Metabolic effects of symptomatic ventricular septal defect (VSD) in infancy

Abstract

Feeding difficulties play a major role in the clinical picture of severe congestive heart failure (CHF) in infancy resulting in poor weight-gain and reduced fat stores and muscle mass. Muscle enzymes and substrates were studied during diagnostic heart catheterization in 20 infants, 1-13 months, with symptomatic VSD. Biopsies from the gracilis muscle were immediately frozen in liquid nitrogen. In a subsample of patients i.v. glucose tolerance tests (0.5 g/kg) and insulin determinations were performed with simultaneous sampling from femoral artery (FA) and main pulmonary artery (MPA). In muscle the cone of ATP, creatine-phosphate and glycogen were low compared to healthy controls. Succinate dehydrogenase activity (as indicator of aerobic energy capacity) was decreased, while lactate dehydrogenase (anaerobic glycolysis) was not. Infants with manifest CHF and poor weight-gain had slower disappearance rate of glucose (k_G) and lower insulin response than infants who had overcome the failure and were gaining weight. Insulin levels in MPA and FA didnot differ significantly. Max insulin response (FA) didnot correlate to the degree of left to right shunt. Reduced muscle blood supply, nutritional deficiency and inactivity may be responsible for the muscle enzyme and substrate reductions. The differences in k_G and insulin response may be due calorie deficiency and/or inhibition of insulin release by high catecholamines present in CHF Increased insulin clearance by the lung in large left to right shunts is not supported by our results.

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