High-dose methylprednisolone and endothelial glycocalyx in paediatric heart surgery

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Abstract

Background:

Corticosteroids are used in paediatric heart surgery to attenuate systemic inflammatory response. Glycocalyx regulates vascular permeability, shear stress and cell adhesion on the endothelium. Syndecan-1 serves as a biomarker of glycocalyx degradation. Hydrocortisone decreased endothelial glycocalyx degradation in an experimental model. Our hypothesis was that high-dose methylprednisolone decreases glycocalyx degradation as measured by plasma sydecan-1 concentration in children undergoing cardiac surgery.

Methods:

Two double-blinded, randomized, placebo-controlled trials were conducted. In the first trial (‘neonatal trial’), 40 neonates undergoing open heart surgery received either 30 mg/kg intravenous methylprednisolone (n = 20) or placebo (n = 20). In the second trial (‘VSD trial’), 45 infants and very young children, undergoing ventricular or atrioventricular septal defect correction received one of the following: 30 mg/kg of methylprednisolone intravenously after anaesthesia induction (n = 15), 30 mg/kg methylprednisolone in the cardiopulmonary bypass prime solution (n = 15) or placebo (n = 15). Plasma syndecan-1 concentrations were measured. Results were expressed both as absolute concentrations and in relative concentrations as multiples of the baseline values of syndecan-1.

Results:

There were no statistically significant differences between the neonate trial groups for absolute syndecan-1 concentrations. However, operative administration of methylprednisolone to neonates significantly reduced the relative increases of syndecan-1 at weaning from cardiopulmonary bypass (P = 0.008) and at 6 h post-operatively (P = 0.018). There were no statistically significant differences in absolute or relative increases of syndecan-1 between the VSD trial study groups.

Conclusion:

High-dose methylprednisolone reduces shedding of glycocalyx in neonates after complex cardiac surgery but not in older infants after repair of VSD/AVSD with shorter ischaemia times.

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