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Cardiomyopathy
Reversible cardiomyopathy with intraventricular hypertrophy and outflow tract obstruction can occur in up to 30% of IDMs. Cardiomyopathy may be
caused by congestive failure due to a poorly functioning myocardium or hypertrophy of the intraventricular septum and one or both ventricular walls.
Occasionally, the outflow tract obstruction becomes so profound as to require extracorporeal membrane oxygenation while awaiting regression of the
obstruction.
The mechanism by which hypertrophic cardiomyopathy occurs is not completely understood. The human heart is rich in insulin receptors. It is
postulated that the fetus of the diabetic mother in whom hyperinsulinism develops will have increased myocardial receptor sites and increased affinity
for insulin. This could lead to increased protein, glycogen, and fat synthesis in the myocardium and subsequent hyperplasia and hypertrophy of the
myocardium. Postnatally, as serum insulin levels and the number of insulin receptors decrease, the septal hypertrophy should decrease as well.
Although this hypothesis is consistent with the natural history of this disease process, other yet unidentified factors may be important as well. Fetuses
of diabetic mothers who were thought to be in good glycemic control, as compared with normal controls, had evidence of cardiac hypertrophy at the
level of the intraventricular septum and at the right and left ventricular free wall by late gestation.27 More sensitive markers of maternal metabolic
control may be needed to define better the in utero environment that promotes this type of cardiac growth.