Evidence map›Paper›PMID 31993492›Full record

ReviewInternational journal of cardiology. Heart & vasculature2020

Brugada syndrome: A comprehensive review of pathophysiological mechanisms and risk stratification strategies.

Ka Hou Christien Li, Sharen Lee, Chengye Yin, Tong Liu, Tachapong Ngarmukos, Giulio Conte, Gan-Xin Yan, Raymond W Sy, Konstantinos P Letsas, Gary Tse

Erratum issuedOpen access · goldAbstract readReview
In one paragraph

Review in International journal of cardiology. Heart & vasculature, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Hypokalaemia and bradycardia unmask the loss-of-function phenotype of a Brugada Syndrome SCN5A mutation.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 · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Beyond the type 1 pattern: comprehensive risk stratification in Brugada syndrome.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Hyperkalemia-induced Brugada phenocopy: a systematic review of case reports.Clinical research in cardiology : official journal of the German Cardiac Society · 2025
    Review
  14. Review
  15. Zebrafish as a Model System for Brugada Syndrome.Reviews in cardiovascular medicine · 2024
    Review
  16. Review
  17. Review
  18. Brugada syndrome update.Frontiers in physiology · 2024
    Review
  19. A large population-based study on the prevalence of electrocardiographic abnormalities: A result of Mashhad stroke and heart atherosclerotic disorder cohort study.Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc · 2023
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 9 institutions in 7 countries.

Ka Hou Christien LiFaculty of Medicine, Newcastle University, Newcastle, United Kingdom.
Sharen LeeLaboratory of Cardiovascular Physiology, Li Ka Shing Institute of Health Sciences, Hong Kong, SAR, PR China.
Chengye YinSchool of Biological and Chemical Sciences, Queen Mary University of London, London, United Kingdom.
Tong LiuTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin 300211, PR China.
Tachapong NgarmukosDepartment of Medicine Faculty of Medicine Ramathibodi Hospital Mahidol University, Bangkok, Thailand.
Giulio ConteDivision of Cardiology, Cardiocentro Ticino, Lugano, Switzerland.
Gan-Xin YanLankenau Institute for Medical Research and Lankenau Medical Center, Wynnewood, PA, USA.
Raymond W SyDepartment of Cardiology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia.
Konstantinos P LetsasSecond Department of Cardiology, Laboratory of Cardiac Electrophysiology, Evangelismos General Hospital of Athens, Athens, Greece.
Gary TseTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin 300211, PR China.
Epatocentro Ticino · CHEvangelismos Hospital · GRLankenau Institute for Medical Research · USNewcastle University · GBQueen Mary University of London · GBRamathibodi Hospital · THSecond Hospital of Tianjin Medical University · CNTianjin Medical University · CNUniversity of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brugada syndrome (BrS) is an inherited ion channel channelopathy predisposing to ventricular arrhythmias and sudden cardiac death. Originally believed to be predominantly associated with mutations in SCN5A encoding for the cardiac sodium channel, mutations of 18 genes other than SCN5A have been implicated in the pathogenesis of BrS to date. Diagnosis is based on the presence of a spontaneous or drug-induced coved-type ST segment elevation. The predominant electrophysiological mechanism underlying BrS remains disputed, commonly revolving around the three main hypotheses based on abnormal repolarization, depolarization or current-load match. Evidence from computational modelling, pre-clinical and clinical studies illustrates that molecular abnormalities found in BrS lead to alterations in excitation wavelength (λ), which ultimately elevates arrhythmic risk. A major challenge for clinicians in managing this condition is the difficulty in predicting the subset of patients who will suffer from life-threatening ventricular arrhythmic events. Several repolarization risk markers have been used thus far, but these neglect the contributions of conduction abnormalities in the form of slowing and dispersion. Indices incorporating both repolarization and conduction based on the concept of λ have recently been proposed. These may have better predictive values than the existing markers. Current treatment options include pharmacological therapy to reduce the occurrence of arrhythmic events or to abort these episodes, and interventions such as implantable cardioverter-defibrillator insertion or radiofrequency ablation of abnormal arrhythmic substrate.

Indexed as

Brugada syndromeDepolarizationIon channelRepolarizationRisk stratification

Identifiers

PMID31993492
PMCPMC6974766
OpenAlexW3001756357

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.