Balli Sevket, Kibar Ayse Esin, Ece Ibrahim, Oflaz Mehmet Burhan, Yilmaz Ozcan
Department of Pediatric Cardiology, Balıkesir Atatürk Hospital, Yıldız Mahallesi, Soma Caddesi, Balıkesir, Turkey,
Pediatr Cardiol. 2013 Oct;34(7):1674-9. doi: 10.1007/s00246-013-0702-8. Epub 2013 Apr 17.
This study investigated cardiac function in 65 fetuses of mildly preeclamptic mothers and 55 fetuses of healthy mothers at 26-40 weeks of gestation. Fetuses with intrauterine growth restriction were excluded. Cardiac functions were evaluated by M-mode, pulsed-wave, and tissue Doppler echocardiography. The two groups were similar in terms of maternal age, gravidity, parity, and gestational age. Peak systolic aortic and pulmonary artery velocities were significantly lower in the fetuses of the preeclamptic mothers than in the fetuses of the healthy mothers. The two groups did not differ significantly in terms of shortening fraction or with regard to mitral or tricuspid annular plane systolic excursion. Pulsed-wave Doppler-derived E/A ratios in the mitral and tricuspid valves were similar in the two groups. The deceleration time of early mitral inflow was prolonged in the fetuses of the preeclamptic mothers. The Ea, Aa, and Ea/Aa ratios in the interventricular septum, left ventricle posterior wall, and right ventricle free wall were lower in the preeclampsia group than in the control group. The E/Ea ratio was higher in the preeclampsia group than in the control group. The isovolumic relaxation time and the right and left myocardial performance indices were higher in the fetuses of the preeclamptic mothers than in the fetuses of the healthy mothers. An increased ductus venosus pulsatility index (PI) and a decreased middle cerebral artery (MCA) PI were found in the fetuses of the preeclamptic mothers. All the fetuses were asymptomatic. The results suggest that the increase in fetal cardiac afterload in mild preeclampsia may have caused early subclinical changes in fetal systolic and diastolic cardiac function. In addition, the decrease in MCA-PI may have been caused by redistribution of fetal cardiac output in favor of the left ventricle, secondary to increased placental vascular resistance.
本研究调查了妊娠26 - 40周的65例轻度子痫前期母亲的胎儿和55例健康母亲的胎儿的心脏功能。排除了宫内生长受限的胎儿。通过M型、脉冲波和组织多普勒超声心动图评估心脏功能。两组在母亲年龄、孕次、产次和孕周方面相似。子痫前期母亲的胎儿的主动脉和肺动脉收缩期峰值速度显著低于健康母亲的胎儿。两组在缩短分数或二尖瓣或三尖瓣环平面收缩期偏移方面无显著差异。两组二尖瓣和三尖瓣的脉冲波多普勒衍生E/A比值相似。子痫前期母亲的胎儿二尖瓣早期血流减速时间延长。子痫前期组室间隔、左心室后壁和右心室游离壁的Ea、Aa和Ea/Aa比值低于对照组。子痫前期组的E/Ea比值高于对照组。子痫前期母亲的胎儿的等容舒张时间以及左右心肌性能指数高于健康母亲的胎儿。子痫前期母亲的胎儿中发现静脉导管搏动指数(PI)增加,而大脑中动脉(MCA)PI降低。所有胎儿均无症状。结果表明,轻度子痫前期胎儿心脏后负荷增加可能导致胎儿心脏收缩和舒张功能早期亚临床变化。此外,MCA-PI降低可能是由于胎盘血管阻力增加,胎儿心输出量重新分配有利于左心室所致。