title: Infant cardiopulmonary bypass: a procoagulant state.
abstract: BACKGROUND
  Procoagulant activity after cardiopulmonary bypass (CPB) in infants may predispose to thrombotic and bleeding complications. The induction of tissue factor and prothrombinase activity on endothelial cell membranes is a primary step in the activation of the extrinsic clotting cascade. The purpose of this study is to characterize the fibrinolytic and endothelial procoagulant state in infants undergoing congenital cardiac repairs with and without CPB.
  
  
  METHODS
  Fourteen infants (aged 1 to 12 weeks) underwent repair of congenital cardiac defects. Two patients had closed procedures (controls) and 12 had open cardiac procedures. Serum samples were taken before and after CPB, 1, 4, and 24 hours after CPB. Tissue plasminogen activator, plasminogen activator inhibitor-1, interleukin-1beta, interleukin-6, plasma tissue factor, and factor V levels were measured. Human umbilical vein endothelial cell cultures were incubated with serum taken from the above time points and assayed for induction of tissue factor and prothrombinase activity.
  
  
  RESULTS
  Control patients had no change from preoperative values in any of the parameters examined. In experimental patients, tissue plasminogen activator levels peaked at 1 hour after CPB and then decreased to normal by 24 hours. Plasminogen activator inhibitor-1 levels peaked at 4 hours after CPB and returned to baseline by 24 hours. The plasma of all patients had no intrinsic tissue factor activity. Induction of tissue factor activity on umbilical vein endothelial cells peaked immediately and again at 24 hours, whereas prothrombinase activity peaked early and stayed elevated. Serum factor V levels were significantly reduced after CPB, but returned to near baseline levels by 24 hours.
  
  
  CONCLUSIONS
  Cardiopulmonary bypass is associated with derangement of the coagulation and fibrinolytic systems in infants. The serum of these patients promotes the induction of endothelial procoagulant activity, suggesting that there may be a hypercoagulable state in the postbypass period.
authors.affiliation: Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA. jagge003@mc.duke.edu
authors.forename: J J
authors.initials: JJ
authors.lastname: Jaggers
authors.forename: M C
authors.initials: MC
authors.lastname: Neal
authors.forename: P K
authors.initials: PK
authors.lastname: Smith
authors.forename: R M
authors.initials: RM
authors.lastname: Ungerleider
authors.forename: J H
authors.initials: JH
authors.lastname: Lawson
mesh_terms: D001779:Blood Coagulation Factors / Q000378:metabolism; D002315:Cardiopulmonary Bypass; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005342:Fibrinolysis / Q000502:physiology*; D006330:Heart Defects, Congenital / Q000097:blood / Q000601:surgery*; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D019106:Postoperative Hemorrhage / Q000097:blood*; D012016:Reference Values; D012307:Risk Factors; D019851:Thrombophilia / Q000097:blood*; D013925:Thromboplastin / Q000378:metabolism
chemical_list: D001779:Blood Coagulation Factors; D013925:Thromboplastin