000098:blood supply* / Q000473:pathology; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011152:Popliteal Vein / Q000473:pathology; D011237:Predictive Value of Tests; D011446:Prospective Studies; D012307:Risk Factors; D012737:Sex Factors; D010959:Tissue Plasminogen Activator / Q000097:blood; D014654:Vascular Patency / Q000502:physiology*; D014682:Vena Cava, Inferior / Q000473:pathology; D020246:Venous Thrombosis / Q000097:blood* / Q000503:physiopathology*; D014861:Washington / Q000453:epidemiology
chemical_list: D015415:Biomarkers; D017395:Plasminogen Activator Inhibitor 1; D010959:Tissue Plasminogen Activator