Evidence map›Paper›PMID 27076564›Full record

Observational studyJournal of the American Heart Association2016

Low Homoarginine Levels in the Prognosis of Patients With Acute Chest Pain.

Dorothee Atzler, Christina Baum, Francisco Ojeda, Till Keller, Kathrin Cordts, Renate B Schnabel, Chi-un Choe, Karl J Lackner, Thomas Münzel, Rainer H Böger and 3 more

Open access · goldAbstract readMulticenter StudyObservational Study
In one paragraph

Observational study in Journal of the American Heart Association, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Trial
  2. Oral supplementation with L-homoarginine in young volunteers.British journal of clinical pharmacology · 2016
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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

13 authors at 7 institutions in 2 countries.

Dorothee AtzlerDepartment of Cardiovascular Medicine, University of Oxford, United Kingdom German Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, Germany dorothee.atzler@well.ox.ac.uk dorothee.atzler@gmail.com.
Christina BaumGerman Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, Germany Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Hamburg, Germany.
Francisco OjedaDepartment of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Hamburg, Germany.
Till KellerDivision of Cardiology, Department of Medicine III, Goethe University Frankfurt, Frankfurt, Germany German Center for Cardiovascular Research (DZHK), Partner Site Rhein/Main, Germany.
Kathrin CordtsGerman Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, Germany Department of Clinical Pharmacology and Toxicology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Renate B SchnabelGerman Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, Germany Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Hamburg, Germany.
Chi-un ChoeDepartment of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Karl J LacknerGerman Center for Cardiovascular Research (DZHK), Partner Site Rhein/Main, Germany Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Thomas MünzelGerman Center for Cardiovascular Research (DZHK), Partner Site Rhein/Main, Germany Department of Medicine II, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Rainer H BögerGerman Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, Germany Department of Clinical Pharmacology and Toxicology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Stefan BlankenbergGerman Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, Germany Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Hamburg, Germany.
Edzard SchwedhelmGerman Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, Germany Department of Clinical Pharmacology and Toxicology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Tanja ZellerGerman Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, Germany Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Hamburg, Germany.
German Centre for Cardiovascular Research · DEUniversität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DEGoethe University Frankfurt · DEJohannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DEUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe endogenous amino acid homoarginine predicts mortality in cerebro- and cardiovascular disease. The objective was to explore whether homoarginine is associated with atrial fibrillation (AF) and outcome in patients with acute chest pain. METHODS AND

resultsOne thousand six hundred forty-nine patients with acute chest pain were consecutively enrolled in this study, of whom 589 were diagnosed acute coronary syndrome (ACS). On admission, plasma concentrations of homoarginine as well as brain natriuretic peptide (BNP), and high-sensitivity assayed troponin I (hsTnI) were determined along with electrocardiography (ECG) variables. During a median follow-up of 183 days, 60 major adverse cardiovascular events (MACEs; 3.8%), including all-cause death, myocardial infarction, or stroke, were registered in the overall study population and 43 MACEs (7.5%) in the ACS subgroup. Adjusted multivariable Cox regression analyses revealed that an increase of 1 SD of plasma log-transformed homoarginine (0.37) was associated with a hazard reduction of 26% (hazard ratio [HR], 0.74; 95% CI, 0.57-0.96) for incident MACE and likewise of 35% (HR, 0.65; 95% CI, 0.49-0.88) in ACS patients. In Kaplan-Meier survival curves, homoarginine was predictive for patients with high-sensitivity assayed troponin I (hsTnI) above 27 ng/L (P<0.05). Last, homoarginine was inversely associated with QTc duration (P<0.001) and prevalent AF (OR, 0.83; 95% CI, 0.71-0.95).

conclusionLow plasma homoarginine was identified as a risk marker for incident MACEs in patients with acute chest pain, in particular, in those with elevated hsTnI. Impaired homoarginine was associated with prevalent AF. Further studies are needed to investigate the link to AF and evaluate homoarginine as a therapeutic option for these patients.

Indexed as

Acute Coronary SyndromeAcute PainAgedAtrial FibrillationBiomarkersChest PainFemaleHomoarginineHumansKaplan-Meier EstimateMaleMiddle AgedMyocardial InfarctionNatriuretic Peptide, BrainPrognosisProportional Hazards ModelsBiomarkersHomoarginineNatriuretic Peptide, Brainacute coronary syndromeatrial fibrillationhomoargininel‐arginine:glycine amidinotransferase

Identifiers

PMID27076564
PMCPMC4859271
OpenAlexW2339672648

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Registered trials

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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.