Objectives: Few data exist for counseling and perinatal management of women after an antenatal diagnosis of early‐onset fetal growth restriction. Yet, the consequences of preterm delivery and its attendant morbidity for both mother and baby are far reaching. The objective of this study was to describe perinatal morbidity and mortality following early‐onset fetal growth restriction based on time of antenatal diagnosis and delivery.Methods: We report cohort outcomes for a prospective multicenter randomized management study of fetal growth restriction (Trial of Randomized Umbilical and Fetal Flow in Europe (TRUFFLE)) performed in 20 European perinatal centers between 2005 and 2010. Women with a singleton fetus at 26–32 weeks of gestation, with abdominal circumference < 10^th percentile and umbilical artery Doppler pulsatility index > 95^th percentile, were recruited. The main outcome measure was a composite of fetal or neonatal death or severe morbidity: survival to discharge with severe brain injury, bronchopulmonary dysplasia, proven neonatal sepsis or necrotizing enterocolitis.Results: Five‐hundred and three of 542 eligible women formed the study group. Mean ± SD gestational age at diagnosis was 29 ± 1.6 weeks and mean ± SD estimated fetal weight was 881 ± 217 g; 12 (2.4%) babies died in utero. Gestational age at delivery was 30.7 ± 2.3 weeks, and birth weight was 1013 ± 321 g. Overall, 81% of deliveries were indicated by fetal condition and 97% were by Cesarean section. Of 491 liveborn babies, outcomes were available for 490 amongst whom there were 27 (5.5%) deaths and 118 (24%) babies suffered severe morbidity. These babies were smaller at birth (867 ± 251 g) and born earlier (29.6 ± 2.0 weeks). Death and severe morbidity were significantly related to gestational age, both at study entry and delivery and also with the presence of maternal hypertensive morbidity. The median time to delivery was 13 days for women without hypertension, 8 days for those with gestational hypertension, 4 days for pre‐eclampsia and 3 days for HELLP syndrome.Conclusions: Fetal outcome in this study was better than expected from contemporary reports: perinatal death was uncommon (8%) and 70% survived without severe neonatal morbidity. The intervals to delivery, death and severe morbidity were related to the presence and severity of maternal hypertensive conditions. Copyright © 2013 ISUOG. Published by John Wiley & Sons Ltd.

OBJECTIVE: To identify specific estimates and predictors of neonatal morbidity and mortality in early onset fetal growth restriction due to placental dysfunction. METHODS: Prospective multicenter study of prenataly diagnosed growth-restricted liveborn neonates of less than 33 weeks of gestational age. Relationships between perinatal variables (arterial and venous Dopplers, gestational age, birth weight, acid-base status, and Apgar scores) and major neonatal complications, neonatal death, and intact survival were analyzed by logistic regression. Predictive cutoffs were determined by receiver operating characteristic curves. RESULTS: Major morbidity occurred in 35.9% of 604 neonates: bronchopulmonary dysplasia in 23.2% (n=140), intraventricular hemorrhage in 15.2% (n=92), and necrotizing enterocolitis in 12.4% (n=75). Total mortality was 21.5 % (n=130), and 58.3% survived without complication (n=352). From 24 to 32 weeks, major morbidity declined (56.6% to 10.5%), coinciding with survival that exceeded 50% after 26 weeks. Gestational age was the most significant determinant (P<.005) of total survival until 26^6/7 weeks (r²=0.27), and intact survival until 29^2/7 weeks (r²=0.42). Beyond these gestational-age cutoffs, and above birth weight of 600 g, ductus venosus Doppler and cord artery pH predicted neonatal mortality (P<.001, r²=0.38), and ductus venosus Doppler alone predicted intact survival (P<.001, r²=0.34). CONCLUSION: This study provides neonatal outcomes specific for early-onset placenta-based fetal growth restriction quantifying the impact of gestational age, birth weight, and fetal cardiovascular parameters. Early gestational age and birth weight are the primary quantifying parameters. Beyond these thresholds, ductus venosus Doppler parameters emerge as the primary cardiovascular factor in predicting neonatal outcome. LEVEL OF EVIDENCE: II

