<p>This prospective observational study investigated the hemodynamic changes in cardiac function and cerebral blood flow velocity (CBFV) in neonates with hypoxic-ischemic encephalopathy (HIE) requiring therapeutic hypothermia (TH). Data were collected at five timepoints, viz., pre-TH (T0), 0–24&#xa0;h of TH (T1), 24–48&#xa0;h of TH (T2), 48–72&#xa0;h of TH (T3), and within 24&#xa0;h postrewarming (T4). Healthy neonates served as the control group (<i>n</i> = 20). A total of 43 neonates with HIE requiring TH were enrolled. Left ventricular output was significantly lower than that in the control group at T1 and T2 and increased from T1 to T4 (92.8 ± 29.5&#xa0;ml/kg/min vs. 103 ± 29.7&#xa0;ml/kg/min vs. 109.5 ± 28&#xa0;ml/kg/min vs. 144.5 ± 34.4&#xa0;ml/kg/min (T4 vs. T1, T2, or T3: <i>p</i> &lt; 0.05). Systolic mitral annular velocity and systolic tricuspid annular velocity were lower than those in the control group across T1–T4 (<i>p</i> &lt; 0.05). Middle cerebral artery peak systolic flow velocities increased across T1–T3 (T1 vs. T2, <i>p</i> &lt; 0.05; T1 vs. T3, <i>p</i> &lt; 0.05; T1 vs. T4, <i>p</i> &lt; 0.05).</p><p> <i>Conclusion</i>: Irrespective of HIE severity, left cardiac output reduced but consistently increased over time in neonates with HIE who required TH. The trend of CBFV gradually increased throughout the TH and rewarming phase.<Table Float="No" ID="Taba"> <tgroup cols="1"> <colspec align="left" colname="c1" colnum="1" /> <tbody> <row> <entry align="left" colname="c1"> <p><b>What is Known:</b></p> <p>• <i>TH is the standard neuroprotective treatment for moderate-to-severe neonatal HIE, yet survivors continue to face significant neurological sequelae.</i></p> <p>• <i>Hypoxic-ischemic injury often leads to myocardial dysfunction, and TH itself induces hemodynamic alterations; however, the dynamic evolution of cardiac function and cerebral hemodynamics in neonates with HIE during TH has not been fully elucidated.</i></p> </entry> </row> <row> <entry align="left" colname="c1"> <p><b>What is New:</b></p> <p>• <i>This study demonstrates that, regardless of HIE severity, left cardiac output decreases initially during TH but consistently recovers over time, and biventricular longitudinal systolic function does not deteriorate during the hypothermia phase.</i></p> <p>• <i>We further observed a gradual increase in CBFV throughout both TH and rewarming.</i></p> </entry> </row> </tbody> </tgroup> </Table></p>

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Hemodynamic changes in neonatal hypoxic-ischemic encephalopathy requiring therapeutic hypothermia

  • Shuhan Yu,
  • Tiantian Xiao,
  • Biao Li,
  • Qi Zhang,
  • Jingyi Zhang,
  • Juetao Fu,
  • Xueli Lu,
  • Yongzhong Zhou,
  • Mingsheng Zheng,
  • Xin Ding,
  • Sheng Yang,
  • Qing Gao,
  • Yiyong Fu,
  • Rong Ju

摘要

This prospective observational study investigated the hemodynamic changes in cardiac function and cerebral blood flow velocity (CBFV) in neonates with hypoxic-ischemic encephalopathy (HIE) requiring therapeutic hypothermia (TH). Data were collected at five timepoints, viz., pre-TH (T0), 0–24 h of TH (T1), 24–48 h of TH (T2), 48–72 h of TH (T3), and within 24 h postrewarming (T4). Healthy neonates served as the control group (n = 20). A total of 43 neonates with HIE requiring TH were enrolled. Left ventricular output was significantly lower than that in the control group at T1 and T2 and increased from T1 to T4 (92.8 ± 29.5 ml/kg/min vs. 103 ± 29.7 ml/kg/min vs. 109.5 ± 28 ml/kg/min vs. 144.5 ± 34.4 ml/kg/min (T4 vs. T1, T2, or T3: p < 0.05). Systolic mitral annular velocity and systolic tricuspid annular velocity were lower than those in the control group across T1–T4 (p < 0.05). Middle cerebral artery peak systolic flow velocities increased across T1–T3 (T1 vs. T2, p < 0.05; T1 vs. T3, p < 0.05; T1 vs. T4, p < 0.05).

Conclusion: Irrespective of HIE severity, left cardiac output reduced but consistently increased over time in neonates with HIE who required TH. The trend of CBFV gradually increased throughout the TH and rewarming phase.

What is Known:

TH is the standard neuroprotective treatment for moderate-to-severe neonatal HIE, yet survivors continue to face significant neurological sequelae.

Hypoxic-ischemic injury often leads to myocardial dysfunction, and TH itself induces hemodynamic alterations; however, the dynamic evolution of cardiac function and cerebral hemodynamics in neonates with HIE during TH has not been fully elucidated.

What is New:

This study demonstrates that, regardless of HIE severity, left cardiac output decreases initially during TH but consistently recovers over time, and biventricular longitudinal systolic function does not deteriorate during the hypothermia phase.

We further observed a gradual increase in CBFV throughout both TH and rewarming.