Evidence map›Paper›PMID 27236656›Full record

ArticleHeart and vessels2016

Effect of irbesartan on development of atrial fibrosis and atrial fibrillation in a canine atrial tachycardia model with left ventricular dysfunction, association with p53.

Naoya Kataoka, Kunihiro Nishida, Koshi Kinoshita, Tamotsu Sakamoto, Yosuke Nakatani, Yasushi Tsujino, Koichi Mizumaki, Hiroshi Inoue, Koichiro Kinugawa

Abstract read
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In one paragraph

Article in Heart and vessels, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed, 18 citations in OpenAlex.

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  10. Irbesartan prevents sodium channel remodeling in a canine model of atrial fibrillation.Journal of the renin-angiotensin-aldosterone system : JRAAS
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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 2 institutions in 1 country.

Naoya KataokaSecond Department of Internal Medicine, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Kunihiro NishidaSecond Department of Internal Medicine, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan. knishida@med.u-toyama.ac.jp.
Koshi KinoshitaDepartment of Legal Medicine, University of Toyama, Toyama, Japan.
Tamotsu SakamotoSecond Department of Internal Medicine, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Yosuke NakataniSecond Department of Internal Medicine, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Yasushi TsujinoSecond Department of Internal Medicine, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Koichi MizumakiClinical Research and Ethics Center, University of Toyama, Toyama, Japan.
Hiroshi InoueSaiseikai Toyama Hospital, Toyama, Japan.
Koichiro KinugawaSecond Department of Internal Medicine, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
University of Toyama · JPToyama University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Effects of an angiotensin II receptor blocker, irbesartan (IRB), on the development of atrial fibrosis and atrial fibrillation (AF) were assessed in a canine model of atrial tachycardia remodeling (ATR) with left ventricular dysfunction, together with its possible association with involvement of p53. Atrial tachypacing (400 bpm for 4 weeks) was used to induce ATR in beagles treated with placebo (ATR-dogs, n = 6) or irbesartan (IRB-dogs, n = 5). Non-paced sham dogs served as control (Control-dogs, n = 4). ATR- and IRB-dogs developed tachycardia-induced left ventricular dysfunction. Atrial effective refractory period (AERP) shortened (83 ± 5 ms, p < 0.05), inter-atrial conduction time prolonged (72 ± 2 ms, p < 0.05), and AF duration increased (29 ± 5 s, p < 0.05 vs. baseline) after 4 weeks in ATR-dogs. ATR-dogs also had a larger area of atrial fibrous tissue (5.2 ± 0.5 %, p < 0.05 vs. Control). All these changes, except for AERP, were attenuated in IRB-dogs (92 ± 3 ms, 56 ± 3 ms, 9 ± 5 s, and 2.5 ± 0.7 %, respectively; p < 0.05 vs. ATR for each). In ATR-dogs, p53 expression in the left atrium decreased by 42 % compared with Control-dogs (p < 0.05); however, it was highly expressed in IRB-dogs (+89 % vs. ATR). Transforming growth factor (TGF)-β1 expression was enhanced in ATR-dogs (p < 0.05 vs. Control) but reduced in IRB-dogs (p < 0.05 vs. ATR). Irbesartan suppresses atrial fibrosis and AF development in a canine ATR model with left ventricular dysfunction in association with p53.

Indexed as

Angiotensin II Type 1 Receptor BlockersAnimalsAtrial FibrillationAtrial RemodelingBiphenyl CompoundsDisease Models, AnimalDogsEchocardiographyFibrosisHeart AtriaHemodynamicsIrbesartanTachycardia, SupraventricularTetrazolesTime FactorsTransforming Growth Factor beta1Angiotensin II Type 1 Receptor BlockersBiphenyl CompoundsIrbesartanTetrazolesTransforming Growth Factor beta1Tumor Suppressor Protein p53Angiotensin IIp53RemodelingTGF-β1

Identifiers

PMID27236656
OpenAlexW2405560221

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.