ReviewBiology2017
Cardiac Channelopathies and Sudden Death: Recent Clinical and Genetic Advances.
Review in Biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04832126 (Genetic Analysis of Heart Channelopathies in Brazilian Patients and Their Relatives), which is not on this map. Cited by 64 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.
Genetic Analysis of Heart Channelopathies in Brazilian Patients and Their Relatives
Who cites it
64 citing papers in PubMed, 146 citations in OpenAlex.
- Repurposing polyamines to prevent life-threatening arrhythmias in Short QT Syndrome type 3.Nature communications · 2026Article
- Genetics of Sudden Cardiac Death.Diseases (Basel, Switzerland) · 2025Review
- Electrophysiological characterization of the state-dependent inhibition of Kv7.1 and IMolecular pharmacology · 2025Article
- Insights into Pre-COVID sudden cardiac deaths-: An autopsy study in South India.Journal of family medicine and primary care · 2025Article
- Catecholaminergic polymorphic ventricular tachycardia: A narrative review of recent advances in genetics, mechanisms, diagnosis, and treatment.Asian heart journal · 2025Review
- The Diagnostic Value of Copy Number Variants in Genetic Cardiomyopathies and Channelopathies.Journal of cardiovascular development and disease · 2025Review
- Exploring transcriptomic signatures in sudden unexplained death (SUD) cases.International journal of legal medicine · 2025Article
- Human induced pluripotent stem cell-derived cardiomyocytes for disease modeling and drug discovery.Frontiers in bioengineering and biotechnology · 2025Review
- Genetics of Sudden Cardiac Arrest: Overview of Genetic Risk Factors and Aetiologies.Arrhythmia & electrophysiology review · 2025Review
- An hiPSC-CM approach for electrophysiological phenotyping of a patient-specific case of short-coupled TdP.Stem cell research & therapy · 2024Article
- Prevalence and associated factors of ECG abnormality patterns indicative of cardiac channelopathies among adult general population of Tehran, Iran: a report from the Tehran Cohort Study (TeCS).BMC cardiovascular disorders · 2024Article
- Novel heterozygous mutation of CACNA2D1 gene in a Chinese family with arrhythmia.BMC cardiovascular disorders · 2024Article
- Review
- Management of Long QT Syndrome: A Systematic Review.Cureus · 2024Review
- The Kir2.1E299V mutation increases atrial fibrillation vulnerability while protecting the ventricles against arrhythmias in a mouse model of short QT syndrome type 3.Cardiovascular research · 2024Article
- Human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) for modeling cardiac arrhythmias: strengths, challenges and potential solutions.Frontiers in physiology · 2024Review
- Review
- Review
- Mechanistic insights into robust cardiac IeLife · 2023Article
- Human atrial fibrillation and genetic defects in transient outward currents: mechanistic insights from multi-scale computational models.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sudden cardiac death poses a unique challenge to clinicians because it may be the only symptom of an inherited heart condition. Indeed, inherited heart diseases can cause sudden cardiac death in older and younger individuals. Two groups of familial diseases are responsible for sudden cardiac death: cardiomyopathies (mainly hypertrophic cardiomyopathy, dilated cardiomyopathy, and arrhythmogenic cardiomyopathy) and channelopathies (mainly long QT syndrome, Brugada syndrome, short QT syndrome, and catecholaminergic polymorphic ventricular tachycardia). This review focuses on cardiac channelopathies, which are characterized by lethal arrhythmias in the structurally normal heart, incomplete penetrance, and variable expressivity. Arrhythmias in these diseases result from pathogenic variants in genes encoding cardiac ion channels or associated proteins. Due to a lack of gross structural changes in the heart, channelopathies are often considered as potential causes of death in otherwise unexplained forensic autopsies. The asymptomatic nature of channelopathies is cause for concern in family members who may be carrying genetic risk factors, making the identification of these genetic factors of significant clinical importance.
Indexed as
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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.