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Thrombosis research · Mar 1996
Clinical TrialFlush heparin during cardiac catheterisation prevents long-term coagulation activation in children without APC-resistance-preliminary results.
- H Vielhaber, B Kohlhase, H G Koch, H G Kehl, M Fliedner, D Kececioglu, B Kehrel, H Veltmann, J Vogt, and U Nowak-Göttl.
- Paediatric Cardiology, University Hospital, Münster, Germany.
- Thromb. Res. 1996 Mar 15; 81 (6): 651-6.
AbstractThis study was designed to prospectively evaluate haemostatic activation in 75 children undergoing cardiac catheterisation with intermittent flush heparin (10 IU/ml saline) and to relate these data to clinical findings and inherited risk factors for thrombophilia. In addition to flush heparin in infants < 6 months of age in whom additional arterial catheterisation was performed (n = 5) or patients with thrombophilia, heparin (300-400 IU/kg/d) was administered for a further 24 h. APTT was prolonged and anti Xa activity was significantly increased at the end of catheterisation and returned to normal 24 hours later. Whereas thrombin generation (F1 + 2) showed a significant coagulation activation at the end of catheterisation, no concomitant fibrinolytic activation (D-Dimer) was observed. Four children showed resistance to APC: one of them in whom stroke had occurred before and one additional child heterozygous for APCR received further prophylactic heparin. Two neonates with APCR and flush heparin only suffered from thrombosis after catheterisation. No further thrombotic events occurred. This study indicates that low-dose flush heparin during catheterisation may prevent long-term haemostatic activation in children without thrombophilia. Whether further heparin after cardiac catheterisation in children with APCR prevents vascular insults requires a more intensive study.
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