Influence of gestational diabetes on fetal autonomic nervous system: a study using phase‐rectified signal‐averaging analysis

Objectives Maternal gestational diabetes (GDM) is known to influence fetal physiology. Phase-rectified signal averaging (PRSA), an innovative signal processing technique, can be used to investigate signals obtained from fetal heart. The PRSA calculated variables “average acceleration capacity” (AAC) and “average deceleration capacity” (ADC) are established indices of autonomic nervous system (ANS) function. The aim of this study was to evaluate the influence of gestational diabetes on the fetal ANS in human pregnancy using PRSA. Methods In a prospective human clinical case-control study during the third trimester of pregnancy, 58 mothers with diagnosed GDM and 58 gestational-age matched healthy controls were included. Fetal CTG registrations were performed in all cases at study entry and in 19 cases of gestational diabetes the registration was repeated again close to delivery. The ultrasound technique based innovative CTG parameters AAC, ADC as well as fetal heart rate short-term variation (STV) according to Dawes/Redman criteria were calculated. Results Mean gestational age of both groups at study entry was 35.7 ± 2.3 weeks. There was a significant difference in AAC (mean ± SD: 1.97 ± 0.33 vs. 2.42 ± 0.57 bpm; p<0.001) and ADC (1.94 ± 0.32 vs. 2.28 ± 0.46, p<0.001) between controls and fetuses of diabetic mothers. This difference between groups could not be demonstrated using standard computerized fetal CTG analysis (STV controls 10.8 ± 3.0 vs. cases 11.3 ± 2.5 ms; p=0.32). The longitudinal measurements in the diabetes group did not show significantdifferences to measurements at study entry. Conclusions These data show increased ANS activity in late gestation fetuses of diabetic mothers. Analysis of human fetal cardiovascular and autonomic nervous system function by PRSA may offer improved surveillance over conventional techniques linking gestational diabetes pregnancy with future cardiovascular dysfunction in the offspring.