Evidence map›Paper›PMID 25849089›Full record

Trial reportPloS one2015

Association of small dense LDL serum levels and circulating monocyte subsets in stable coronary artery disease.

Konstantin A Krychtiuk, Stefan P Kastl, Stefan Pfaffenberger, Max Lenz, Sebastian L Hofbauer, Anna Wonnerth, Lorenz Koller, Katharina M Katsaros, Thomas Pongratz, Georg Goliasch and 8 more

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Nature versus Number: Monocytes in Cardiovascular Disease.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Observational
  11. Article
  12. Review
  13. Article
  14. Observational
  15. Article
  16. 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

18 authors at 2 institutions in 2 countries.

Konstantin A KrychtiukDepartment of Internal Medicine II-Division of Cardiology, Medical University of Vienna, Waehringerguertel 18-20, 1090, Vienna, Austria; Ludwig Boltzmann Cluster for Cardiovascular Research, Waehringerguertel 18-20, 1090, Vienna, Austria.
Stefan P KastlDepartment of Internal Medicine II-Division of Cardiology, Medical University of Vienna, Waehringerguertel 18-20, 1090, Vienna, Austria.
Stefan PfaffenbergerDepartment of Internal Medicine II-Division of Cardiology, Medical University of Vienna, Waehringerguertel 18-20, 1090, Vienna, Austria.
Max LenzDepartment of Internal Medicine II-Division of Cardiology, Medical University of Vienna, Waehringerguertel 18-20, 1090, Vienna, Austria.
Sebastian L HofbauerDepartment of Internal Medicine II-Division of Cardiology, Medical University of Vienna, Waehringerguertel 18-20, 1090, Vienna, Austria.
Anna WonnerthDepartment of Internal Medicine II-Division of Cardiology, Medical University of Vienna, Waehringerguertel 18-20, 1090, Vienna, Austria.
Lorenz KollerDepartment of Internal Medicine II-Division of Cardiology, Medical University of Vienna, Waehringerguertel 18-20, 1090, Vienna, Austria.
Katharina M KatsarosDepartment of Internal Medicine II-Division of Cardiology, Medical University of Vienna, Waehringerguertel 18-20, 1090, Vienna, Austria.
Thomas PongratzKrankenanstalten Dr. Dostal, Saarplatz 9, 1190, Vienna, Austria.
Georg GoliaschDepartment of Internal Medicine II-Division of Cardiology, Medical University of Vienna, Waehringerguertel 18-20, 1090, Vienna, Austria.
Alexander NiessnerDepartment of Internal Medicine II-Division of Cardiology, Medical University of Vienna, Waehringerguertel 18-20, 1090, Vienna, Austria.
Ludovit Gaspar2nd Department of Internal Medicine, Faculty of Medicine, Comenius University, Vajanského nábrežie, 811 02, Bratislava, Slovakia.
Kurt HuberLudwig Boltzmann Cluster for Cardiovascular Research, Waehringerguertel 18-20, 1090, Vienna, Austria; 3rd Medical Department, Wilhelminenhospital, Montleartstraße 37, 1160, Vienna, Austria.
Gerald MaurerDepartment of Internal Medicine II-Division of Cardiology, Medical University of Vienna, Waehringerguertel 18-20, 1090, Vienna, Austria.
Elisabeth DostalKrankenanstalten Dr. Dostal, Saarplatz 9, 1190, Vienna, Austria.
Johann WojtaDepartment of Internal Medicine II-Division of Cardiology, Medical University of Vienna, Waehringerguertel 18-20, 1090, Vienna, Austria; Ludwig Boltzmann Cluster for Cardiovascular Research, Waehringerguertel 18-20, 1090, Vienna, Austria; Core Facilities, Medical University of Vienna, Waehringerguertel 18-20, 1090, Vienna, Austria.
Stanislav OravecKrankenanstalten Dr. Dostal, Saarplatz 9, 1190, Vienna, Austria; 2nd Department of Internal Medicine, Faculty of Medicine, Comenius University, Vajanského nábrežie, 811 02, Bratislava, Slovakia.
Walter S SpeidlDepartment of Internal Medicine II-Division of Cardiology, Medical University of Vienna, Waehringerguertel 18-20, 1090, Vienna, Austria.
Wiener Krankenanstaltenverbund · ATComenius University Bratislava · SK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAtherosclerosis is considered to be an inflammatory disease in which monocytes and monocyte-derived macrophages play a key role. Circulating monocytes can be divided into three distinct subtypes, namely in classical monocytes (CM; CD14++CD16-), intermediate monocytes (IM; CD14++CD16+) and non-classical monocytes (NCM; CD14+CD16++). Low density lipoprotein particles are heterogeneous in size and density, with small, dense LDL (sdLDL) crucially implicated in atherogenesis. The aim of this study was to examine whether monocyte subsets are associated with sdLDL serum levels.

methodsWe included 90 patients with angiographically documented stable coronary artery disease and determined monocyte subtypes by flow cytometry. sdLDL was measured by an electrophoresis method on polyacrylamide gel.

resultsPatients with sdLDL levels in the highest tertile (sdLDL≥4mg/dL;T3) showed the highest levels of pro-inflammatory NCM (15.2±7% vs. 11.4±6% and 10.9±4%, respectively; p<0.01) when compared with patients in the middle (sdLDL=2-3mg/dL;T2) and lowest tertile (sdLDL=0-1mg/dL;T1). Furthermore, patients in the highest sdLDL tertile showed lower CM levels than patients in the middle and lowest tertile (79.2±8% vs. 83.9±7% and 82.7±5%; p<0.01 for T3 vs. T2+T1). Levels of IM were not related to sdLDL levels (5.6±4% vs. 4.6±3% vs. 6.4±3% for T3, T2 and T1, respectively). In contrast to monocyte subset distribution, levels of circulating pro- and anti-inflammatory markers were not associated with sdLDL levels.

conclusionThe atherogenic lipoprotein fraction sdLDL is associated with an increase of NCM and a decrease of CM. This could be a new link between lipid metabolism dysregulation, innate immunity and atherosclerosis.

Indexed as

AgedBiomarkersCoronary AngiographyCoronary Artery DiseaseCross-Sectional StudiesFemaleFlow CytometryHumansLipoproteins, LDLMaleMiddle AgedMonocytesBiomarkersLipoproteins, LDL

Identifiers

PMID25849089
PMCPMC4388574
OpenAlexW2046905970

What OpenQuestion holds

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LicenceCC BY
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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.