BackgroundThere is no consensus on the most effective and best tolerated first‐line antiarrhythmic treatment for fetal tachyarrhythmia. The purpose of this systematic review and meta‐analysis was to compare the efficacy, safety, and fetal–maternal tolerance of first‐line monotherapies for fetal supraventricular tachycardia and atrial flutter.Methods and ResultsA comprehensive search of several databases was conducted through January 2017. Only studies that made a direct comparison between first‐line treatments of fetal tachyarrhythmia were included. Outcomes of interest were termination of fetal tachyarrhythmia, fetal demise, and maternal complications. Ten studies met inclusion criteria, with 537 patients. Overall, 291 patients were treated with digoxin, 137 with flecainide, 102 with sotalol, and 7 with amiodarone. Digoxin achieved a lower rate of supraventricular tachycardia termination compared with flecainide (odds ratio [OR]: 0.773; 95% confidence interval [CI], 0.605–0.987; I2=34%). In fetuses with hydrops fetalis, digoxin had lower rates of tachycardia termination compared with flecainide (OR: 0.412; 95% CI, 0.268–0.632; I2=0%). There was no significant difference in the incidence of maternal side effects between digoxin and flecainide groups (OR: 1.134; 95% CI, 0.129–9.935; I2=80.79%). The incidence of maternal side effects was higher in patients treated with digoxin compared with sotalol (OR: 3.148; 95% CI, 1.468–6.751; I2=0%). There was no difference in fetal demise between flecainide and digoxin (OR: 0.767; 95% CI, 0.140–4.197; I2=44%).ConclusionsFlecainide may be more effective treatment than digoxin as a first‐line treatment for fetal supraventricular tachycardia.

In the fetus with critical left heart obstruction, a threshold forward/reverse time-velocity integral ratio of 3 or less optimizes specificity for predicting emergency atrial septostomy. Most late second trimester values will not change over time with regard to threshold levels.

Right ventricular outflow tract abnormalities impact ∼ 9% of recipient twins in twin-twin transfusion syndrome, many of whom will have persistent abnormalities despite otherwise successful therapy. These data justify efforts to increase awareness and monitoring of the cardiac sequelae of twin-twin transfusion syndrome in these high-risk pregnancies.

Background: Hypoplastic left heart syndrome (HLHS) is associated with significant mortality and morbidity. Fetal head growth abnormalities have been identified in a subset of HLHS fetuses, but it is unclear whether specific patterns of maladaptive growth affect clinical outcomes. We hypothesized that poor fetal head growth is associated with an increased frequency of adverse clinical outcomes. Methods: We retrospectively examined a cohort of HLHS patients from midgestation to 1 y of age. Fetal and birth anthropometric measurements were analyzed using the Olsen standard, and clinical outcomes were obtained. results: A total of 104 HLHS patients were identified over a 12-y period; fetal data were available in 38 cases. HLHS neonates demonstrated a high incidence of microcephaly (12%), small head size (27%), and poor head growth (32%). Allcause mortality was 31% at 30 d and 43% at 1 y. Neurologic outcomes were observed in 12% of patients and were significantly increased with microcephaly (43 vs. 4%; P = 0.02). The average length of hospital stay following stage I palliation was 33.4 ± 33 d, correcting for early death. conclusion: In term nonsyndromic HLHS, fetal and neonatal microcephaly are associated with early adverse neurologic outcomes but not mortality.

Purpose We designed this retrospective observational study on the use of a 2 -agonist dexmedetomidine to determine the optimum intranasal dose to achieve sedation for pediatric transthoracic echocardiography and to identify any dose-related adverse effects. Methods Outpatient children aged three months to three years with diverse diagnoses of congenital heart disease, including cyanotic cardiac defects, underwent transthoracic echocardiography under dexmedetomidine sedation. Aerosolized intranasal dexmedetomidine was administered with initial doses ranging from 1-3 lgÁkg -1 . A rescue dose of 1 lgÁkg -1 was administered if adequate sedation was not achieved within 45 min following the first dose. The primary study outcome was the achievement of adequate sedation to allow transthoracic echocardiography (TTE) scanning, including subxiphoid and suprasternal probe manipulation.Results Sedation with intranasal dexmedetomidine for transthoracic echocardiography was successful in 62 of the 63 (98%) patients studied, with an intranasal rescue dose required in 13 (21%) patients. Intranasal doses of dexmedetomidine 2.5-3.0 lgÁkg -1 were required for tolerating TTE probe placement, including subxiphoid and suprasternal manipulation, with minimal response and a 90% success rate. Excluding patients who required a second dose of dexmedetomidine, the mean (standard deviation) time from administration to achieving such sedation (onset time) was 26 (8) min for low-dose (1-2 lgÁkg -1 ) dexmedetomidine and 28 (8) min for moderate-dose (2.5-3.0 lgÁkg -1 ) dexmedetomidine (P = 0.33). Time from administration of low-dose dexmedetomidine to discharge, including TTE scan time, was 80 (14) min, and it increased with moderate-dose dexmedetomidine to 91 (22) min (P = 0.05). Mild to moderate bradycardia and hypotension were observed, but no interventions were required. Conclusion We found that aerosolized intranasal dexmedetomidine offers satisfactory conditions for TTE in children three months to three years of age with an optimal dose of 2.5-3.0 lgÁkg -1 administered under the supervision of a pediatric cardiac anesthesiologist. RésuméObjectif Nous avons conçu cette étude observationnelle rétrospective sur l'utilisation de la dexmédétomidine, un agoniste des récepteurs a 2 , afin de déterminer la dose intranasale optimale pour obtenir une sédation pour l'échocardiographie transthoracique chez l'enfant et d'identifier tout effet secondaire néfaste lié à la dose.Presentation: Children's Hospital of Philadelphia ''Cardiology 2015''; Scottsdale, AZ, USA.

Background: Fetal growth abnormalities in hypoplastic left heart syndrome (HLHS) have been documented primarily by birth measurements. Fetal growth trajectory has not been described. We hypothesized that fetal growth trajectory declines across late gestation in this population. Methods: Infants with a prenatal diagnosis of HLHS and no history of prematurity or a genetic syndrome were identified. Fetal ultrasound measurements and birth anthropometrics were obtained from clinical records. z-Scores for estimated fetal weight (EFWz) and birth weight (BWTz) were compared. BWTz for three neonatal standards were compared. results: Paired fetal and neonatal data were identified in 33 cases of HLHS. Mean gestational age at ultrasound and birth were 27 and 38 wk, respectively. BWTz was lower than EFWz by a mean of 0.82 (SD: 0.72, P < 0.0001), with 64% of subjects demonstrating a decrease in z-score of >0.5. Umbilical artery (UA) Doppler found no evidence of significant placental insufficiency. Modest differences in BWTz were seen across BWT standards in this cohort. conclusion: The majority of fetuses with HLHS demonstrate decreased growth velocity during later pregnancy, suggesting growth abnormalities manifest in utero. The potential relationship to future clinical outcomes warrants further study.

We found no associations of CCO or MCA- and UA-PI with late gestational weight gain or biometry at birth in fetuses with CHD. This does not support fetal hemodynamics as the primary driver of suboptimal fetal growth in fetuses with SV. Future research could further explain genetic and placental abnormalities that may affect fetal growth in those with CHD. Copyright © 2017 ISUOG. Published by John Wiley & Sons Ltd.

ABSTRACT