In newborns with hypoxic-ischaemic encephalopathy, more profound altered right and left ventricular function has been associated with mortality or brain injury. Mechanisms underlying cardiac dysfunction in this population are thought to be related to the persistence of increased pulmonary vascular resistance and myocardial ischaemia. We sought to compare cardiac function in newborns with hypoxic-ischaemic encephalopathy to controls using echocardiography.

We did a retrospective case–control study with moderate or severe hypoxic-ischaemic encephalopathy between 2008 and 2017. Conventional and speckle-tracking echocardiography measures were extracted to quantify right and left ventricular systolic and diastolic function. Fifty-five newborns with hypoxic-ischaemic encephalopathy were compared to 28 controls.

Hypoxic-ischaemic encephalopathy newborns had higher estimated systolic pulmonary pressure (62.5 ± 15.0 versus 43.8 ± 17.3 mmHg, p < 0.0001) and higher systolic pulmonary artery pressure/systolic blood pressure ratio [101 ± 16 (iso-systemic) versus 71 ± 27 (2/3 systemic range) %, p < 0.0001]. Tricuspid annular plane systolic excursion was decreased (7.5 ± 2.2 versus 9.0 ± 1.4 mm, p = 0.002), E/e’ increased (7.9 ± 3.3 versus 5.8 ± 2.0, p = 0.01), and right ventricle-myocardial performance index increased (68.1 ± 21.5 versus 47.8 ± 9.5, p = 0.0001) in hypoxic-ischaemic encephalopathy. Conventional markers of left ventricle systolic function were similar, but e’ velocity (0.059 ± 0.019 versus 0.070 ± 0.01, p = 0.03) and left ventricle-myocardial performance index were statistically different (77.9 ± 26.2 versus 57.9 ± 11.2, p = 0.001). The hypoxic-ischaemic encephalopathy group had significantly altered right and left ventricular deformation parameters by speckle-tracking echocardiography. Those with decreased right ventricle-peak longitudinal strain were more likely to have depressed left ventricle-peak longitudinal strain.

Newborns with hypoxic-ischaemic encephalopathy have signs of increased pulmonary pressures and altered biventricular systolic and diastolic function.

在患有缺氧缺血性脑病的新生儿中，右心室和左心室功能的更深刻改变与死亡或脑损伤有关。该人群心脏功能障碍的机制被认为与持续增加的肺血管阻力和心肌缺血有关。我们试图使用超声心动图将缺氧缺血性脑病新生儿的心脏功能与对照组进行比较。

我们在 2008 年至 2017 年间对中度或重度缺氧缺血性脑病进行了一项回顾性病例对照研究。提取常规超声心动图和斑点追踪超声心动图测量值来量化右心室和左心室收缩和舒张功能。将 55 名患有缺氧缺血性脑病的新生儿与 28 名对照新生儿进行了比较。

缺氧缺血性脑病新生儿的估计收缩压肺动脉压较高（62.5 ± 15.0 对比 43.8 ± 17.3 mmHg，p < 0.0001），收缩压肺动脉压/收缩压比值较高 [101 ± 16（等全身）对比 71 ± 27（等全身） 2/3 全身范围)%, p < 0.0001]。三尖瓣环平面收缩期偏移减少（7.5 ± 2.2 与 9.0 ± 1.4 mm，p = 0.002），E/e' 增加（7.9 ± 3.3 与 5.8 ± 2.0，p = 0.01），右心室心肌性能指数增加（缺氧缺血性脑病中为 68.1 ± 21.5 与 47.8 ± 9.5，p = 0.0001）。左心室收缩功能的常规标志物相似，但 e' 速度（0.059 ± 0.019 与 0.070 ± 0.01，p = 0.03）和左心室心肌性能指数有统计学差异（77.9 ± 26.2 与 57.9 ± 11.2，p = 0.001） 。通过斑点追踪超声心动图，缺氧缺血性脑病组的右心室和左心室变形参数显着改变。那些右心室峰值纵向应变降低的人更有可能左心室峰值纵向应变降低。

患有缺氧缺血性脑病的新生儿有肺动脉压升高和双心室收缩和舒张功能改变的迹象。