Variations in inclusion criteria across studies lead to differences in mortality rates within patient populations [7]. Mortality rates can range from 23% in populations with isolated high-risk cardiac anomalies [2] to 6%, 7.9%, and 8.4% in others [5, 9, 14]. In our study, the neonatal mortality rate was found to be 20.9%. The distribution of the severity of fetal heart disease in cases included in the study (such as single ventricle physiology, cardiac dysfunction, etc.) could alter neonatal mortality rates. Most cases reaching our perinatology unit are referred from external centers and are at high risk of postnatal hemodynamic instability. Therefore, the higher number of group 2 and 3 cases in our study might have contributed to the higher neonatal mortality rate compared to the literature [5, 14]. According to Lucron H and Derridj N, the severity of cardiac disease is a key determinant of mortality, with having group-2 heart disease increasing neonatal mortality by 2.9 times and group-3 heart disease by 5.3 times in our study [5, 6]. Surgical success and thus neonatal outcomes can vary based on the technical capabilities of the center where the cardiac surgery is performed [10], the experience of the surgical team, the presence of a cardiac surgical unit at the place of birth, and the conditions of the neonatal intensive care unit [25]. Our hospital is a tertiary prenatal diagnosis center with good neonatal intensive care conditions but, like many hospitals in our country, does not have a cardiac surgical unit. In many centers in our country with a cardiac surgical unit, there is no delivery unit. Therefore, prenatal diagnosis, planned delivery, and pre-delivery counseling are important for many clinics, including our perinatology clinic. Even though newborns are transferred under appropriate conditions in emergency deliveries where the delivery room is not prepared and/or communication with the cardiac surgical center cannot be established, this situation can still affect neonatal outcomes. According to Purkey NJ and Jowett VC, being born in a tertiary center or a hospital close to a tertiary center improves neonatal outcomes [10, 26]. If our study had been conducted in a hospital with a delivery unit, neonatal intensive care, and a cardiac surgical center, different neonatal outcomes might have been observed. The presence of genetic diseases and extracardiac anomalies are other factors that can affect mortality [8, 15, 21, 27]. When planning our study, we excluded cases of multiple pregnancies and cases with chromosomal diseases, as these could change neonatal outcomes. Since most of our cases with fetal heart disease also had extracardiac anomalies and the number of cases with isolated cardiac disease was low, we included patients with extracardiac anomalies in our study. In cases where neonatal mortality occurred, CNS anomalies were more frequently present, with the statistical significance being borderline. When cases with CNS anomalies were examined, the number of cases with cerebellar anomalies, severe hydrocephalus, and vermis anomalies was high. Due to the nature of the anomaly, CNS anomalies were considered a confounding factor in predicting mortality. There was no difference in the presence of skeletal system anomalies between cases with and without neonatal mortality. However, when factors predicting neonatal mortality were modeled, the presence of a skeletal system anomaly increased the risk of neonatal mortality by 5.1 times, and the presence of GUS anomalies increased the risk by 4.03 times. The presence of anomalies in multiple systems did not contribute additional risk to mortality. The presence of extracardiac anomalies increased neonatal mortality in fetal heart disease, consistent with the literature [1, 7, 15, 27, 28]. Being born before the 34th week of gestation did not affect mortality, contrary to the literature [4, 6, 7, 27]. This result was thought to be due to the low number of preterm births. The mode of delivery (vaginal/cesarean) did not affect neonatal mortality in our study. Although an increase in urgent cesarean section rates due to fetal distress caused by non-reassuring fetal heart rate was reported, urgent cesarean section due to fetal distress did not affect neonatal mortality in our study [12, 13, 17]. To enable births to occur during working hours, the need for labor induction has increased, providing an opportunity to assess its impact on neonatal mortality. Regardless of whether the birth was vaginal or cesarean, the neonatal mortality rate was significantly higher in cases where prostaglandin ± oxytocin was administered compared to those who received only oxytocin or did not undergo induction. This raises the question of whether prostaglandins could be responsible for this effect. According to Rossi, the intolerance of a fetus with heart disease to labor induction is 13 times higher compared to a fetus without heart disease [13]. In Asoglu's study, there was no difference in terms of Apgar score and blood pH in newborns between the group that underwent labor induction and the group that did not [15]. Although the use of induction in the delivery of pregnant women with fetal heart disease has been evaluated in current studies, the type/dose of drugs used in induction has not been specified, and its effect on neonatal outcomes has not been analyzed [12, 13, 15]. Since there were few cases in our study where induction of labor was performed using only prostaglandins, the effect of prostaglandins on mortality could not be analyzed. The current data does not provide a solid statistical basis for the interpretation that "The use of prostaglandins in labor induction increases neonatal mortality." This observation requires further validation through studies involving larger sample sizes.
Our study has several limitations and strengths. Some pregnant women in our study chose not to undergo prenatal genetic analysis, which could have affected our ability to exclude genetic syndromes not diagnosed at birth, despite excluding aneuploidies through physical examination at birth. Additionally, births were planned near-term rather than at term due to hospital conditions, which may have influenced obstetric and neonatal outcomes. However, the study was conducted in a single center, ensuring consistency in data collection and management. Furthermore, pregnant women were followed up according to 'written delivery protocols,' minimizing individual differences in decisions such as labor induction and labor follow-up.
In conclusion, the severity of fetal heart disease, particularly the presence of group-3 heart disease, low BW, and the presence of extracardiac anomalies, are significant factors influencing neonatal mortality. Our findings suggest that labor induction with prostaglandin ± oxytocin may increase neonatal mortality, although further validation through studies with larger sample sizes is needed. Obstetricians are advised to consider this when deciding on labor induction, opting for prostaglandin use selectively. The study underscores the importance of a personalized approach in managing fetal heart diseases to accurately predict and address neonatal outcomes.