Evidence map›Paper›PMID 20935153›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2011

Ionic mechanisms of cellular electrical and mechanical abnormalities in Brugada syndrome.

Min Dong, Paul J Niklewski, Hong-Sheng Wang

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Acute exposure to low-dose bisphenol A delays cardiac repolarization in female canine heart - Implication for proarrhythmic toxicity in large animals.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2023
    Article
  5. Improved CaJournal of molecular and cellular cardiology · 2022
    Article
  6. Article
  7. Effects of human atrial ionic remodelling by β-blocker therapy on mechanisms of atrial fibrillation: a computer simulation.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 · 2014
    Article
  8. Article
  9. Dependence of phase-2 reentry and repolarization dispersion on epicardial and transmural ionic heterogeneity: a simulation study.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 · 2014
    Article
  10. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Min DongDepartment of Pharmacology and Cell Biophysics, 2Neuroscience Program, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0575, USA.
Paul J Niklewski
Hong-Sheng Wang
University of Cincinnati Medical Center · US

Funding

Ionic Basis of the Brugada SyndromeR21HL084539 · NHLBI · UNIVERSITY OF CINCINNATI · PI WANG, HONG-SHENG · 2007 to 2008
$402k
NHLBI NIH HHS HL084539
6 · The paper itself

Abstract

The Brugada syndrome (BrS) is a right ventricular (RV) arrhythmia that is responsible for up to 12% of sudden cardiac deaths. The aims of our study were to determine the cellular mechanisms of the electrical abnormality in BrS and the potential basis of the RV contractile abnormality observed in the syndrome. Tetrodotoxin was used to reduce cardiac Na(+) current (I(Na)) to mimic a BrS-like setting in canine ventricular myocytes. Moderate reduction (<50%) of I(Na) with tetrodotoxin resulted in all-or-none repolarization in a fraction of RV epicardial myocytes. Dynamic clamp and modeling show that reduction of I(Na) shifts the action potential (AP) duration-transient outward current (I(to)) density curve to the left and has a biphasic effect on AP duration. In the presence of a large I(to), I(Na) reduction either prolongs or collapses the AP, depending on the exact density of I(to). These repolarization changes reduce Ca(2+) influx and sarcoplasmic reticulum load, resulting in marked attenuation of myocyte contraction and Ca(2+) transient in RV epicardial myocytes. We conclude that I(Na) reduction alters repolarization by reducing the threshold for I(to)-induced all-or-none repolarization. These cellular electrical changes suppress myocyte excitation-contraction coupling and contraction and may be a contributing factor to the contractile abnormality of the RV wall in BrS.

Indexed as

Action PotentialsAnimalsBrugada SyndromeCalciumComputer SimulationDogsElectrophysiologyHeart VentriclesMaleModels, BiologicalMyocytes, CardiacSarcoplasmic ReticulumCalcium

Identifiers

PMID20935153
PMCPMC3023248
OpenAlexW2009766668

What OpenQuestion holds

Textmetadata
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.