Evidence map›Paper›PMID 25046857›Full record

ArticleHeart rhythm2014

Cellular mechanism of premature ventricular contraction-induced cardiomyopathy.

Yuhong Wang, Jose M Eltit, Karoly Kaszala, Alex Tan, Min Jiang, Mei Zhang, Gea-Ny Tseng, Jose F Huizar

Abstract read
In one paragraph

Article in Heart rhythm, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
4.7field-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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

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  13. Alterations of sarcoplasmic reticulum-mediated CaMolecular and cellular biochemistry · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Yuhong WangDepartment of Physiology and Biophysics, Virginia Commonwealth University.
Jose M EltitDepartment of Physiology and Biophysics, Virginia Commonwealth University.
Karoly KaszalaDepartment of Physiology and Biophysics, Virginia Commonwealth University; McGuire VA Medical Center.
Alex TanDepartment of Physiology and Biophysics, Virginia Commonwealth University; McGuire VA Medical Center.
Min JiangDepartment of Physiology and Biophysics, Virginia Commonwealth University.
Mei ZhangDepartment of Physiology and Biophysics, Virginia Commonwealth University.
Gea-Ny TsengDepartment of Physiology and Biophysics, Virginia Commonwealth University. Electronic address: gtseng@vcu.edu.
Jose F HuizarDepartment of Physiology and Biophysics, Virginia Commonwealth University; McGuire VA Medical Center; Pauley Heart Center of Virginia Commonwealth University, Richmond, Virginia.
Virginia Commonwealth University · US

Funding

VCU Neuroscience Center Core GrantP30NS047463 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI POVLISHOCK, JOHN T · 2003 to 2013
$5.0M
STRUCTURE-FUNCTION RELATION & MODULATION OF Kv CHANNELSR01HL107294 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI TSENG, GEA-NY · 2012 to 2015
$1.5M
NHLBI NIH HHS R01 HL107294NINDS NIH HHS 5P30NS047463NINDS NIH HHS P30 NS047463
6 · The paper itself

Abstract

backgroundFrequent premature ventricular contractions (PVCs) are associated with increased risk of sudden cardiac death and can cause secondary cardiomyopathy.

objectiveWe sought to determine the mechanism(s) responsible for prolonged refractory period and left ventricular (LV) dysfunction demonstrated in our canine model of PVC-induced cardiomyopathy.

methodsSingle myocytes were isolated from LV free wall of PVC and control canines and used for patch-clamp recording, intracellular Ca(2+) measurements, and immunocytochemistry/confocal microscopy. LV tissues adjacent to the area of myocyte isolation were used for the immunoblot quantification of protein expression.

resultsIn the PVC group, LV ejection fraction decreased from 57.6% ± 1.5% to 30.4% ± 3.1% after ≥4 months of ventricular bigeminy. Compared to control myocytes, PVC myocytes had decreased densities of both outward (transient outward current [Ito] and inward rectifier current [IK1]) and inward (L-type Ca current [ICaL]) currents, but no consistent changes in rapid or slow delayed rectifier currents. The reduction in Ito, IK1, and ICaL was accompanied by decreased protein levels of their channel subunits. The extent of reduction in Ito, IK1, and ICaL varied among PVC myocytes, creating marked heterogeneity in action potential configurations and durations. PVC myocytes showed impaired Ca-induced Ca release from the sarcoplasmic reticulum (SR), without increase in SR Ca leak or decrease in SR Ca store. This was accompanied by a decrease in dyad scaffolding protein, junctophilin-2, and loss of Cav1.2 registry with Ca-releasing channels (ryanodine receptor 2).

conclusionPVCs increase dispersion of action potential configuration/duration, a risk factor for sudden cardiac death, because of the heterogeneous reduction in Ito, IK1, and ICaL. The excitation-contraction coupling is impaired because of the decrease in ICaL and Cav1.2 misalignment with respect to ryanodine receptor 2.

Indexed as

AnimalsCardiomyopathiesDisease Models, AnimalDogsImmunoblottingImmunohistochemistryMicroscopy, ConfocalMuscle CellsPatch-Clamp TechniquesVentricular Premature ComplexesCardiomyopathyElectrical remodelingExcitation-contraction couplingPremature ventricular contraction

Identifiers

PMID25046857
PMCPMC4252777
OpenAlexW1982898867

What OpenQuestion holds

Textmetadata
LicenceTDM
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.