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  • Title: Power spectrum analysis of heart rate and blood flow velocity variability measured in the umbilical and uterine arteries in early pregnancy: a comparative study.
    Author: Struijk PC, Ursem NT, Mathews J, Clark EB, Keller BB, Wladimiroff JW.
    Journal: Ultrasound Obstet Gynecol; 2001 Apr; 17(4):316-21. PubMed ID: 11339188.
    Abstract:
    OBJECTIVE: To compare power spectral derived variability parameters from the fetal side of the placental circulation with those from the maternal side of the placental circulation, during early pregnancy. METHODS: Doppler velocity waveforms were obtained from both the umbilical and the uterine arteries in a study group of 40 pregnant women between 10 and 14 (n = 25) and 15 and 20 (n = 15) weeks of gestation. The coefficient of variation of both the beat-to-beat heart rate variability and the blood flow velocity variability was determined. The ratio of the integrated low-frequency components (< 0.2 Hz) and the integrated high-frequency components (> 0.2 Hz) from normalized power spectrum analysis (LH-ratio) was established, to reflect sympathovagal balance. RESULTS: The coefficient of variation and LH-ratio of fetal heart rate variability constitute only a fraction of the same maternal heart rate variability parameters. Nevertheless a highly significant increase (P < 0.001) in LH-ratio was demonstrated with advancing gestational age. The coefficient of variation and LH-ratio of blood flow velocity variability were significantly lower in the fetal umbilical artery only in the 10-14-weeks' gestation group. Due to a decrease of the maternal uterine blood flow velocity variability parameters with advancing gestational age, statistically equal fetal and maternal values for coefficient of variation and LH-ratio were found in the 15-20 weeks' gestation group. CONCLUSIONS: The increase in LH-ratio of fetal heart rate variability indicates functional development of the fetal autonomic nervous system at 15-20 weeks' gestation. The umbilical blood flow velocity variability may be secondary to maternal uterine arterial flow variability rather than due to primary changes in fetal cardiovascular function.
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