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This 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.

Resistance to activated protein C (APCR) has emerged as the most important hereditary cause of venous thromboembolism. Using an aPTT-based method together with DNA technique we investigated 120 healthy neonates and infants < 12 months of age and 24 infants with septicaemia for the presence of this mutation. In addition, data of 11 neonates with vascular occlusion, heterozygous (+/-) for the Arg 506 Gln mutation were included. Results of an aPTT-based method (clotting time using the APC/CaCl2 solution obtained in an undiluted, 1:5 and 1:11 dilution with factor V deficient plasma divided by clotting time with CaCl2 in the same plasma dilution) are shown: Whereas 7 (5.5%) out of 120 healthy neonates were (+/-) carriers for the factor V Arg 506 Gln mutation, concordance with the aPTT-based method (cut-off defined as ratio < 2) was found only when using the 1:11 plasma dilution. Six (four) out of 24 infants with sepsis, not carrying the factor V mutation, would have been classified as APC resistant when using the 1:1 (1:5) plasma dilution. Four (two) out of 18 patients, (+/-) for the Arg 506 Gln mutation showed APC ratios > 2 in the 1:1(1:5) plasma dilution.