Decreased fetal cardiac performance in the first trimester correlates with hyperglycemia in pregestational maternal diabetes.

OBJECTIVE: In-vitro animal studies suggest that high glucose levels impair fetal cardiac function early in gestation. We aimed to study whether evidence of first-trimester myocardial dysfunction can be detected in fetuses of women with pregestational diabetes mellitus.
METHODS: Women with diabetes mellitus underwent fetal echocardiography at 11-14 weeks' gestational age. In fetuses with normal anatomy, the cardiac preload, diastolic function, global myocardial performance and placental afterload were studied by Doppler of the ductus venosus (DV), mitral and tricuspid early/atrial (E/A) ratios, left and right ventricular myocardial performance index (MPI) and umbilical artery (UA) Doppler, respectively. Cases were matched for gestational age and UA and DV Doppler with controls that had no diabetes mellitus.
RESULTS: Sixty-three singleton diabetic pregnancies were matched with 63 controls. Mean gestational age at enrollment was 12.6 (range, 11.1-13.6) weeks. Diabetic mothers had moderate to poor glycemic control (median (range) glycosylated hemoglobin A1 (HbA1c), 7.5 (5.1-12.7)%, and the HbA1c level was ≥ 7% in 37 (59%)). Fetuses of diabetic mothers exhibited worse measures of diastolic dysfunction: the isovolumetric relaxation time (IRT) was significantly prolonged (left ventricle: 36.9 ± 7.4 ms vs. 45.8 ± 6.8 ms; right ventricle: 35.6 ± 8 ms vs. 46.4 ± 7.3 ms, P < 0.0001 for both). The mitral E/A ratio was lower in diabetics (0.55 ± 0.06 vs. 0.51 ± 0.08, P = 0.03), and the global myocardial performance was lower in both ventricles (left ventricle MPI: 0.5 ± 0.08; right ventricle MPI: 0.52 ± 0.08, P = 0.03 and P < 0.0001, respectively). This lower global myocardial performance was caused by a prolonged myocardial relaxation time, which was most marked in diabetics with an HbA1c of ≥ 7% (P < 0.001 vs. controls for both ventricles). There were no significant correlations between cardiac Doppler parameters and DV, UA indices and fetal heart rate (P > 0.05 for all).
CONCLUSIONS: Fetuses of poorly controlled diabetic mothers demonstrate significant differences in first-trimester diastolic myocardial function compared with non-diabetic controls. The decrease in myocardial performance is more marked with increasing HbA1c and appears to be independent of preload and afterload. The ability to document these cardiac functional changes this early in pregnancy opens potential new avenues to understand the consequences of maternal glycemic status.