Assessment of Fetal Cardiac Function in Mild Preeclampsia


Balli S., Kibar A. E. , Ece I. , OFLAZ M. B. , Yilmaz O.

PEDIATRIC CARDIOLOGY, cilt.34, ss.1674-1679, 2013 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 34 Konu: 7
  • Basım Tarihi: 2013
  • Doi Numarası: 10.1007/s00246-013-0702-8
  • Dergi Adı: PEDIATRIC CARDIOLOGY
  • Sayfa Sayıları: ss.1674-1679

Özet

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.