title: Children undergoing cardiac surgery for complex cardiac defects show imbalance between pro- and anti-thrombotic activity.
abstract: BACKGROUND
  Cardiac surgery with cardiopulmonary bypass (CPB) is associated with the activation of inflammatory mediators that possess prothrombotic activity and could cause postoperative haemostatic disorders. This study was conducted to investigate the effect of cardiac surgery on prothrombotic activity in children undergoing cardiac surgery for complex cardiac defects.
  
  
  METHODS
  Eighteen children (ages 3 to 163 months) undergoing univentricular palliation with total cavopulmonary connection (TCPC) (n = 10) or a biventricular repair (n = 8) for complex cardiac defects were studied. Prothrombotic activity was evaluated by measuring plasma levels of prothrombin fragment 1+2 (F1+2), thromboxane B2 (TxB2), and monocyte chemoattractant protein-1 (MCP-1). Anti-thrombotic activity was evaluated by measuring levels of tissue factor pathway inhibitor (TFPI) before, during, and after cardiac surgery.
  
  
  RESULTS
  In all patients, cardiac surgery was associated with a significant but transient increase of F1+2, TxB2, TFPI, and MCP-1. Maximal values of F1+2, TxB2, and MCP-1 were found at the end of CPB. In contrast, maximal levels of TFPI were observed at the beginning of CPB. Concentrations of F1+2 at the end of CPB correlated negatively with the minimal oesophageal temperature during CPB. Markers of prothrombotic activity returned to preoperative values from the first postoperative day on. Early postoperative TFPI levels were significantly lower and TxB2 levels significantly higher in patients with TCPC than in those with biventricular repair. Thromboembolic events were not observed.
  
  
  CONCLUSIONS
  Our data suggest that children with complex cardiac defects undergoing cardiac surgery show profound but transient imbalance between pro- and anti-thrombotic activity, which could lead to thromboembolic complications. These alterations are more important after TCPC than after biventricular repair but seem to be determined mainly by low antithrombin III.
authors.affiliation: Department of Pediatric Cardiology, University Hospital, RWTH-Aachen, Pauwelsstrasse 30, 52074 Aachen, Germany. heying@uni-duesseldorf.de
authors.forename: Ruth
authors.initials: R
authors.lastname: Heying
authors.forename: Wim
authors.initials: W
authors.lastname: van Oeveren
authors.forename: Stefanie
authors.initials: S
authors.lastname: Wilhelm
authors.forename: Katharina
authors.initials: K
authors.lastname: Schumacher
authors.forename: Ralph G
authors.initials: RG
authors.lastname: Grabitz
authors.forename: Bruno J
authors.initials: BJ
authors.lastname: Messmer
authors.forename: Marie-Christine
authors.initials: MC
authors.lastname: Seghaye
mesh_terms: D000990:Antithrombin III / Q000032:analysis; D001777:Blood Coagulation; D001780:Blood Coagulation Tests; D006348:Cardiac Surgical Procedures / Q000009:adverse effects*; D002648:Child; D002675:Child, Preschool; D018610:Heart Bypass, Right / Q000009:adverse effects*; D006330:Heart Defects, Congenital / Q000601:surgery*; D006801:Humans; D011446:Prospective Studies; D013927:Thrombosis / Q000209:etiology / Q000503:physiopathology*
chemical_list: D000990:Antithrombin III