Alan M. Groves

Background: Maternal obesity may increase offspring risk of cardiovascular disease. We assessed the impact of maternal obesity on cardiac structure and function in newborns as a marker of fetal cardiac growth. Methods: Neonates born to mothers of healthy weight (body mass index (BMI) 20–25 kg/m², n=56) and to mothers who were obese (BMI ≥30 kg/m², n=31) underwent 25-minute continuous ECG recording and non-sedated, free-breathing cardiac MRI within 72 hours of birth. Results: Mean (SD) heart rate during sleep was higher in infants born to mothers who were versus were not obese (123 (12.6) vs 114 (9.8) beats/min, p=0.002). Heart rate variability during sleep was lower in infants born to mothers who were versus were not obese (SD of normal-to-normal R-R interval 34.6 (16.8) vs 43.9 (16.5) ms, p=0.05). Similar heart rate changes were seen during wakefulness. Left ventricular end-diastolic volume (2.35 (0.14) vs 2.54 (0.29) mL/kg, p=0.03) and stroke volume (1.50 (0.09) vs 1.60 (0.14), p=0.04) were decreased in infants born to mothers who were versus were not obese. There were no differences in left ventricular end-systolic volume, ejection fraction, output or myocardial mass between the groups. Conclusion: Maternal obesity was associated with increased heart rate, decreased heart rate variability and decreased left ventricular volumes in newborns. If persistent, these changes may provide a causal mechanism for the increased cardiovascular risk in adult offspring of mothers with obesity. In turn, modifying antenatal and perinatal maternal health may have the potential to optimise long-term cardiovascular health in offspring.

Objective To evaluate the relationship between systolic (SBP), diastolic (DBP), mean (MBP) blood pressures and pulse pressure (PP), and left ventricular output (LVO), a surrogate of systemic blood flow. Study design This retrospective study included neonates who underwent targeted neonatal echocardiography (TNE) in 3-tertiary NICUs over 2 years. Associations between LVO and BP components were investigated. Analysis was adjusted for relevant covariates. Result 1060 studies from 485 neonates were included, with a mean GA of 28.4 ± 4.6 weeks and birth weight of 1234 ± 840 grams. LVO was associated positively with SBP and PP, and negatively with GA. PP demonstrated the highest predictive value for identifying infants with LVO < 150 ml/kg/min (area under the curve 0.75 [95% CI 0.68, 0.82]). MBP and DBP demonstrated no correlation with LVO. Conclusion BP parameters correlate poorly with LVO, irrespective of GA and underlying etiology. Narrow PP may be more reflective of low LVO than low SBP.

Premature birth is associated with ventricular remodeling, early heart failure, and altered left ventricular (LV) response to physiological stress. Using computational cardiac magnetic resonance (CMR) imaging, we aimed to quantify preterm ventricular remodeling in the neonatal period, and explore contributory clinical factors. Seventy-three CMR scans (34 preterm infants, 10 term controls) were performed to assess in-utero development and preterm ex-utero growth. End-diastolic computational atlases were created for both cardiac ventricles; t statistics, linear regression modeling, and principal component analysis (PCA) were used to describe the impact of prematurity and perinatal factors on ventricular volumetrics, ventricular geometry, myocardial mass, and wall thickness. All preterm neonates demonstrated greater weight-indexed LV mass and higher weight-indexed end-diastolic volume at term-corrected age (P < 0.05 for all preterm gestations). Independent associations of increased term-corrected age LV myocardial wall thickness were (false discovery rate 48 h postnatal respiratory support. PCA of LV geometry showed statistical differences between all preterm infants at term-corrected age and term controls. Computational CMR demonstrates that significant LV remodeling occurs soon after preterm delivery and is associated with definable clinical situations. This suggests that neonatal interventions could reduce long-term cardiac dysfunction.

High flow therapy works partly by washout of airway dead space, the volume of which has not been quantified in newborns. This observational study aimed to quantify airway dead space in infants and to compare efficacy of washout between high flow devices in three-dimensional (3D) printed airway models of infants weighing 2.5–3.8 kg. Nasopharyngeal airway dead space volume was 1.5–2.0 mL/kg in newborns. A single cannula device produced lower carbon dioxide (CO₂) levels than a dual cannula device (33.7, 31.2, 23.1, 15.9, 10.9 and 6.3 mm Hg vs 36.8, 35.5, 32.1, 26.8, 23.1 and 18.8 mm Hg at flow rates of 1, 2, 3, 4, 6 and 8 L/min, respectively; p2 washout with lower airway pressure.

Cardiac ultrasound techniques are increasingly used in the neonatal intensive care unit to guide cardiorespiratory care of the sick newborn. This is the first in a series of eight review articles discussing the current status of “neonatologist-performed echocardiography” (NPE). The aim of this introductory review is to discuss four key elements of NPE. Indications for scanning are summarized to give the neonatologist with echocardiography skills a clear scope of practice. The fundamental physics of ultrasound are explained to allow for image optimization and avoid erroneous conclusions from artifacts. To ensure patient safety during echocardiography recommendations are given to prevent cardiorespiratory instability, hypothermia, infection, and skin lesions. A structured approach to echocardiography, with the same standard views acquired in the same sequence at each scan, is suggested in order to ensure that the neonatologist confirms normal structural anatomy or acquires the necessary images for a pediatric cardiologist to do so when reviewing the scan.

Neonatal heart failure (HF) is a progressive disease caused by cardiovascular and non-cardiovascular abnormalities. The most common cause of neonatal HF is structural congenital heart disease, while neonatal cardiomyopathy represents the most common cause of HF in infants with a structurally normal heart. Neonatal cardiomyopathy is a group of diseases manifesting with various morphological and functional phenotypes that affect the heart muscle and alter cardiac performance at, or soon after birth. The clinical presentation of neonates with cardiomyopathy is varied, as are the possible causes of the condition and the severity of disease presentation. Echocardiography is the selected method of choice for diagnostic evaluation, follow-up and analysis of treatment results for cardiomyopathies in neonates. Advances in neonatal echocardiography now permit a more comprehensive assessment of cardiac performance that could not be previously achieved with conventional imaging. In this review, we discuss the current and emerging echocardiographic techniques that aid in the correct diagnostic and pathophysiological assessment of some of the most common etiologies of HF that occur in neonates with a structurally normal heart and acquired cardiomyopathy and we provide recommendations for using these techniques to optimize the management of neonate with HF.

Simulation is used in many aspects of medical training but less so for echocardiography instruction in paediatric cardiology. We report our experience with the introduction of simulator-based echocardiography training at Weill Cornell Medicine for paediatric cardiology fellows of the New York–Presbyterian Hospital of Columbia University and Weill Cornell Medicine. Knowledge of CHD and echocardiographic performance improved following simulation-based training. Simulator training in echocardiography can be an effective addition to standard training for paediatric cardiology trainees.