title: Activation of coagulation and fibrinolytic systems in patients with CLI is not normalized after surgical revascularisation.
abstract: OBJECTIVE
  To study the activation of coagulation and fibrinolysis before, during and after surgical revascularisation in patients with critical limb ischemia (CLI).
  
  
  METHODS
  Prospective clinical study.
  
  
  METHODS
  Forty patients with CLI underwent femoro-popliteal or femoro-distal reconstruction and were compared to a control-group. Measurements of prothrombin-fragment 1+2 (F1+2) and thrombin-antithrombin complex (TAT) assessed activation of coagulation. Fibrinolysis was determined by tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI-1) and fibrin degradation product (D-dimer). The inflammatory mediators: Interleukin 2 receptor (IL-2-rec), Interleukin 6 (IL-6), Interleukin 10 (IL-10) and Monocyte chemoattractant protein 1 (MCP-1) was also analysed.
  
  
  RESULTS
  Patients (in 35 of the 40 reconstruction was possible) were operated upon using either vein (n=23) or ePTFE (n=12) grafts. Patients with CLI had a preoperative prothrombotic state as indicated by high TAT-levels and also ongoing fibrinolysis with high levels of t-PA and D-dimer. After reperfusion an ongoing prothrombotic state for the first week was demonstrated. A significant as well as defective fibrinolysis was also seen with increased levels of tPA and D-dimer unopposed by PAI-1 after one week and also after 30 days. Increased levels of inflammatory mediators IL-6, IL-10 and MCP-1 was observed after reperfusion and normalised after 30 days.
  
  
  CONCLUSIONS
  This study demonstrates significant disturbances of both the coagulation and fibrinolytic systems before, during and after revascularisation for CLI. This was accompanied by release of inflammatory mediators. A prothrombotic state and increased fibrinolysis were evident also 30 days after successful revascularisation.
authors.affiliation: Institution for Surgical Science, Uppsala, Sweden.
authors.forename: H
authors.initials: H
authors.lastname: Pärsson
authors.forename: A
authors.initials: A
authors.lastname: Holmberg
authors.forename: A
authors.initials: A
authors.lastname: Siegbahn
authors.forename: D
authors.initials: D
authors.lastname: Bergqvist
mesh_terms: D000368:Aged; D000990:Antithrombin III / Q000378:metabolism; D001777:Blood Coagulation; D019917:Blood Vessel Prosthesis Implantation; D016022:Case-Control Studies; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005342:Fibrinolysis; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007511:Ischemia / Q000097:blood* / Q000601:surgery*; D007866:Leg / Q000098:blood supply*; D008297:Male; D010446:Peptide Fragments / Q000378:metabolism; D010447:Peptide Hydrolases / Q000378:metabolism; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D011138:Polytetrafluoroethylene; D011184:Postoperative Period; D011498:Protein Precursors / Q000378:metabolism; D011516:Prothrombin / Q000378:metabolism; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000378:metabolism
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D018836:Inflammation Mediators; D010446:Peptide Fragments; D017395:Plasminogen Activator Inhibitor 1; D011498:Protein Precursors; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; C029733:prothrombin fragment 1; D000990:Antithrombin III; D011516:Prothrombin; D011138:Polytetrafluoroethylene; D010447:Peptide Hydrolases; D010959:Tissue Plasminogen Activator