STUDY OBJECTIVE: Preterm birth delays maturation of autonomic cardiovascular control, reflected in reduced heart rate variability (HRV) in preterm compared to term infants at term-equivalent age. It has been suggested that immature cardiovascular control contributes to the increased risk for the sudden infant death syndrome (SIDS) in preterm infants. However, the effects of prone sleeping, the major SIDS risk factor, and of gestational age (GA) at birth on HRV have not been assessed in preterm infants beyond term-equivalent age. SUBJECTS AND METHODS: Very preterm (n = 21; mean GA 29.4 ± 0.3 weeks), preterm (n = 14; mean GA 33.5 ± 0.3 weeks), and term (n = 17; mean GA 40.1 ± 0.3 weeks) infants were recruited and underwent daytime polysomnography at 2-4 weeks, 2-3 months, and 5-6 months post-term corrected age (CA). Infants slept both supine and prone. HRV was assessed in the low frequency (LF) and high frequency (HF) ranges. RESULTS: There was no effect of prone sleeping on HRV parameters in either preterm group. In term infants LF/HF was significantly elevated in the prone position in AS at 2-4 weeks (P < 0.05). HF HRV was significantly reduced (P < 0.05) and LF/HF increased (P < 0.05) in very preterm compared to both preterm and term infants at 2-3 months CA. CONCLUSION: Prone sleeping did not significantly impact on heart rate variability (HRV) in preterm infants. However, reduced maturation of high frequency HRV in very preterm infants resulted in significantly altered sympathovagal balance at 2-3 months corrected age, the age of peak sudden infant death syndrome (SIDS) risk. This may contribute to the increased risk of SIDS in infants born at earlier gestational age.
STUDY OBJECTIVE: Preterm birth delays maturation of autonomic cardiovascular control, reflected in reduced heart rate variability (HRV) in preterm compared to term infants at term-equivalent age. It has been suggested that immature cardiovascular control contributes to the increased risk for the sudden infant death syndrome (SIDS) in preterm infants. However, the effects of prone sleeping, the major SIDS risk factor, and of gestational age (GA) at birth on HRV have not been assessed in preterm infants beyond term-equivalent age. SUBJECTS AND METHODS: Very preterm (n = 21; mean GA 29.4 ± 0.3 weeks), preterm (n = 14; mean GA 33.5 ± 0.3 weeks), and term (n = 17; mean GA 40.1 ± 0.3 weeks) infants were recruited and underwent daytime polysomnography at 2-4 weeks, 2-3 months, and 5-6 months post-term corrected age (CA). Infants slept both supine and prone. HRV was assessed in the low frequency (LF) and high frequency (HF) ranges. RESULTS: There was no effect of prone sleeping on HRV parameters in either preterm group. In term infants LF/HF was significantly elevated in the prone position in AS at 2-4 weeks (P < 0.05). HF HRV was significantly reduced (P < 0.05) and LF/HF increased (P < 0.05) in very preterm compared to both preterm and term infants at 2-3 months CA. CONCLUSION: Prone sleeping did not significantly impact on heart rate variability (HRV) in preterm infants. However, reduced maturation of high frequency HRV in very preterm infants resulted in significantly altered sympathovagal balance at 2-3 months corrected age, the age of peak sudden infant death syndrome (SIDS) risk. This may contribute to the increased risk of SIDS in infants born at earlier gestational age.
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