title: Heparin coating of extracorporeal circuits inhibits contact activation during cardiac operations.
abstract: OBJECTIVE
  Heparin coating reduces complement activation on the surface of extracorporeal circuits. In this study we investigated its effect on activation of the contact system in 30 patients undergoing coronary artery bypass grafting with the use of a heparin-coated (Duraflo II, Baxter Healthcare Corp., Edwards Division, Santa Ana, Calif.; n = 15) or an uncoated extracorporeal circuit (n = 15).
  
  
  METHODS
  Plasma markers that reflect activation of contact (kallikrein-C1-inhibitor complexes), coagulation (prothrombin fragments F1 + 2), or fibrinolytic (plasmin-alpha 2-antiplasmin complexes) systems were determined before and during the operation. The generation of kallikrein-C1-inhibitor complexes was reduced by 62% (p = 0.06) after the onset of cardiopulmonary bypass and by 43% (p = 0.026) after the cessation of bypass in the group in which a heparin-coated circuit was used compared with the group in which the circuit was uncoated. Generation was reduced by 58% (p = 0.06) when the ratio of kallikrein-C1-inhibitor to prekallikrein after onset of bypass was considered. We detected significant increases in F1 + 2 levels in both groups and increases in plasmin-alpha 2-antiplasmin complexes in the heparin-coated group at cessation of bypass, but no intergroup differences were observed. Thus use of heparin-coated extracorporeal circuits during cardiac operations reduces formation of kallikrein-C1-inhibitor complexes when compared with use of uncoated circuits. The heparin coating is not accompanied by similar reductions in coagulation or fibrinolysis, suggesting that thrombin and plasmin formation during cardiopulmonary bypass occurs mainly independently of the contact system activation.
authors.affiliation: Department of Pathophysiology of Plasma Proteins, Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Amsterdam, The Netherlands.
authors.forename: H
authors.initials: H
authors.lastname: te Velthuis
authors.forename: C
authors.initials: C
authors.lastname: Baufreton
authors.forename: P G
authors.initials: PG
authors.lastname: Jansen
authors.forename: C M
authors.initials: CM
authors.lastname: Thijs
authors.forename: C E
authors.initials: CE
authors.lastname: Hack
authors.forename: A
authors.initials: A
authors.lastname: Sturk
authors.forename: C R
authors.initials: CR
authors.lastname: Wildevuur
authors.forename: D Y
authors.initials: DY
authors.lastname: Loisance
mesh_terms: D000368:Aged; D000933:Antifibrinolytic Agents; D001777:Blood Coagulation / Q000187:drug effects; D002315:Cardiopulmonary Bypass / Q000295:instrumentation*; D003174:Complement C1 Inactivator Proteins / Q000187:drug effects*; D001026:Coronary Artery Bypass; D005174:Factor XII / Q000187:drug effects; D005260:Female; D005341:Fibrinolysin / Q000187:drug effects; D005342:Fibrinolysis / Q000187:drug effects; D006493:Heparin / Q000008:administration & dosage / Q000494:pharmacology*; D006801:Humans; D007610:Kallikreins / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000187:drug effects; D011516:Prothrombin / Q000187:drug effects; D000979:alpha-2-Antiplasmin / Q000187:drug effects
chemical_list: D000933:Antifibrinolytic Agents; D003174:Complement C1 Inactivator Proteins; D010446:Peptide Fragments; D000979:alpha-2-Antiplasmin; C037742:plasmin-plasmin inhibitor complex; C045879:prothrombin fragment 1.2; D011516:Prothrombin; D005174:Factor XII; D006493:Heparin; D007610:Kallikreins; D005341:Fibrinolysin