Evidence map›Paper›PMID 26771573›Full record

ArticlePloS one2016

Left Atrial Size and Function in a Canine Model of Chronic Atrial Fibrillation and Heart Failure.

Adam Goldberg, Kenya Kusunose, Salima Qamruddin, L Leonardo Rodriguez, Todor N Mazgalev, Brian P Griffin, David R Van Wagoner, Youhua Zhang, Zoran B Popović

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Animal and cellular models of atrial fibrillation: a review.Frontiers in cardiovascular medicine · 2025
    Review
  2. Article
  3. Observational
  4. 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

9 authors at 1 institution in 1 country.

Adam GoldbergDepartment of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America.
Kenya KusunoseDepartment of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America.
Salima QamruddinDepartment of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America.
L Leonardo RodriguezDepartment of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America.
Todor N MazgalevDepartment of Molecular Cardiology, Cleveland Clinic, Cleveland, Ohio, United States of America.
Brian P GriffinDepartment of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America.
David R Van WagonerDepartment of Molecular Cardiology, Cleveland Clinic, Cleveland, Ohio, United States of America.
Youhua ZhangDepartment of Molecular Cardiology, Cleveland Clinic, Cleveland, Ohio, United States of America.
Zoran B PopovićDepartment of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America.
Cleveland Clinic · US

Funding

Functional Genomics of Atrial Fibrillation in Human AtriaR01HL111314 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI BARNARD, JOHN, CHUNG, MINA KAY · 2012 to 2019
$6.1M
NHLBI NIH HHS R01 HL111314
6 · The paper itself

Abstract

backgroundOur aim was to assess how atrial fibrillation (AF) induction, chronicity, and RR interval irregularity affect left atrial (LA) function and size in the setting of underlying heart failure (HF), and to determine whether AF effects can be mitigated by vagal nerve stimulation (VNS).

methodsHF was induced by 4-weeks of rapid ventricular pacing in 24 dogs. Subsequently, AF was induced and maintained by atrial pacing at 600 bpm. Dogs were randomized into control (n = 9) and VNS (n = 15) groups. In the VNS group, atrioventricular node fat pad stimulation (310 μs, 20 Hz, 3-7 mA) was delivered continuously for 6 months. LA volume and LA strain data were calculated from bi-weekly echocardiograms.

resultsRR intervals decreased with HF in both groups (p = 0.001), and decreased further during AF in control group (p = 0.014), with a non-significant increase in the VNS group during AF. LA size increased with HF (p<0.0001), with no additional increase during AF. LA strain decreased with HF (p = 0.025) and further decreased after induction of AF (p = 0.0001). LA strain decreased less (p = 0.001) in the VNS than in the control group. Beat-by-beat analysis showed a curvilinear increase of LA strain with longer preceding RR interval, (r = 0.45, p <0.0001) with LA strain 1.1% higher (p = 0.02) in the VNS-treated animals, independent of preceding RR interval duration. The curvilinear relationship between ratio of preceding and pre-preceding RR intervals, and subsequent LA strain was weaker, (r = 0.28, p = 0.001). However, VNS-treated animals again had higher LA strain (by 2.2%, p = 0.002) independently of the ratio of preceding and pre-preceding RR intervals.

conclusionsIn the underlying presence of pacing-induced HF, AF decreased LA strain, with little impact on LA size. LA strain depends on the preceding RR interval duration.

Indexed as

AnimalsAtrial FibrillationDisease Models, AnimalDogsEchocardiographyHeart AtriaHeart Failure

Identifiers

PMID26771573
PMCPMC4714887
OpenAlexW2235935487

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.