title: Tissue factor and tissue factor pathway inhibitor levels in unstable angina patients during short-term low-molecular-weight heparin administration.
abstract: High tissue factor (TF), tissue factor pathway inhibitor (TFPI) levels and a hypercoagulability state have been documented in unstable angina patients. We evaluated whether short-term enoxaparin administration (100 IU/kg b.i.d. for 3 d) reduces the high TF levels and the hypercoagulability state, and whether it influences the fibrinolytic system in 20 unstable angina patients. On d 3, we observed a significant reduction in TF levels both 1 h and 4 h after the morning injection (-25.6% and -21.7%; P < 0.001 respectively) in comparison with the base-line levels. Both 1 and 4 h after the morning injection on the d 3, TFPI levels significantly (P < 0.001) increased (+96.4%, +96.9% respectively) with respect to the base-line values. After enoxaparin administration, at all observation times, thrombin-antithrombin complexes and prothrombin fragment F1 + 2 levels were significantly (P < 0.001) lower with respect to base-line levels. We observed a slight but significant increase in tissue plasminogen activator antigen levels in preinjection samples, as well as 1 h and 4 h after enoxaparin administration, in comparison with the base-line values. This study provides evidence that low-molecular-weight heparin (LMWH) administration, in addition to a reduction of hypercoagulability and a mild fibrinolytic activation, is associated with decreased TF levels, so indicating a novel mechanism of interference of LMWH with the haemostatic system.
authors.affiliation: Department of Medical and Surgical Critical Care, Clinical Medicine and Cardiology, University of Florence-Azienda Ospedaliera Careggi, Viale Morgagni 85, 50134 Florence, Italy.
authors.forename: A M
authors.initials: AM
authors.lastname: Gori
authors.forename: S
authors.initials: S
authors.lastname: Fedi
authors.forename: G
authors.initials: G
authors.lastname: Pepe
authors.forename: M
authors.initials: M
authors.lastname: Falciani
authors.forename: A
authors.initials: A
authors.lastname: Rogolino
authors.forename: D
authors.initials: D
authors.lastname: Prisco
authors.forename: G F
authors.initials: GF
authors.lastname: Gensini
authors.forename: R
authors.initials: R
authors.lastname: Abbate
mesh_terms: D000328:Adult; D000368:Aged; D000789:Angina, Unstable / Q000097:blood / Q000188:drug therapy*; D000925:Anticoagulants / Q000627:therapeutic use*; D000990:Antithrombin III / Q000378:metabolism; D004334:Drug Administration Schedule; D017984:Enoxaparin / Q000627:therapeutic use*; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006801:Humans; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000378:metabolism; D010447:Peptide Hydrolases / Q000378:metabolism; D011498:Protein Precursors / Q000378:metabolism; D011516:Prothrombin / Q000378:metabolism; D013925:Thromboplastin / Q000378:metabolism*; D010959:Tissue Plasminogen Activator / Q000097:blood
chemical_list: D000925:Anticoagulants; D017984:Enoxaparin; D005343:Fibrinolytic Agents; D008074:Lipoproteins; D010446:Peptide Fragments; D011498:Protein Precursors; C046193:antithrombin III-protease complex; C051928:lipoprotein-associated coagulation inhibitor; C029733:prothrombin fragment 1; C044183:prothrombin fragment 2; D000990:Antithrombin III; D011516:Prothrombin; D013925:Thromboplastin; D010447:Peptide Hydrolases; D010959:Tissue Plasminogen Activator