Evidence map›Paper›PMID 33121665›Full record

ArticleJACC. Clinical electrophysiology2020

Dyssynchrony and Fibrosis Persist After Resolution of Cardiomyopathy in a Swine Premature Ventricular Contraction Model.

Tomos E Walters, Judit Szilagyi, Christina Alhede, Richard Sievers, Qizhi Fang, Jeffrey Olgin, Edward P Gerstenfeld

Abstract read
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In one paragraph

Article in JACC. Clinical electrophysiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

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  5. Role of conduction system pacing in ablate and pace strategies for atrial fibrillation.European heart journal supplements : journal of the European Society of Cardiology · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Tomos E WaltersSection of Cardiac Electrophysiology, Department of Medicine, University of California, San Francisco, San Francisco, California, USA.
Judit SzilagyiSection of Cardiac Electrophysiology, Department of Medicine, University of California, San Francisco, San Francisco, California, USA.
Christina AlhedeSection of Cardiac Electrophysiology, Department of Medicine, University of California, San Francisco, San Francisco, California, USA.
Richard SieversSection of Cardiac Electrophysiology, Department of Medicine, University of California, San Francisco, San Francisco, California, USA.
Qizhi FangSection of Cardiac Electrophysiology, Department of Medicine, University of California, San Francisco, San Francisco, California, USA.
Jeffrey OlginSection of Cardiac Electrophysiology, Department of Medicine, University of California, San Francisco, San Francisco, California, USA.
Edward P GerstenfeldSection of Cardiac Electrophysiology, Department of Medicine, University of California, San Francisco, San Francisco, California, USA. Electronic address: Edward.Gerstenfeld@ucsf.edu.
University of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThis study sought to prospectively study the development and then regression of premature ventricular contraction (PVC)-induced cardiomyopathy, with the hypothesis that structural left ventricular (LV) changes that are of potential clinical significance may endure beyond the period of exposure to PVCs.

backgroundRecovery of LV function after eradication of PVCs in PVC-induced cardiomyopathy is incompletely defined.

methodsFifteen swine were exposed to: 1) 50% paced PVCs from the LV lateral epicardium for 12 weeks (LV PVC, n = 5); 2) no pacing for 12 weeks (Control, n = 5); or 3) 50% paced LV PVCs for 12 weeks followed by pacing cessation for 4 weeks (Recovery, n = 5). LV function was quantified biweekly in sinus rhythm with echocardiography. Dyssynchrony was measured from pressure-volume loops at baseline and terminal studies. LV fibrosis was quantified after sacrifice.

resultsLV ejection fraction during sinus rhythm fell between baseline and terminal studies in the LV PVC group (65.8 ± 3.0 to 39.3 ± 3.2; p < 0.05), whereas there was no significant change in the Control group (69.6 ± 3.0 to 72.2 ± 3.0; p = NS) or after Recovery (64.5 ± 3.4% to 61.4 ± 3.4%; p = NS) groups. There was a significant increase in LV dyssynchrony measured during sinus rhythm between baseline and terminal studies in the LV PVC group (4.0 ± 1.5% to 9.0 ± 1.5%; p < 0.05); there was a similar increase in dyssynchrony that persisted 4 weeks after PVC cessation in the Recovery group (4.4 ± 1.7% to 12.8 ± 1.7%; p < 0.05). After sacrifice, percent fibrosis was higher in the LV PVC group compared with Control (5.7 ± 0.3% vs. 3.0 ± 0.3%; p < 0.05) and remained elevated in Recovery (4.1 ± 0.3% vs. 3.0 ± 0.3%; p < 0.05) despite return to baseline LV ejection fraction.

conclusionsIn a swine model of PVC-induced cardiomyopathy, cessation of PVCs for 4 weeks leads to normalization of LV systolic function but significant changes in myocardial fibrosis and LV dyssynchrony during sinus rhythm persist.

Indexed as

CardiomyopathiesVentricular Premature ComplexesAnimalsFibrosisHumansStroke VolumeSwineVentricular Function, Leftcardiomyopathydyssynchronyfibrosispremature ventricular contraction

Identifiers

PMID33121665
OpenAlexW3087535374

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.