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.
- magnetic resonance imaging
Data availability statement
Data are available upon reasonable request. MRI sequence data are available from Anthony.email@example.com. Anonymised cohort outcome data are available from Alan.firstname.lastname@example.org.
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Contributors AMG, ANP, MCV, DP, ADE, PJC, LP and PDT contributed to study design. ANP, TR-W, SJ, YY, EEB, PTS, KWDS, JC, SS, FM, ALB and CS were involved in data collection and analysis. All authors were involved in writing and reviewing the manuscript. AMG is responsible for the overall content as guarantor.
Funding Funded by the British Heart Foundation Grant (Ref PG/13/38/30289), Biomedical Research Centre, Guy’s and St Thomas’ NHS Foundation Trust and KCL. LP and DP are supported by Tommy’s charity, UK.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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