Evidence map›Paper›PMID 33742565›Full record

ArticleESC heart failure2021

Neprilysin inhibition does not alter dynamic of proenkephalin-A 119-159 and pro-substance P in heart failure.

Henrike Arfsten, Georg Goliasch, Philipp E Bartko, Suriya Prausmüller, Georg Spinka, Anna Cho, Johannes Novak, Julia Mascherbauer, Helmuth Haslacher, Guido Strunk and 2 more

Open access · goldAbstract read
In one paragraph

Article in ESC heart failure, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 42% 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, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  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

12 authors at 2 institutions in 1 country.

Henrike ArfstenDepartment of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Waehringer Guertel 18-20, Vienna, 1090, Austria.ORCID 0000-0002-5836-7759
Georg GoliaschDepartment of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Waehringer Guertel 18-20, Vienna, 1090, Austria.
Philipp E BartkoDepartment of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Waehringer Guertel 18-20, Vienna, 1090, Austria.
Suriya PrausmüllerDepartment of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Waehringer Guertel 18-20, Vienna, 1090, Austria.
Georg SpinkaDepartment of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Waehringer Guertel 18-20, Vienna, 1090, Austria.
Anna ChoDepartment of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Waehringer Guertel 18-20, Vienna, 1090, Austria.
Johannes NovakDepartment of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Waehringer Guertel 18-20, Vienna, 1090, Austria.
Julia MascherbauerDepartment of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Waehringer Guertel 18-20, Vienna, 1090, Austria.
Helmuth HaslacherDepartment of Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Waehringer Guertel 18-20, Vienna, 1090, Austria.
Guido StrunkComplexity Research, Schönbrunner Straße 32, Vienna, 1050, Austria.
Martin HülsmannDepartment of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Waehringer Guertel 18-20, Vienna, 1090, Austria.
Noemi PavoDepartment of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Waehringer Guertel 18-20, Vienna, 1090, Austria.
Medical University of Vienna · ATComplexity Science Hub · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsAs NEP degrades many substrates, the specific therapeutic mechanism of NEP inhibition with angiotensin receptor neprilysin inhibitor (ARNi) in heart failure with reduced ejection fraction (HFrEF) is not entirely evident. The aim of this study was to investigate the response of two substrates of NEP-the tachykinin and enkephalin systems-to the initiation of ARNi therapy in HFrEF. METHODS AND

resultsBetween 2016 and 2018, 141 consecutive patients with stable HFrEF [74 with initiation of ARNi and 67 controls on continuous angiotensin converting enzyme inhibitor (ACEi) or angiotensin receptor blocker (ARB) therapy] were prospectively enrolled. Plasma proenkephalin-A 119-159 (PENK) and pro-substance P (pro-SP) were serially determined. Proenkephalin-A 119-159 and pro-SP correlated strongly with each other (r

conclusionsAlthough enkephalins and SP are known substrates of NEP, NEP inhibition by ARNi does not clearly affect the circulating precursors PENK and pro-SP in HFrEF.

Indexed as

Heart FailureNeprilysinAngiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsEnkephalinsHumansProtein PrecursorsStroke VolumeSubstance PAngiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsEnkephalinsNeprilysinproenkephalinProtein PrecursorsSubstance PARNiEnkephalinHeart failureNeprilysinSubstance P

Identifiers

PMID33742565
PMCPMC8120349
OpenAlexW3136706118

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.