Development of a system to record precordial echocardiographic signals continuously in the newborn

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Foetal blood flow measured using phase contrast cardiovascular magnetic resonance – preliminary data comparing 1.5 T with 3.0 T

Abstract Background Phase contrast cardiovascular magnetic resonance (PC CMR) has emerged as a clinical tool for blood flow quantification but its use in the foetus has been hampered by the need for gating with the foetal heart beat. The previously described metric optimized gating (MOG) technique has been successfully used to measure foetal blood flow in late gestation foetuses on a 1.5 T CMR magnet. However, there is increasing interest in performing foetal cardiac imaging using 3.0 T CMR. We describe our pilot investigation of foetal blood flow measured using 3.0 T CMR. Methods Foetal blood flows were quantified in 5 subjects at late gestational age (35–38 weeks). Three were normal pregnancies and two were pregnancies with ventricular size discrepancy. Data were obtained at 1.5 T and 3.0 T using a previously described PC CMR protocol. After reconstruction using MOG, blood flow was quantified independently by two observers. Intra- and inter-observer reproducibility of flow measurements at the two field strengths was assessed by Pearson correlation coefficient (R2), linear regression and Bland Altman analysis. Results PC CMR flow measurements were obtained in 36 of 40 target vessels. Strong intra-observer agreement was obtained between measurements at each field strength (R2 = 0.78, slope = 0.83 ± 0.11), with a mean bias of −1 ml/min/kg and 95% confidence limits of ±71 ml/min/kg. Inter-observer agreement was similarly high for measurements at both 1.5 T (R2 = 0.86, slope = 0.95 ± 0.13, bias = 6 ± 52 ml/min/kg) and 3.0 T (R2 = 0.88, slope = 0.94 ± 0.13, bias = 4 ± 47 ml/min/kg). Across all PC CMR measurements, SNR per pixel was expectedly higher at 3.0 T relative to 1.5 T (165 ± 50%). The relative differences in flow measurements between observers were low (range: 4–16%) except for pulmonary blood flow which showed much higher variability at 1.5 T (34%) versus that at 3.0 T (11%). This was attributed to the poorly visualized, small pulmonary vessels at 1.5 T, which made delineation inconsistent between observers. Conclusions This is the first pilot study to measure foetal blood flow using PC CMR at 3.0 T. The flow data obtained were in good correlation with those measured at 1.5 T, both within and between observers. With increased SNR at 3.0 T, smaller pulmonary vessels were better visualized which improved inter-observer agreement of associated flows

Pulmonary arterial response to hypoxia in survivors of chronic lung disease of prematurity

Background It is unclear whether increased pulmonary arterial (PA) reactivity to hypoxia observed in preterm infants who develop chronic lung disease of prematurity (CLD) persists into childhood. Aim We assessed and compared PA pulse wave velocity (PWV) in air and after 12% hypoxia using velocity-encoded MRI between children who had CLD in infancy and preterm-born and term-born controls. Methods From 67 recruited children, 59 (13 CLD, 21 preterm, 25 term), 9–12-year-old children successfully completed the study. Velocity-encoded phase-contrast MR PA images were acquired breathing air and during breathing 12% hypoxia. PA PWV was derived as the ratio of flow to area changes during early systole. Results There were no differences in mean (SD) PA PWV between the groups breathing air (CLD=1.3 (0.4) m/s, preterm control=1.3 (0.4) m/s, term control=1.3 (0.3) m/s)) but increased following hypoxia to 1.9 (0.7) m/s, 1.6 (0.6) m/s and 1.5 (0.5) m/s in CLD, preterm and term groups, respectively. The mean differences (95% CI) for PA PWV between CLD and the preterm and control groups were 0.37 (0.08 to 0.70) and 0.34 (0.05 to 0.70), respectively. There was no difference for change in PA PWV with hypoxia between the two control groups, mean difference 0.23 (−0.2 to 0.3). Conclusions Children who had CLD in infancy had increased pulmonary arterial reactivity during hypoxia, thus long-term follow-up is warranted in this population

Assessment of pulmonary artery pulse wave velocity in children: An MRI pilot study

Purpose To assess the feasibility of measuring pulmonary artery (PA) pulse wave velocity (PWV) in children breathing ambient air and 12% oxygen. Methods Velocity-encoded phase-contrast MR images of the PA were acquired in 15 children, aged 9–12 years, without evidence of cardiac or pulmonary diseases. PWV was derived as the ratio of flow to area changes during early systole. Each child was scanned twice, in air and after at least 20 minutes into inspiratory hypoxic challenge. Intra-observer and inter-observer variability and repeatability were also compared. Results PA PWV, which was successfully measured in all subjects, increased from 1.31 ± 0.32 m/s in air to 1.61 ± 0.58 m/s under hypoxic challenge (p = 0.03). Intra- and inter-observer coefficients of variations were 9.0% and 15.6% respectively. Good correlation within and between observers of r = 0.92 and r = 0.72 respectively was noted for PA PWV measurements. Mean (95% limit of agreement) intra- and inter-observer agreement on Bland–Altman analysis were − 0.02 m/s (− 0.41–0.38 m/s) and -0.28 m/s (− 1.06–0.49 m/s). Conclusion PA PWV measurement in children using velocity-encoded MRI is feasible, reproducible and sufficiently sensitive to detect differences in PA compliance between normoxia and hypoxia. This technique can be used to detect early changes of PA compliance and monitor PAH in children