Angiogenic Gene Expression in Down Syndrome Fetal Hearts

Sánchez, Olga; Domı́nguez, Carmen; Ruiz, Alba; Ribera, I.; Alijotas, J; Cabero, L.; Carreras, Elena; Llurba, Elisa

doi:10.1159/000441356

Cited by 13 publications

(12 citation statements)

References 40 publications

(40 reference statements)

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“…Recent studies [6,27,28] gave a potential insight into the connection between impaired fetal growth and CHD, suggesting a common pathway between cardiovascular (angio)genesis and placental function. Interestingly, a Spanish study [29] explored the gene expression profile of Down syndrome fetal heart tissue and found an antiangiogenic profile that was very similar to that found in the CHD fetal heart tissue gene profile. This was confirmed also at a cerebral level: Sanchez et al [30] compared brain tissue from CHD fetuses undergoing termination of pregnancy to normal fetal brain tissue, detecting an overall dysregulation of angiogenesis with a net balance towards an antiangiogenic environment in the CHD fetuses.…”

Section: Discussionmentioning

confidence: 70%

Prenatal Growth in Fetuses with Isolated Cyanotic and Non-Cyanotic Congenital Heart Defects

Inversetti¹,

Fesslová²,

Deprest³

et al. 2018

Fetal Diagn Ther

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Background: Fetal growth may vary significantly in different congenital heart defects (CHDs). Objectives: To investigate prenatal growth of CHD fetuses and its correlation with classifications based upon expected oxygen delivery to the fetal brain or structural findings. Methods: Seventy-nine euploid fetuses with isolated CHD were recruited prospectively and categorized by the expected oxygen supply to the brain (low, intermediate, and high) or by the expected arterial mixing considering two categories (cyanotic or non-cyanotic). Biometry and Doppler were recorded, and Z-scores (Zs) calculated. Growth changes at different time points were analyzed and compared with 150 controls. Results: A total of 664 exams were performed on 229 fetuses. Median head circumference (HC) Zs were lower in all CHD fetuses from the second trimester onwards and in cyanotic CHD fetuses from the first onwards, with associated smaller abdominal circum-ference (AC) in the third trimester (first-trimester biparietal diameter Zs cyanotic: -1.3 [-2.36; -0.98], non-cyanotic -0.72 [-1.25; -0.6], p = 0.044, second-trimester HC Zs cyanotic: -1.47 [-2.3; -0.84]; non-cyanotic -0.45 [-0.83; -0.02], p < 0.0001; AC Zs cyanotic 0.0 [-0.44; 0.86]; non-cyanotic 0.65 [0.31; 1], p = 0.0006). Birth-weight centiles were smaller in CHDs (particularly in cyanotic) with no differences between categories of brain oxygen delivery. Conclusions: Fetuses with cyanotic CHD have fetal growth restriction, impaired head growth, yet normal posterior fossa dimensions and fetal-placental Doppler.

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Section: Discussionmentioning

confidence: 70%

Prenatal Growth in Fetuses with Isolated Cyanotic and Non-Cyanotic Congenital Heart Defects

Inversetti¹,

Fesslová²,

Deprest³

et al. 2018

Fetal Diagn Ther

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“…Histopathological studies have identified abnormal lung development and lung hypoplasia as common features of PAH, CHD, CDH, and Down syndrome [ 14 , 16 ]. While the mechanisms for impaired lung development are not known, altered expression of angiogenic and anti-angiogenic genes likely contribute [ 17 , 18 , 19 , 20 ]. Decreased lung vascular and alveolar growth predispose one to vascular injury during susceptible periods of growth and adaptation.…”

Section: Introductionmentioning

confidence: 99%

Genetics and Genomics of Pediatric Pulmonary Arterial Hypertension

Welch

Chung

2020

Genes

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Pulmonary arterial hypertension (PAH) is a rare disease with high mortality despite recent therapeutic advances. The disease is caused by both genetic and environmental factors and likely gene–environment interactions. While PAH can manifest across the lifespan, pediatric-onset disease is particularly challenging because it is frequently associated with a more severe clinical course and comorbidities including lung/heart developmental anomalies. In light of these differences, it is perhaps not surprising that emerging data from genetic studies of pediatric-onset PAH indicate that the genetic basis is different than that of adults. There is a greater genetic burden in children, with rare genetic factors contributing to ~42% of pediatric-onset PAH compared to ~12.5% of adult-onset PAH. De novo variants are frequently associated with PAH in children and contribute to at least 15% of all pediatric cases. The standard of medical care for pediatric PAH patients is based on extrapolations from adult data. However, increased etiologic heterogeneity, poorer prognosis, and increased genetic burden for pediatric-onset PAH calls for a dedicated pediatric research agenda to improve molecular diagnosis and clinical management. A genomics-first approach will improve the understanding of pediatric PAH and how it is related to other rare pediatric genetic disorders.

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“…Congenital heart disease in infants born following exposure to preeclampsia management of these newborns but also their survival. [24,25] The association between preeclampsia and CHD may suggest that clinicians managing women with preeclampsia in addition to other fetal surveillance screening, consider including the screening for congenital heart diseases in order to improve the early diagnosis and management of these newborns who may have CHD. This will help improve the survival of the infants of women with preeclampsia.…”

Section: Plos Onementioning

confidence: 99%

Profile of congenital heart disease in infants born following exposure to preeclampsia

et al. 2020

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BackgroundEvents in pregnancy play an important role in predisposing the newborn to the risk of developing CHD. This study evaluated the association between maternal preeclampsia and her offspring risk of CHD. MethodsThis is a cohort study of 90 sex-matched neonates (45 each born to women with preeclampsia and normal pregnancy) in Jos, Nigeria. Anthropometry was taken shortly after delivery using standard protocols. Echocardiography was performed within 24 hours of life and repeated 7 and 28 days later. SPSS version 25 was used in all analyses. Statistical significance was set at p<0.05. ResultsCongenital heart disease (CHD) was observed in 27 (30.0%) of newborns of women with preeclampsia compared with 11 (12.1%) of newborns without preeclampsia (p<0.001) at the end of 7 days and in 19 (21.1%) of newborns of women with preeclampsia and 3 (3.3%) of newborns of women without preeclampsia by the end of the 4 th week of life (p<0.001). Overall, ASD (4 newborns), PDA (21 newborns), patent foramen ovale (14 newborns) and VSD (2 newborns) were the prevalent lesions found among all the newborns studied in the first week of life. Isolated atrial and ventricular septal defects were seen in 4 (4.4%) of the newborns of women with preeclampsia. Being the infant of a woman with preeclampsia was associated with about 8-fold increased risk of having CHD (OR = 7.9, 95% CI = 2.5-24.9, p<0.001).

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Angiogenic Gene Expression in Down Syndrome Fetal Hearts

Cited by 13 publications

References 40 publications

Prenatal Growth in Fetuses with Isolated Cyanotic and Non-Cyanotic Congenital Heart Defects

Prenatal Growth in Fetuses with Isolated Cyanotic and Non-Cyanotic Congenital Heart Defects

Genetics and Genomics of Pediatric Pulmonary Arterial Hypertension

Profile of congenital heart disease in infants born following exposure to preeclampsia

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