Maternal Diabetes, Birth Weight, and Neonatal Risk of Congenital Heart Defects in Norway, 1994–2009

Leirgul, Elisabeth; Brodwall, Kristoffer; Greve, Gottfried; Vollset, Stein Emil; Holmstrøm, Henrik; Tell, Grethe S.; Øyen, Nina

doi:10.1097/aog.0000000000001694

Cited by 57 publications

(69 citation statements)

References 29 publications

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“…Maternal obesity has been shown to increase the risk of congenital heart defects [ 9 , 10 , 38 ], as is also the case for maternal diabetes [ 39 , 40 ]. In our study, we only detected minor cardiac defects, 8/55 (15%) in the NOW group and 2/20 (10%) in the NNW group.…”

Section: Discussionmentioning

confidence: 99%

Cardiac function in newborns of obese women and the effect of exercise during pregnancy. A randomized controlled trial

et al. 2018

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BackgroundThe prevalence of maternal obesity is rising. Pre-pregnancy obesity is associated with later cardiovascular disease in the child and the underlying pathogenesis begins in early life. Therefore, pregnancy and infancy are key periods for potential intervention. The aim of this study was to study the cardiac function in newborns of obese women compared to newborns of normal-weight women, and to determine if exercise intervention during pregnancy could have an effect on cardiac function of newborns to obese women.Material and methodsFifty-five pregnant women, 51 obese (BMI ≥ 30 kg/m2) and four overweight (BMI 28–30 kg/m2), were randomized to an exercise training group (n = 27) or a control group (standard maternity care, n = 28). From gestational week 14 until delivery participants in the intervention group were offered supervised training sessions three times weekly. In addition, they were told to exercise at home once weekly. All newborns had an echocardiogram performed 1–3 days and 6–8 weeks after delivery. The results were compared with newborns of normal weight women (n = 20, standard maternity care).ResultsNewborns of obese women had an impaired systolic and diastolic cardiac function with reduced global strain, strain rate, tissue Doppler velocities and a thicker intraventricular septum at birth and after 6–8 weeks after delivery compared to newborns of normal weight women. Exercise had no statistically significant effect on either of the cardiac function parameters. The mean (± standard deviation) adherence to the exercise protocol was 1.3 ± 0.8 sessions per week for supervised training and 0.8 ± 0.7 sessions per week for home-based exercise training.ConclusionsNewborns of obese women had reduced cardiac function and thicker intraventricular septum compared to newborns of normal weight women. Exercise training during pregnancy had no significant effect, potentially due to a low number of subjects and low adherence to the exercise protocol.Trial registrationClinicalTrials.gov NCT01243554.

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Section: Discussionmentioning

confidence: 99%

Cardiac function in newborns of obese women and the effect of exercise during pregnancy. A randomized controlled trial

et al. 2018

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“…Formally, these risk factors may be regarded as confounders, because they influence both the “exposure” (older sibling) and the “outcome” (younger sibling). Some of the shared risk factors are well known, such as maternal diabetes mellitus which may predispose the offspring to CHD (Leirgul et al, ; Øyen et al, ). One purpose of this study was to evaluate the recurrence risk after adjusting for known risk factors, and maternal diabetes and maternal age were therefore included as covariates.…”

Section: Discussionmentioning

confidence: 99%

Recurrence of congenital heart defects among siblings—a nationwide study

Brodwall

Greve

Leirgul

et al. 2017

American J of Med Genetics Pt A

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Congenital heart defects (CHD) constitute the largest group of congenital malformations. In most families, only one person has CHD; however, the risk of CHD increases for children born into families already affected. In this study, all births from 1994 through 2009 were identified in the Medical Birth Registry of Norway, including supplemental information on CHD from clinical and administrative registers, as part of the CVDNOR project. By using the unique personal identification number of each parent we were able to link 16,078 pairs of twins, 445,584 pairs of full siblings, and 106,840 pairs of half-siblings. Sibling recurrence risk ratio (RRR) was calculated using CHD status in the oldest sibling as exposure and CHD status in the younger sibling as outcome, adjusted for year of birth, maternal age, and maternal diabetes. Among full sibling pairs with CHD in the older sibling, the younger sibling had CHD in 4.1% compared to 1.1% of the pairs without CHD in the older sibling (adjusted RRR 3.6; 95% confidence interval (CI) 3.1-4.1). In same-sex twins the RRR was 14.0 (95% CI 10.6-18.6), and in opposite-sex twins the RRR was 11.9 (95% CI 7.1-19.9). For half-siblings the RRR was 1.5 (95% CI 0.8-2.8). When restricting to severe types of CHD, the RRR was 6.9 (95% CI 4.9-9.8) for full siblings. In 50% of the pairs with recurrent CHD, the siblings had similar types of CHD. The high relative risk of recurrence indicates that familial risk factors are important in the etiology of CHD.

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“…In terms of cardiac septal defects, the risk for atrioventricular septal defects (AVSD) was higher than for atrial or ventricular septal defects (ASD, VSD). Likewise, gestational diabetes has been shown to confer risk of heart defects, with a twofold to threefold increased risk seen for large for gestational age babies ( Leirgul et al, 2016 ). Overall, all forms of diabetes are a significant risk factor for all CHD.…”

Section: Chronic Diseasesmentioning

confidence: 99%

Recent Advances in Placenta–Heart Interactions

Maslen

2018

Front. Physiol.

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Congenital heart defects (CHD) occur in ∼1 in every 100 live births. In addition, an estimated 10% of fetal loss is due to severe forms of CHD. This makes heart defects the most frequently occurring birth defect and single cause of in utero fatality in humans. There is considerable evidence that CHD is heritable, indicating a strong contribution from genetic risk factors. There are also known external environmental exposures that are significantly associated with risk for CHD. Hence, the majority of CHD cases have long been considered to be multifactorial, or generally caused by the confluence of several risk factors potentially from genetic, epigenetic, and environmental sources. Consequently, a specific cause can be very difficult to ascertain, although patterns of associations are very important to prevention. While highly protective of the fetus, the in utero environment is not immune to insult. As the conduit between the mother and fetus, the placenta plays an essential role in maintaining fetal health. Since it is not a fully-formed organ at the onset of pregnancy, the development of the placenta must keep pace with the growth of the fetus in order to fulfill its critical role during pregnancy. In fact, the placenta and the fetal heart actually develop in parallel, a phenomenon known as the placenta–heart axis. This leaves the developing heart particularly vulnerable to early placental insufficiency. Both organs share several developmental pathways, so they also share a common vulnerability to genetic defects. In this article we explore the coordinated development of the placenta and fetal heart and the implications for placental involvement in the etiology and pathogenesis of CHD.

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Maternal Diabetes, Birth Weight, and Neonatal Risk of Congenital Heart Defects in Norway, 1994–2009

Cited by 57 publications

References 29 publications

Cardiac function in newborns of obese women and the effect of exercise during pregnancy. A randomized controlled trial

Cardiac function in newborns of obese women and the effect of exercise during pregnancy. A randomized controlled trial

Recurrence of congenital heart defects among siblings—a nationwide study

Recent Advances in Placenta–Heart Interactions

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