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
Summary
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
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have