A 17-year experience with mitral valve repair with artificial chordae in infants and children.

OBJECTIVES: We sought to examine our long-term results of mitral valve (MV) repair with expanded polytetrafluoroethylene (ePTFE) sutures and to determine the predictors for the outcome of this procedure. METHODS: Between 1995 and 2011, MV repair with chordal reconstruction by artificial chordae was achieved in 78 patients (34 males and 44 females). Median age at repair was 1.5 years (range 3.6 months-13.4) and weight was 9.1 kg (2.5-31.4). The mean follow-up was 8.3 years. A Cox proportional hazards model was used to analyse the risk factors for a composite outcome of death, conversion to other MV repair techniques or MV replacement, reoperation on MV and recurrent mitral regurgitation (MR). RESULTS: According to Carpentier classification, 65 (83.3%) patients were Type 2 and 13 (16.7%) were Type 3. Mitral annuloplasty was performed in all cases, except 2. During MV repair, 8 (10.3%) patients were ineffective with artificial chordae and converted to other techniques. Six (7.7%) patients underwent MV reoperation (three repairs and three replacements). Freedom from MV reoperation was 92.5 and 90.4% at 5 and 10 years, respectively. There was 1 in-hospital death. At the latest follow-up, moderate or more MR was observed in 3 (3.8%) patients. Risks for the composite outcome were low body weight at operation and Carpentier classification Type 3. CONCLUSIONS: MV repair with artificial chordae in infants and children is safe and effective and associated with a low reoperation rate. Further investigation into the long-term durability and biological adaptation of ePTFE sutures after patient growth is mandatory.

Adsorption of inflammatory cytokines using a heparin-coated extracorporeal circuit.

Cardiopulmonary bypass (CPB) surgeries cause an increase in plasma inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) along with whole-body inflammatory responses. The inflammatory responses during a CPB treatment are reduced when using a heparin-coated extracorporeal circuit. Because many cytokines, growth factors, and complements are known to interact with heparin, the reduction of inflammatory responses by a heparin-coated circuit is likely to depend on this heparin-binding nature of the inflammatory cytokines. In this study, the inflammatory cytokines, TNF-alpha and IL-6, in fetal bovine serum (FBS) bound to a heparin-agarose beads (heparin beads)-column and the adsorptions were competitively inhibited on addition of heparin in a concentration-dependent manner. TNF-alpha in FBS required a higher concentration of heparin (50% concentration inhibition [IC50] > 20microg/ml) to inhibit adsorption to the heparin beads-column compared with IL-6, probably because of a stronger interaction between TNF-alpha and heparin-beads. TNF-alpha and IL-6 concentrations in human heparinized blood significantly increased after a CPB treatment. Although the adsorbed amount of IL-6 onto the heparin-coated circuit was low (less than 6% of free circulating IL-6), a significant amount of TNF-alpha adsorbed onto the circuit (23.9-755% of free circulating TNF-alpha). Therefore, the adsorption of inflammatory cytokines, especially TNF-alpha, onto the inner heparin-coated surface of an extracorporeal circuit may partly account for a reduction in inflammatory responses.