Preeclampsia is associated with asymptomatic global left ventricular abnormal function and geometry during the acute phase of the disorder. These subclinical abnormalities in cardiac findings are known to be important in cardiovascular risk stratification for nonpregnant patients. Furthermore, epidemiological studies have also demonstrated a relationship between preeclampsia and cardiac morbidity and mortality later in life. The aim of this study was to evaluate the postpartum natural history and clinical significance of asymptomatic left ventricular impairment known to occur with acute preeclampsia. This was a prospective longitudinal case-control study of 64 subjects with preeclampsia and 78 matched controls. There were 3 time point assessments, pregnancy and 1 and 2 years postpartum. The assessments included a medical and family history, blood pressure profile, echocardiography, and 12-lead ECG. At 1 year postpartum, asymptomatic left ventricular moderate-severe dysfunction/hypertrophy was significantly higher in preterm preeclampsia (56%) compared with term preeclampsia (14%) or matched controls (8%; P values <0.001). The risk of developing essential hypertension within 2 years was significantly higher in both preterm preeclamptic women and those with persistent left ventricular moderate-severe abnormal function/geometry. The cardiovascular implications of preeclampsia do not end with the birth of the infant and placenta. The majority of preterm preeclamptic women have stage B asymptomatic heart failure postpartum, and 40% develop essential hypertension within 1 to 2 years after pregnancy. Women with a history of preterm preeclampsia may benefit from formal cardiovascular risk assessment in the 1 to 2 years after delivery to identify those who would benefit from targeted therapeutic intervention.

Objective: To evaluate the effectiveness of adding outlet views to the four chamber view in routine prenatal ultrasound screening for major congenital heart defects (CHD) as performed by trained sonographers, and to compare the procedure with current practice. Design and setting: Prospective observational study at a London teaching hospital. Participants and methods: 9277 women booked at a single institution (80% had first trimester nuchal translucency measurement) due to have routine fetal cardiac screening using the four chamber and outflow tract views at > 18 weeks of gestation. Main outcome measure: Identification of major CHD in chromosomally normal and abnormal pregnancies antenatally or postnatally. Results: There were 40 abnormalities (4.3/1000), of which 30 were chromosomally normal (3.3/1000). The overall antenatal detection rate was 75% (95% confidence interval (CI) 59% to 87%) and 70% (95% CI 51% to 85%) for euploid pregnancies. Abnormal cardiac views accounted for 70% of all prenatal diagnoses, 30% of which were made at ≤ 18 weeks. The sensitivity of cardiac views during the first scan at > 18 weeks was 52%. Of all patients undergoing nuchal translucency screening, 34 had major CHD, nine with increased nuchal translucency (26.5%). Factors influencing the results of this screening programme were training and audit of operators, adequate equipment for antenatal examination, ease of access, and low threshold for referral to specialised fetal echocardiography. Conclusion: Adding ventricular outlet views to the four chamber assessment of the heart at routine fetal anomaly scans at > 18 weeks is the most effective technique to detect CHD prenatally. The success of such a programme depends on an infrastructure committed to continuous in house training of obstetric ultrasonographers coupled with feedback from specialised fetal cardiologists, as well as adequate resource allocation to obstetric hospitals involved with antenatal screening.

Background—Patients with heart failure and chronic anemia frequently demonstrate left ventricular (LV) trabeculations, which may be compatible with the diagnosis of LV noncompaction. We used the pregnancy model, which is characterized by a reversible increase in cardiac preload and other changes in cardiac function, to assess the development of de novo LV trabeculations in women with morphologically normal hearts. Methods and Results—One hundred two primigravida pregnant women were evaluated longitudinally with a series of echocardiograms in the first trimester, in the third trimester, and postpartum. Echocardiograms were analyzed according to established guidelines. Increased LV trabeculations and the presence of LV noncompaction were based on established criteria. Pregnancy was associated with an increased heart rate, stroke volume, and cardiac output, as well as increased LV volume and mass. During pregnancy, 26 women (25.4%) developed increased trabeculations. Eight women showed sufficient trabeculations to fulfill criteria for LV noncompaction. During the postpartum follow-up period of 24±3 months, 19 women (73%) demonstrated complete resolution of trabeculations, and 5 showed a marked reduction in the trabeculated layer. Conclusions—Pregnancy induces de novo LV trabeculations in a significant proportion of women. The results suggest that LV trabeculations occur in response to increased LV loading conditions or other physiological responses to pregnancy and are not specific for LV noncompaction. These factors should be considered in the assessment of individuals with LV trabeculations outside the context of symptoms of heart failure or familial cardiomyopathy.