Pregnancy Outcomes in Women after the Fontan Procedure.

Women with single ventricle physiology after the Fontan procedure, despite numerous possible complications, can reach adulthood and give birth. Pregnancy poses a hemodynamic burden for distorted physiology of Fontan circulation, but according to the literature, it is usually well tolerated unless the patient is a "failing" Fontan. Our study aimed to assess maternal and fetal outcomes in patients after the Fontan procedure followed up in two tertiary Polish medical centers. We retrospectively evaluated all pregnancies in women after the Fontan procedure who were followed up between 1995-2022. During the study period, 15 women after the Fontan procedure had 26 pregnancies. Among 26 pregnancies, eleven ended with miscarriages, and 15 pregnancies resulted in 16 live births. Fetal complications were observed in 9 (56.3%) live births, with prematurity being the most common complication (n = 7, 43.8%). We recorded 3 (18.8%) neonatal deaths. Obstetrical complications were present in 6 (40%) out of 15 completed pregnancies-two (13.3%) cases of abruptio placentae, two (13.3%) pregnancies with premature rupture of membranes, and two (13.3%) patients with antepartum hemorrhage. There was neither maternal death nor heart failure decompensation during pregnancy. In two (13.3%) women, atrial arrhythmia developed. One (6.7%) patient in the second trimester developed ventricular arrhythmia. None of the patients suffered from systemic thromboembolism during pregnancy. Pregnancy in women after the Fontan procedure is well tolerated. However, it is burdened by a high risk of miscarriage and multiple obstetrical complications. These women require specialized care provided by both experienced cardiologists and obstetricians.

Does the Blood-Brain Barrier Integrity Change in Regard to the Onset of Fetal Growth Restriction?

The aim of the study was to determine whether early-onset and late-onset fetal growth restriction (FGR) differentially affects the blood-brain barrier integrity. Furthermore, the purpose of the study was to investigate the relationship between the blood-brain barrier breakdown and neurological disorders in FGR newborns. To evaluate the serum tight junction (TJ) proteins and the placental TJ proteins expression, an ELISA method was used. A significant difference in serum OCLN concentrations was noticed in pregnancies complicated by the early-onset FGR, in relation to the intraventricular hemorrhage (IVH) occurrence in newborns. No significant differences in concentrations of the NR1 subunit of the N-methyl-d-aspartate receptor (NR1), nucleoside diphosphate kinase A (NME1), S100 calcium-binding protein B (S100B), occludin (OCLN), claudin-5 (CLN5), zonula occludens-1 (zo-1), the CLN5/zo-1 ratio, and the placental expression of OCLN, CLN5, claudin-4 (CLN4), zo-1 were noticed between groups. The early-onset FGR was associated with a higher release of NME1 into the maternal circulation in relation to the brain-sparing effect and premature delivery. Additionally, in late-onset FGR, the higher release of the S100B into the maternal serum in regard to fetal distress was observed. Furthermore, there was a higher release of zo-1 into the maternal circulation in relation to newborns' moderate acidosis in late-onset FGR. Blood-brain barrier disintegration is not dependent on pregnancy advancement at the time of FGR diagnosis. NME1 may serve as a biomarker useful in the prediction of fetal circulatory centralization and extremely low birth weight in pregnancies complicated by the early-onset FGR. Moreover, the serum zo-1 concentration may have prognostic value for moderate neonatal acidosis in late-onset FGR pregnancies.

Preeclampsia and Fetal Growth Restriction as Risk Factors of Future Maternal Cardiovascular Disease-A Review.

Cardiovascular diseases (CVDs) remain the leading cause of death in women worldwide. Although traditional risk factors increase later-life CVD, pregnancy-associated complications additionally influence future CVD risk in women. Adverse pregnancy outcomes, including preeclampsia and fetal growth restriction (FGR), are interrelated disorders caused by placental dysfunction, maternal cardiovascular maladaptation to pregnancy, and maternal abnormalities such as endothelial dysfunction, inflammation, hypercoagulability, and vasospasm. The pathophysiologic pathways of some pregnancy complications and CVDs might be linked. This review aimed to highlight the associations between specific adverse pregnancy outcomes and future CVD and emphasize the importance of considering pregnancy history in assessing a woman's CVD risk. Moreover, we wanted to underline the role of maternal cardiovascular maladaptation in the development of specific pregnancy complications such as FGR.

The role of corticoliberin concentration levels and placental CRH receptors 1 and 2 in the prolongation of pregnancy.

OBJECTIVE: To examine the changes in CRH concentrations in the blood serum of pregnant women and in the placenta of patients after the 41st week of gestation, and to determine its influence on the effectiveness of inducing labor and its progress. MATERIALS AND METHODS: The study group comprised pregnant patients who did not deliver until the 41 week of gestation (n = 114). The control group was divided into two subgroups: patients in whom delivery started spontaneously before the 41st week of gestation (n = 24) and pregnant patients in whom delivery started spontaneously after the 41st week of gestation (n = 23). Blood serum and placenta were obtained from the patients. Corticoliberin originating from blood serum was assessed with the use of ELISA Kit. Parts of the placenta were stained with monoclonal antibodies for the presence of corticoliberin, corticoliberin receptors 1 and 2. RESULTS: No statistically significant differences were found with regard to corticoliberin concentrations in the blood or during a qualitative assessment of the number of CRH R1 in the placenta between the research groups. However, corticoliberin receptor 2 had a statistically higher expression rate in the control group in which the delivery started spontaneously before the 41st week of gestation. CONCLUSION: In post-term pregnancy, the up-regulation of CRH R2 receptor is disturbed with no change in CRH R1 expression, which complicates the initiation of labor despite correct corticoliberin levels in both blood serum and the placenta. Pregnancy duration over 41 weeks and the effectiveness of preinducing or inducing labor do not depend on corticoliberin concentrations.

Does platelet aggregation have any importance in fetal growth restriction pregnancies?

OBJECTIVES: The aim of the study was to evaluate platelet (PLT) concentration, mean platelet volume (MPV), PLT aggregation and its velocity in pregnancy complicated with fetal growth restriction (FGR) and to analyze the PLT aggregation according to the gestational age and Doppler velocimetry. MATERIAL AND METHODS: The study group included 29 pregnant women diagnosed with FGR. The control group-consisted of 27 females in uncomplicated pregnancy. Then both groups were divided according to the gestational week (< and ≥ 36 weeks) and Doppler velocimetry results. The adenosine diphosphate (ADP) induced PLT aggregation was performed with the help of the electrical impedance. RESULTS: There was a significant positive correlation between gestational age and PLT aggregation and between gestational age and velocity of PLT aggregation in FGR. Patients with FGR ≥ 36 weeks of gestation had 73% higher PLT aggregation than control group. Within the FGR group, the PLT aggregation was 135% higher in pregnancies ≥ 36 weeks as compared to < 36 weeks of gestation. In FGR pregnancies ≥ 36 weeks with impaired flow in both uterine arteries (UtA), 2.3-fold higher PLT aggregation was found as compared to FGR patients with normal flow or abnormal flow in one UtA. CONCLUSIONS: The increased PLT aggregation in FGR is related to gestational week and occurs in pregnancies ≥ 36 weeks of gestation. The PLT hyperaggregability in growth-restricted pregnancies is associated with abnormal Doppler velocimetry in both UtA, comparing to patients with altered blood flow in one UtA or normal pulsatility index in both UtA, suggesting the PLT activation due to impaired uteroplacental circulation.