Evidence map›Paper›PMID 22090166›Full record

ArticleCirculation2012

Brugada-like syndrome in infancy presenting with rapid ventricular tachycardia and intraventricular conduction delay.

Ronald J Kanter, Ryan Pfeiffer, Dan Hu, Héctor Barajas-Martinez, Michael P Carboni, Charles Antzelevitch

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Circulation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.1field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 70 citations in OpenAlex.

  1. Trial
  2. Functional Profiling ofCirculation. Genomic and precision medicine · 2025
    Article
  3. AHeartRhythm case reports · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. J wave syndromes: What's new?Trends in cardiovascular medicine · 2022
    Review
  8. J wave syndromes as a cause of malignant cardiac arrhythmias.Pacing and clinical electrophysiology : PACE · 2018
    Review
  9. Recent advances in the treatment of Brugada syndrome.Expert review of cardiovascular therapy · 2018
    Review
  10. Review
  11. Article
  12. J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2017
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. [Brugada ECG].Herzschrittmachertherapie & Elektrophysiologie · 2015
    Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Ronald J KanterDuke University Medical Center, Box 3090, 2301 Erwin Road, Durham, NC 27710, USA. kante001@mc.duke.edu
Ryan Pfeiffer
Dan Hu
Héctor Barajas-Martinez
Michael P Carboni
Charles Antzelevitch
Duke University · USMasonic Medical Research Laboratory · US

Funding

ELECTRICAL HETEROGENEITY AND CARDIAC ARRHYTHMIASR01HL047678 · NHLBI · MASONIC MEDICAL RESEARCH LABORATORY, INC · PI ANTZELEVITCH, CHARLES · 1993 to 2014
$5.7M
ELECTRICAL HETEROGENEITY AND CARDIAC ARRHYTHMIASR55HL047678 · NHLBI · MASONIC MEDICAL RESEARCH LABORATORY, INC · PI ANTZELEVITCH, CHARLES · 1992 to 1992
–
NHLBI NIH HHS HL47678NHLBI NIH HHS R01 HL047678
6 · The paper itself

Abstract

backgroundBrugada syndrome is a potentially serious channelopathy that usually presents in adulthood and has only rarely been described in infancy. In the absence of metabolic or structural cardiac disease, rapid ventricular tachycardia (>200 bpm) and primary cardiac conduction disease are uncommon in infancy. We hypothesized that infants having rapid ventricular tachycardia and conduction abnormalities and not having structural or metabolic pathogeneses were likely to have mutations in depolarizing current channels. METHODS AND

resultsA retrospective review of all clinical materials from a single institution over a 9-year period from all infants <2 years old and having a discharge diagnosis of ventricular tachycardia or ventricular fibrillation was performed. Among 32 infants fulfilling inclusion criteria, 12 had a structurally normal heart, and 9 of them had either prolonged QRS duration or Brugada pattern while in sinus rhythm. Of those 5 infants not having a definitive pathogenesis, electrophysiological testing had been performed in 4, and genetic testing had been performed in all 5 of those infants. During electrophysiological testing, a prolonged HV interval was present in 2 of 4, inducible ventricular tachycardia was present in 1 of 4, and a type 1 Brugada pattern was induced by intravenous procainamide in 3 of 4. Genetic testing revealed disease-causing mutations in depolarizing sodium (SCN5A) or calcium (CaCNB2b) channels in all 5 infants.

conclusionsInfants having rapid ventricular tachycardia and conduction abnormalities in the absence of structural or metabolic abnormalities are likely to have disease-causing mutations in cardiac depolarizing channels.

Indexed as

Brugada SyndromeCalcium Channels, L-TypeDiagnosis, DifferentialElectrocardiographyFemaleHeart Conduction SystemHumansInfantInfant, NewbornMaleMutationNAV1.5 Voltage-Gated Sodium ChannelRetrospective StudiesSecondary PreventionSodium ChannelsTachycardia, VentricularCACNB2 protein, humanCalcium Channels, L-TypeNAV1.5 Voltage-Gated Sodium ChannelSCN5A protein, humanSodium Channels

Identifiers

PMID22090166
PMCPMC3519939
OpenAlexW2155773526

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Registered trials

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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.