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Plasma metabolites after a lipid load in infants with congenital heart disease

K H Lundell1, K G Sabel, B O Eriksson

  • 1Department of Paediatrics, Jönköping Central Hospital, Sweden.

Acta Paediatrica (Oslo, Norway : 1992)
|August 14, 1999
PubMed

Insights

Infants with congenital heart defects often experience growth retardation linked to lipid metabolism disturbances. This study found altered linoleic acid and glycerol levels, suggesting impaired fat utilization in affected infants.

Area of Science:

  • Pediatric Cardiology
  • Neonatal Metabolism
  • Biochemistry

Background:

  • Growth retardation is a frequent complication in infants diagnosed with congenital heart defects (CHDs).
  • The underlying mechanisms contributing to this growth failure are not fully understood.
  • Disturbances in lipid metabolism may play a significant role in the pathophysiology of CHDs and associated growth issues.

Purpose of the Study:

  • To investigate the relationship between growth retardation and lipid metabolism in infants with CHDs.
  • To determine if specific types of heart defects (ventricular septal defects vs. transposition of the great arteries) are associated with distinct metabolic profiles.
  • To explore potential alterations in fatty acid utilization and lipolysis in infants with CHDs.

Main Methods:

  • A cohort of 16 infants with ventricular septal defects and 6 with transposition of the great arteries underwent a standardized intravenous lipid emulsion (Intralipid) challenge after an overnight fast.
  • Blood samples were collected at multiple time points (pre-infusion and up to 240 minutes post-infusion) to analyze plasma concentrations of triglycerides, free fatty acids, ketones, lactate, pyruvate, alanine, glycerol, and glucose.
  • Gas chromatography was employed to determine the specific fatty acid patterns within the triglyceride and free fatty acid fractions.

Main Results:

  • Severe growth retardation in infants with CHDs correlated with elevated fasting and peak levels of linoleic acid in plasma free fatty acids.
  • Higher peak levels of linoleic acid in triglycerides were positively associated with weight standard deviation scores.
  • Growth-retarded infants exhibited higher peak glycerol levels, indicative of increased intravascular lipolysis.
  • Linoleic acid in the triglyceride fraction remained elevated for up to 240 minutes post-infusion.
  • Infants with cyanotic heart defects showed higher lactate and alanine levels and potentially reduced capacity for free fatty acid utilization compared to those with VSDs.

Conclusions:

  • The findings support the hypothesis that lipid metabolism is significantly disturbed in infants suffering from congenital heart defects.
  • Altered fatty acid profiles and impaired lipolysis appear to be associated with growth retardation in this population.
  • Differences in metabolic profiles between cyanotic and non-cyanotic heart defects suggest distinct pathophysiological pathways.

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