ArticleThe Journal of pediatrics2019
Damaging Variants in Proangiogenic Genes Impair Growth in Fetuses with Cardiac Defects.
Article in The Journal of pediatrics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Neurodevelopment in congenital heart disease: a review of antenatal mechanisms and therapeutic potentials.Pediatric research · 2025Review
- Placental Malperfusion Is Associated With Adverse Outcomes in Congenital Heart Disease and With Genetic Variants in Placental Developmental Pathways.Journal of the American College of Cardiology · 2025Article
- Convergent evolution of complex adaptive traits modulates angiogenesis in high-altitude Andean and Himalayan human populations.Communications biology · 2025Article
- Article
- Cardiovascular Disease Among Women and Birthing Individuals After Delivering a Child With Congenital Heart Disease.JACC. Advances · 2025Article
- Altered In Utero Metabolic Brain Trajectories in CHD: Going Beyond Fetal Brain Structure and Physiology.Journal of the American College of Cardiology · 2023Article
- Impaired Maternal-Fetal Environment and Risk for Preoperative Focal White Matter Injury in Neonates With Complex Congenital Heart Disease.Journal of the American Heart Association · 2023Article
- Fetal Brain Development in Congenital Heart Disease.The Canadian journal of cardiology · 2023Review
- Placental delayed villous maturation is associated with fetal congenital heart disease.American journal of obstetrics and gynecology · 2023Article
- Associations between Maternal Risk Factors and Intrinsic Placental and Fetal Brain Functional Properties in Congenital Heart Disease.International journal of molecular sciences · 2022Article
- Article
- Neuroplacentology in congenital heart disease: placental connections to neurodevelopmental outcomes.Pediatric research · 2022Review
- Impact of Maternal-Fetal Environment on Mortality in Children With Single Ventricle Heart Disease.Journal of the American Heart Association · 2022Article
- The Congenital Heart Disease Brain: Prenatal Considerations for Perioperative Neurocritical Care.Pediatric neurology · 2020Review
- Effect of parental origin of damaging variants in pro-angiogenic genes on fetal growth in patients with congenital heart defects: Data and analyses.Data in brief · 2019Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveTo determine the impact of damaging genetic variation in proangiogenic pathways on placental function, complications of pregnancy, fetal growth, and clinical outcomes in pregnancies with fetal congenital heart defect. STUDY
designFamilies delivering a baby with a congenital heart defect requiring surgical repair in infancy were recruited. The placenta and neonate were weighed and measured. Hemodynamic variables were recorded from a third trimester (36.4 ± 1.7 weeks) fetal echocardiogram. Exome sequencing was performed on the probands (N = 133) and consented parents (114 parent-child trios, and 15 parent-child duos) and the GeneVetter analysis tool used to identify damaging coding sequence variants in 163 genes associated with the positive regulation of angiogenesis (PRA) (GO:0045766).
resultsIn total, 117 damaging variants were identified in PRA genes in 133 congenital heart defect probands with 73 subjects having at least 1 variant. Presence of a damaging PRA variant was associated with increased umbilical artery pulsatility index (mean 1.11 with variant vs 1.00 without; P = .01). The presence of a damaging PRA variant was also associated with lower neonatal length and head circumference for age z score at birth (mean -0.44 and -0.47 with variant vs 0.23 and -0.05 without; P = .01 and .04, respectively). During median 3.1 years (IQR 2.0-4.1 years) of follow-up, deaths occurred in 2 of 60 (3.3%) subjects with no PRA variant and in 9 of 73 (12.3%) subjects with 1 or more PRA variants (P = .06).
conclusionsDamaging variants in proangiogenic genes may impact placental function and are associated with impaired fetal growth in pregnancies involving a fetus with congenital heart defect.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.