Evidence map›Paper›PMID 26228671›Full record

ArticleJournal of clinical lipidology

Monocyte subset distribution in patients with stable atherosclerosis and elevated levels of lipoprotein(a).

Konstantin A Krychtiuk, Stefan P Kastl, Sebastian L Hofbauer, Anna Wonnerth, Georg Goliasch, Maria Ozsvar-Kozma, Katharina M Katsaros, Gerald Maurer, Kurt Huber, Elisabeth Dostal and 5 more

Abstract read
In one paragraph

Article in Journal of clinical lipidology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. From inflammation to remodelling: A novel BASP1Journal of advanced research · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The Effects of Exercise on Lipid Biomarkers.Methods in molecular biology (Clifton, N.J.) · 2022
    Review
  15. Nature versus Number: Monocytes in Cardiovascular Disease.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Observational
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

15 authors.

Konstantin A KrychtiukDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria; Ludwig Boltzmann Cluster for Cardiovascular Research, Vienna, Austria.
Stefan P KastlDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Sebastian L HofbauerDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Anna WonnerthDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Georg GoliaschDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Maria Ozsvar-KozmaDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Katharina M KatsarosDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Gerald MaurerDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Kurt HuberLudwig Boltzmann Cluster for Cardiovascular Research, Vienna, Austria; 3rd Medical Department, Wilhelminenhospital, Vienna, Austria.
Elisabeth DostalKrankenanstalten Dr. Dostal, Vienna, Austria.
Christoph J BinderDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Stefan PfaffenbergerDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Stanislav OravecKrankenanstalten Dr. Dostal, Vienna, Austria; 2nd Department of Internal Medicine, Faculty of Medicine, Comenius University, Bratislava, Slovakia.
Johann WojtaDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria; Ludwig Boltzmann Cluster for Cardiovascular Research, Vienna, Austria; Core Facilities, Medical University of Vienna, Vienna, Austria.
Walter S SpeidlDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria. Electronic address: walter.speidl@meduniwien.ac.at.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLipoprotein(a) (Lp(a)) is a proatherogenic plasma lipoprotein currently established as an independent risk factor for the development of atherosclerotic disease and as a predictor for acute thrombotic complications. In addition, Lp(a) is the major carrier of proinflammatory oxidized phospholipids (OxPL). Today, atherosclerosis is considered to be an inflammatory disease of the vessel wall in which monocytes and monocyte-derived macrophages are crucially involved. Circulating monocytes can be divided according to their surface expression pattern of CD14 and CD16 into at least 3 subsets with distinct inflammatory and atherogenic potential.

objectiveThe aim of this study was to examine whether elevated levels of Lp(a) and OxPL on apolipoprotein B-100-containing lipoproteins (OxPL/apoB) are associated with changes in monocyte subset distribution.

methodsWe included 90 patients with stable coronary artery disease. Lp(a) and OxPL/apoB were measured, and monocyte subsets were identified as classical monocytes (CMs; CD14++CD16-), intermediate monocytes (IMs; CD14++CD16+), and nonclassical monocytes (NCMs; CD14+CD16++) by flow cytometry.

resultsIn patients with elevated levels of Lp(a) (>50 mg/dL), monocyte subset distribution was skewed toward an increase in the proportion of IM (7.0 ± 3.8% vs 5.2 ± 3.0%; P = .026), whereas CM (82.6 ± 6.5% vs 82.0 ± 6.8%; P = .73) and NCM (10.5 ± 5.3 vs 12.8 ± 6.0; P = .10) were not significantly different. This association was independent of clinical risk factors, choice of statin treatment regime, and inflammatory markers. In addition, OxPL/apoB was higher in patients with elevated Lp(a) and correlated with IM but not CM and NCM.

conclusionsIn conclusion, we provide a potential link between elevated levels of Lp(a) and a proatherogenic distribution of monocyte subtypes in patients with stable atherosclerotic disease.

Indexed as

Oxidation-ReductionAgedApolipoprotein B-100AtherosclerosisCell LineageCoronary Artery DiseaseFemaleGPI-Linked ProteinsHumansLipopolysaccharide ReceptorsLipoprotein(a)MaleMiddle AgedMonocytesPhospholipidsReceptors, IgGApolipoprotein B-100FCGR3B protein, humanGPI-Linked ProteinsLipopolysaccharide ReceptorsLipoprotein(a)PhospholipidsReceptors, IgGAtherosclerosisCoronary artery diseaseLipoprotein(a)Monocyte subsetsOxidized phospholipids

Identifiers

PMID26228671
PMCPMC4533224

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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.