Abstract
Transient hypertrophic cardiomyopathy in human infants of diabetic mothers has been reported by various investigators. In order to clarify the pathogenesis of this unique type of myocardial disease, streptozotocin-induced diabetic rats were used in our study.Obvious asymmetrical septal hypertrophy (ASH), with thickened myocytes and immature intercellular connections, was observed in newborns of diabetic rats. Daily administration of NPH insulin to mother rats did not prevent the development of ASH. However, ASH was no longer seen 4 weeks after the birth. On the other hand, symmetrical cardiac hypertrophy developed when 4 week old rats were treated with NPH insulin for 4 weeks.Thus, transient ASH developed in infants of experimental diabetic rats. Clearly, this cardiac hypertrophy is not genetically transmitted. The author considers the cardiac hypertrophy in infants of diabetic mothers to possibly be a cardiac manifestation of generalized organomegaly caused by hyperinsulinism and/or catecholamine excess. The asymmetry of hypertrophy in this unique myocardial disease might represent only immaturity of the cardiac architecture.
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