Evidence map›Paper›PMID 28082430›Full record

ArticlePhysiological reports2017

Increased cardiac work provides a link between systemic hypertension and heart failure.

Alexander J Wilson, Vicky Y Wang, Gregory B Sands, Alistair A Young, Martyn P Nash, Ian J LeGrice

Abstract read
In one paragraph

Article in Physiological reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

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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

6 authors.

Alexander J WilsonAuckland Bioengineering Institute, University of Auckland, Auckland, New Zealand alexander.wilson@auckland.ac.nz.
Vicky Y WangAuckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
Gregory B SandsAuckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
Alistair A YoungAuckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
Martyn P NashAuckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
Ian J LeGriceAuckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.

Funding

The Cardiac Atlas ProjectR01HL121754 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MCCULLOCH, ANDREW D., OMENS, JEFFREY H. · 2014 to 2023
$5.0M
NHLBI NIH HHS R01 HL121754
6 · The paper itself

Abstract

The spontaneously hypertensive rat (SHR) is an established model of human hypertensive heart disease transitioning into heart failure. The study of the progression to heart failure in these animals has been limited by the lack of longitudinal data. We used MRI to quantify left ventricular mass, volume, and cardiac work in SHRs at age 3 to 21 month and compared these indices to data from Wistar-Kyoto (WKY) controls. SHR had lower ejection fraction compared with WKY at all ages, but there was no difference in cardiac output at any age. At 21 month the SHR had significantly elevated stroke work (51 ± 3 mL.mmHg SHR vs. 24 ± 2 mL.mmHg WKY; n = 8, 4; P < 0.001) and cardiac minute work (14.2 ± 1.2 L.mmHg/min SHR vs. 6.2 ± 0.8 L.mmHg/min WKY; n = 8, 4; P < 0.001) compared to control, in addition to significantly larger left ventricular mass to body mass ratio (3.61 ± 0.15 mg/g SHR vs. 2.11 ± 0.008 mg/g WKY; n = 8, 6; P < 0.001). SHRs showed impaired systolic function, but developed hypertrophy to compensate and successfully maintained cardiac output. However, this was associated with an increase in cardiac work at age 21 month, which has previously demonstrated fibrosis and cell death. The interplay between these factors may be the mechanism for progression to failure in this animal model.

Indexed as

Rats, Inbred SHRAnimalsCardiac OutputDisease ProgressionHeartHeart FailureHeart VentriclesHypertensionHypertrophy, Left VentricularMagnetic Resonance ImagingMaleModels, AnimalRatsRats, Inbred WKYStroke VolumeVentricular Dysfunction, LeftCardiomyopathyheart failurehypertensionhypertrophyventricular dysfunctionventricular remodeling

Identifiers

PMID28082430
PMCPMC5256162

What OpenQuestion holds

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LicenceCC BY
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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.