ReviewPediatric cardiology2019
Fetal Arrhythmias: Genetic Background and Clinical Implications.
Review in Pediatric cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Society for Maternal-Fetal Medicine Consult Series #75: Evaluation and management of non-immune hydrops fetalis.Pregnancy (Hoboken, N.J.) · 2026Article
- scRiskDB: a single-cell epigenomic resource linking complex traits to regulatory mechanisms across human tissues.Database : the journal of biological databases and curation · 2026Article
- Human Genetics of Cardiac Arrhythmias.Advances in experimental medicine and biology · 2024Review
- Article
- Early L-T4 intervention improves fetal heart development in pregnant rats with subclinical hypothyroidism rats by activating BMP4/Smad4 signaling pathway.BMC cardiovascular disorders · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fetal arrhythmias are a common phenomenon of pregnancies. However, debates remain with regard to the etiologies and early treatment of choices for severe fetal arrhythmias. The gene regulatory networks govern cardiac conduction system development to produce distinct nodal and fast conduction phenotypes. The slow conduction properties of nodes that display automaticity are determined by the cardiac ion channel genes, whereas the fast conduction properties are regulated by the transcription factors. Mutations of genes specific for the developmental processes and/or functional status of cardiac conduction system including ion channel promoter (minK-lacZ), GATA family of zinc finger proteins (GATA4), the homeodomain transcription factor (Nkx2.5), the homeodomain-only protein (Hop) and the T-box transcription factors (Tbx2, Tbx3 and Tbx5), hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4) and connexins, may cause fetal arrhythmias. It is expected that development of investigational antiarrhythmic agents based on genetic researches on cardiac conduction system, and clinical application of percutaneously implantable fetal pacemaker for the treatment of fetal arrhythmias would come to true.
Indexed as
Identifiers
What OpenQuestion holds
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.