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Children undergoing cardiac surgery for complex cardiac defects show imbalance between pro- and anti-thrombotic
Ruth Heying1, Wim van Oeveren, Stefanie Wilhelm
1Department of Pediatric Cardiology, University Hospital, RWTH-Aachen, Pauwelsstrasse 30, 52074 Aachen, Germany. heying@uni-duesseldorf.de
Insights
Pediatric cardiac surgery temporarily disrupts the balance of blood clotting factors, increasing prothrombotic activity. These changes, particularly after total cavopulmonary connection, can pose risks for thromboembolic complications in children.
Area of Science:
- Pediatric Cardiology
- Hemostasis and Thrombosis
- Cardiovascular Surgery
Background:
- Cardiac surgery using cardiopulmonary bypass (CPB) can activate inflammatory pathways, leading to prothrombotic states and potential postoperative bleeding or clotting issues.
- Children undergoing complex cardiac defect repair are at risk for haemostatic disorders due to CPB-induced inflammation.
Purpose of the Study:
- To investigate the impact of cardiac surgery on prothrombotic and anti-thrombotic activity in children with complex cardiac defects.
- To compare these effects between univentricular palliation (total cavopulmonary connection) and biventricular repair procedures.
Main Methods:
- Studied 18 children (3-163 months) undergoing either total cavopulmonary connection (TCPC) or biventricular repair.
- Measured plasma levels of prothrombin fragment 1+2 (F1+2), thromboxane B2 (TxB2), monocyte chemoattractant protein-1 (MCP-1), and tissue factor pathway inhibitor (TFPI) pre-, during-, and post-surgery.
Main Results:
- Cardiac surgery caused a transient increase in F1+2, TxB2, MCP-1, and TFPI, with peak prothrombotic markers at CPB's end.
- Lower esophageal temperatures during CPB correlated with higher F1+2 levels post-surgery.
- Postoperative TFPI was lower and TxB2 higher in TCPC patients versus biventricular repair patients; no thromboembolic events occurred.
Conclusions:
- Children with complex cardiac defects exhibit a temporary pro- and anti-thrombotic imbalance after surgery, potentially leading to complications.
- The imbalance is more pronounced after TCPC compared to biventricular repair, possibly linked to low antithrombin III levels.
Introduction:
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.
Conclusion:
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.
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