Abstract

The cause of antepartum fetal heart rate (FHR) short-term variability (STV) interfetal differences and their interaction with the biological environment are poorly understood. We suggest that: i) norepinephrine increases baseline STV (inducing the high frequency component while the low frequency component is due to parasympathetic co-activation, see figure), and ii) transient epinephrine release induces transient FHR accelerations. The norepinephrine/epinephrine ratio is known to increase after childbirth in adults with uncomplicated obesity. To test our hypothesis, we studied the relationship between higher antepartum STV values and several maternal-fetal metabolic syndrome criteria. Our study included 477 unselected single pregnancies (initial weight 62±12 kg) involved in an enhanced prenatal care program (7 FHR tracings per pregnancy; high-risk cases included). STV was calculated by SisPorto version 3.6. As we suspected that some low STV tracings could introduce bias, we focused on the highest STV level of one antepartum tracing, rather than the highest level of the average of all tracings. The case group was defined by the greatest STV ≥ 97th percentile, as well as a low FHR acceleration score. The remaining cases were assigned to the control group. A univariate descriptive analysis was used to compare the case group (12 pregnancies) with the control group data. We observed the following significant higher values in the case group: initial maternal weight (> 100 kg 25% vs. 1%, > 80 kg 17% vs. 7%, p<0.001), gestational diabetes mellitus (42% vs. 7%, p<0.002), incidence of glycemia > 90th percentile at one-hour post second trimester load (36% vs. 9%, p<0.02), and, lastly, infant birth weight (3,717g ± 591 vs. 3,385g ± 470, p<0.03). We confirm the relationship between high antepartum STV and maternal-fetal metabolic syndrome. It supports our hypothesis concerning the respective effects of norepinephrine and epinephrine on FHR. Improved antepartum FHR analysis could help to detect maternal-fetal metabolic syndromes, insulin resistance, and delayed lung maturity.

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