Evidence map›Paper›PMID 27502440›Full record

ArticleScientific reports2016

Pro-arrhythmogenic effects of CACNA1C G1911R mutation in human ventricular tachycardia: insights from cardiac multi-scale models.

Jieyun Bai, Kuanquan Wang, Qince Li, Yongfeng Yuan, Henggui Zhang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Unexpected impairment ofNature cardiovascular research · 2023
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. R-From-T as a Common Mechanism of Arrhythmia Initiation in Long QT Syndromes.Circulation. Arrhythmia and electrophysiology · 2019
    Article
  11. Dysfunctional Cav1.2 channel in Timothy syndrome, from cell to bedside.Experimental biology and medicine (Maywood, N.J.) · 2019
    Article
  12. Article
  13. Calcium Signaling and Cardiac Arrhythmias.Circulation research · 2017
    Review
  14. Article
  15. Review
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

5 authors at 1 institution in 2 countries.

Jieyun BaiSchool of Computer Science and Technology, Harbin Institute Technology, Harbin, 150001, China.
Kuanquan WangSchool of Computer Science and Technology, Harbin Institute Technology, Harbin, 150001, China.
Qince LiSchool of Computer Science and Technology, Harbin Institute Technology, Harbin, 150001, China.
Yongfeng YuanSchool of Computer Science and Technology, Harbin Institute Technology, Harbin, 150001, China.
Henggui ZhangSchool of Computer Science and Technology, Harbin Institute Technology, Harbin, 150001, China.
Harbin Institute of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the CACNA1C gene are associated with ventricular tachycardia (VT). Although the CACNA1C mutations were well identified in patients with cardiac arrhythmias, mechanisms by which cardiac arrhythmias are generated in such genetic mutation conditions remain unclear. In this study, we identified a novel mechanism of VT resulted from enhanced repolarization dispersion which is a key factor for arrhythmias in the CACNA1C G1911R mutation using multi-scale computational models of the human ventricle. The increased calcium influx in the mutation prolonged action potential duration (APD), produced steepened action potential duration restitution (APDR) curves as well as augmented membrane potential differences among different cell types during repolarization, increasing transmural dispersion of repolarization (DOR) and the spatial and temporal heterogeneity of cardiac electrical activities. Consequentially, the vulnerability to unidirectional conduction block in response to a premature stimulus increased at tissue level in the G1911R mutation. The increased functional repolarization dispersion anchored reentrant excitation waves in tissue and organ models, facilitating the initiation and maintenance of VT due to less meandering rotor tip. Thus, the increased repolarization dispersion caused by the G1911R mutation is a primary factor that may primarily contribute to the genesis of cardiac arrhythmias in Timothy Syndrome.

Indexed as

Action PotentialsArrhythmias, CardiacAutistic DisorderCalcium Channels, L-TypeComputer SimulationElectrocardiographyHeart VentriclesHumansLong QT SyndromeMembrane PotentialsModels, CardiovascularMutationPericardiumSyndactylyTachycardia, VentricularCACNA1C protein, humanCalcium Channels, L-Type

Identifiers

PMID27502440
PMCPMC4977499
OpenAlexW2523688192

What OpenQuestion holds

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LicenceCC BY
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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.