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(Circulation. 2004;110:2627-2630.)
© 2004 American Heart Association, Inc.

Heart Failure

Maternal Hyperglycemia Improves Fetal Cardiac Function During Tachycardia-Induced Heart Failure in Pigs

M.R. Schmidt, MD, PhD; M. Smerup, MD; S.B. Kristiansen, MD; H.E. Bøtker, MD, PhD, DMSc; O. Schmitz, MD, DMSc; V.E. Hjortdal, MD, PhD, DMSc; K.E. Sørensen, MD; A.N. Redington, MD, FRCP

From Aarhus University Hospital, Skejby, Aarhus (M.R.S., M.S., S.B.K., H.E.B., V.E.H., K.E.S.), and Aarhus University Hospital, Kommunehospitalet (O.S.), Denmark; and the Hospital for Sick Children, Toronto, Canada (A.N.R.).

Correspondence to Michael Rahbek Schmidt, Department of Cardiology, Aarhus University Hospital, Skejby, Brendstrupgaardsvej, DK-8200 Aarhus N, Denmark. E-mail rahbek{at}dadlnet.dk

Received January 1, 2004; de novo received April 28, 2004; revision received June 17, 2004; accepted June 18, 2004.

Background— Fetal tachycardia often leads to cardiac failure, which in experimental settings can be prevented by direct fetal glucose-insulin administration. In this study, we hypothesize that similar effects can be obtained indirectly by inducing maternal hyperglycemia.

Methods and Results— Systolic and diastolic indices (dP/dt_max and ) of left ventricular function were measured by use of high-fidelity catheters during 180 minutes of aggressive atrial pacing (300 bpm) in 12 preterm porcine fetuses. In 6 fetuses, maternal hyperglycemia (15 mmol/L) was induced for the last 120 minutes of pacing. The remaining fetuses served as controls. Glucose, insulin, and free fatty acid levels were determined, as was fetal myocardial glycogen content. Maternal glucose infusion led to significant fetal hyperglycemia and hyperinsulinemia but did not change the inherently low fetal levels of free fatty acids. There were no differences between groups with regard to dP/dt_max (1025±226 and 1037±207 mm Hg, P=NS) and (20.6±2.0 and 21.4±1.6 ms, P=NS) at baseline (100%). During the 180 minutes of pacing, systolic function (dP/dt_max) and diastolic function () deteriorated more in the control group than in the hyperglycemic group (P<0.001 for both). At 180 minutes, dP/dt_max was 62±18% of baseline in controls and 85±11% in hyperglycemic fetuses (P=0.03), and was 117±12% and 98±4%, respectively (P=0.004).

Conclusions— Induced maternal hyperglycemia improves fetal cardiac function during fetal tachycardia and suggests a possible additional therapeutic option to improve the function of the failing fetal heart before or during antiarrhythmic therapy. The findings may be relevant in fetal heart failure in general.

Key Words: heart failure • tachycardia • glucose