Abstract

Background Foramen ovale (FO) flow may be altered in IUGR. This study was designed to test this hypothesis. Methods Forty pregnant women (24–38 weeks) were divided into 3 groups: group I (IUGR), group II (adequate growth and maternal hypertension), and group III (normal controls). Impedance across the FO was assessed by the FO pulsatility index (FOPI): (systolic velocity − presystolic velocity)/mean velocity. Statistical analysis utilized ANOVA, Tukey test, and ROC curves. Results Mean FOPI in IUGR fetuses (n = 15) was 3.70 ± 0.99 (3.15–4.26); in the group II (n = 12), it was 2.84 ± 0.69 (2.40–3.28), and in the group III (n = 13), it was 2.77 ± 0.44 (2.50–3.04) (p=0.004). FOPI and UtA RI were correlated (r = 0.375, p=0.017), as well as FOPI and UA RI (r = 0.356, p=0.024) and, inversely, FOPI and MCA RI (r = −0.359, p=0.023). Conclusions The FO flow pulsatility index is increased in fetuses with IUGR, probably as a result of impaired left ventricular diastolic function.

Highlights

  • Intrauterine growth restriction (IUGR) is a significant clinical problem, affecting up to 10% of all pregnancies [1] and even 15% of all monochorionic twin pregnancies [2], with high perinatal morbidity and mortality rates due to fetal hypoxia [3, 4]

  • Doppler features of study groups are shown in Table 2. e FO pulsatility index (FOPI) in group I was 3.70 ± 0.99 (95% confidence interval: 3.15 to 4.26), 2.84 ± 0.69 in group II, and 2.77 ± 0.44 in group III (p 0.004) (Figure 2)

  • It was observed that IUGR fetuses had an increased impedance to ow through the Foramen ovale (FO), represented by an increased FOPI compared to control groups, probably as a result of impaired diastolic function. e same e ect has been demonstrated

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Summary

Introduction

Intrauterine growth restriction (IUGR) is a significant clinical problem, affecting up to 10% of all pregnancies [1] and even 15% of all monochorionic twin pregnancies [2], with high perinatal morbidity and mortality rates due to fetal hypoxia [3, 4]. E fetal heart is a central organ in adaptive mechanisms to hypoxia, and cardiac dysfunction is recognized as the pathophysiologic determinant of clinical deterioration in both early- and late-onset IUGR [4]. IUGR fetuses have abnormal placental changes, with increased placental vascular resistance and progressive deterioration of the UA flow [10]. Mean FOPI in IUGR fetuses (n 15) was 3.70 ± 0.99 (3.15–4.26); in the group II (n 12), it was 2.84 ± 0.69 (2.40–3.28), and in the group III (n 13), it was 2.77 ± 0.44 (2.50–3.04) (p 0.004). E FO flow pulsatility index is increased in fetuses with IUGR, probably as a result of impaired left ventricular diastolic function Conclusions. e FO flow pulsatility index is increased in fetuses with IUGR, probably as a result of impaired left ventricular diastolic function

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