Evidence map›Paper›PMID 36620202›Full record

ArticleInternational journal of cardiology. Heart & vasculature2023

Increased

Nils Bögeholz, Vincent Knappe, Paul Pauls, Jan S Schulte, Joshua I Goldhaber, Frank U Müller, Georg Nickenig, Lars Eckardt, Jan W Schrickel, Thomas Beiert

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of cardiology. Heart & vasculature, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Recent highlights from theInternational journal of cardiology. Heart & vasculature · 2024
    Article
  2. Article
  3. Ion channel trafficking implications in heart failure.Frontiers in cardiovascular medicine · 2024
    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

10 authors at 4 institutions in 2 countries.

Nils BögeholzDepartment of Cardiology II - Electrophysiology, University Hospital Münster, Münster, Germany.
Vincent KnappeDepartment of Internal Medicine II, University Hospital Bonn, Bonn, Germany.
Paul PaulsInstitute of Pharmacology and Toxicology, University Hospital Münster, Münster, Germany.
Jan S SchulteInstitute of Pharmacology and Toxicology, University Hospital Münster, Münster, Germany.
Joshua I GoldhaberSmidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Frank U MüllerInstitute of Pharmacology and Toxicology, University Hospital Münster, Münster, Germany.
Georg NickenigDepartment of Internal Medicine II, University Hospital Bonn, Bonn, Germany.
Lars EckardtDepartment of Cardiology II - Electrophysiology, University Hospital Münster, Münster, Germany.
Jan W SchrickelDepartment of Internal Medicine II, University Hospital Bonn, Bonn, Germany.
Thomas BeiertDepartment of Internal Medicine II, University Hospital Bonn, Bonn, Germany.
University Hospital Bonn · DEUniversity Hospital Münster · DECedars-Sinai Medical Center · USSchüchtermann-Klinik · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aims: Na Methods/Results: Programmed ventricular stimulation (PVS) and isoproterenol were applied to a murine heterozygous NCX-knockout model (KO) to investigate ventricular arrhythmia initiation and perpetuation compared to wild-type (WT). KO displayed a reduced susceptibility towards isoproterenol-induced premature ventricular complexes. During PVS, initiation of single or double ectopic beats was similar between KO and WT. But strikingly, perpetuation of ventricular tachycardia (VT) was significantly increased in KO (animals with VT - KO: 82 %; WT: 47 %; p = 0.0122 / median number of VTs - KO: 4.5 (1.0, 6.25); WT: 0.0 (0.0, 4.0); p = 0.0039). The median VT duration was prolonged in KO (in s; KO: 0.38 (0.19, 0.96); WT: 0.0 (0.0, 0.60); p = 0.0239). The ventricular refractory period (VRP) was shortened in KO (in ms; KO: 15.1 ± 0.7; WT: 18.7 ± 0.7; p = 0.0013). Conclusions: Not the initiation, but the perpetuation of provoked whole-heart

Indexed as

Antiarrhythmic strategiesArrhythmia mechanismsAV, AtrioventricularAVNRP, AV-nodal refractory periodCL, Cycle lengthCorrSNRP, Corrected sinus node recovery periodDAD, Delayed afterdepolarizationEAD, Early afterdepolarizationEPS, Electrophysiological studyICa, voltage-dependent l-type Ca2+-currentIQR, Interquartile rangeKO, Heterozygous Na+/Ca2+ exchanger knockout mouse modelNa+/Ca2+ exchangerNCX, Na+/Ca2+ exchangerPCR, Polymerase chain reactionPVC, Premature ventricular complexPVS, Programmed ventricular stimulationSEM, Standard error of the meanVentricular arrhythmiaVRP, Ventricular refractory periodVT, Ventricular tachycardiaWBP, Wenckebach periodicityWT, Wild-type

Identifiers

PMID36620202
PMCPMC9816773
OpenAlexW4313479561

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.