title: Plasma metabolites after a lipid load in infants with congenital heart disease.
abstract: Growth retardation is common in infants with congenital heart defects. The aim of this study was to investigate whether growth retardation or type of heart defect in infants with congenital heart defects is related to disturbances in lipid metabolism. Sixteen infants with ventricular septal defects and six infants with transposition of the great arteries were given an intravenous load of lipid emulsion (Intralipid 20 mg/ml) corresponding to 0.5 g fat/kg body weight for 5 min after fasting for 8 h. Blood samples were drawn immediately before the infusion and 3, 20, 60, 120 and 240 min after the infusion was completed. Plasma concentrations of triglycerides (TG), free fatty acids (FFA), ketones, lactate, pyruvate, alanine, glycerol and glucose were determined. The fatty acid patterns in the TG and FFA fractions were measured using gas chromatography. Severe growth retardation in infants with defects of these kinds was correlated to higher fasting and maximum levels of linoleic acid in plasma FFA. The maximum levels of linoleic acid in the TG fraction were positively correlated to weight SD score, and maximum glycerol levels were higher in the most growth-retarded infants, indicating faster intravascular lipolysis. Linoleic acid in the TG fraction was still elevated at 120 and 240 min after the lipid load. Some differences between the cyanotic and VSD groups could be noted. These indicate decreased metabolic capacity to utilize released FFA in the cyanotic group. Infants with cyanotic heart defects also had higher lactate and alanine levels compared to infants with VSD. Our results support the hypothesis that lipid metabolism is disturbed in infants with congenital heart defects.
authors.affiliation: Department of Paediatrics, Jönköping Central Hospital, Sweden.
authors.forename: K H
authors.initials: KH
authors.lastname: Lundell
authors.forename: K G
authors.initials: KG
authors.lastname: Sabel
authors.forename: B O
authors.initials: BO
authors.lastname: Eriksson
mesh_terms: D000409:Alanine / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D002849:Chromatography, Gas / Q000379:methods; D002855:Chromatography, Thin Layer / Q000379:methods; D005217:Fat Emulsions, Intravenous / Q000378:metabolism*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005470:Fluorometry / Q000379:methods; D005990:Glycerol / Q000097:blood; D006130:Growth Disorders / Q000150:complications* / Q000175:diagnosis; D006330:Heart Defects, Congenital / Q000150:complications* / Q000378:metabolism*; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007659:Ketones / Q000097:blood; D007773:Lactates / Q000097:blood; D019787:Linoleic Acid / Q000097:blood; D008066:Lipolysis / Q000502:physiology; D019289:Pyruvic Acid / Q000097:blood; D012720:Severity of Illness Index; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D005217:Fat Emulsions, Intravenous; D005230:Fatty Acids, Nonesterified; D007659:Ketones; D007773:Lactates; D014280:Triglycerides; D019289:Pyruvic Acid; D019787:Linoleic Acid; D000409:Alanine; D005990:Glycerol