Evidence map›Paper›PMID 24760552›Full record

ArticleCardiovascular research2014

Lipoprotein (a) concentrations, apolipoprotein (a) phenotypes, and peripheral arterial disease in three independent cohorts.

Anja Laschkolnig, Barbara Kollerits, Claudia Lamina, Christa Meisinger, Barbara Rantner, Marietta Stadler, Annette Peters, Wolfgang Koenig, Andrea Stöckl, Doreen Dähnhardt and 5 more

Open access · greenAbstract read
In one paragraph

Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 2 pooled it
5.9field-weighted citation impact, top 3% 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

63 citing papers in PubMed, 2 syntheses or guidelines pooled it, 150 citations in OpenAlex.

  1. Pooled it
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  12. Observational
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  16. Review
  17. Lipoprotein (a): Underrecognized Risk with a Promising Future.Reviews in cardiovascular medicine · 2024
    Review
  18. Article
  19. Lipoprotein(a): from Causality to Treatment.Current atherosclerosis reports · 2024
    Review
  20. Lipoprotein(a) as a Risk Factor for Cardiovascular Diseases: Pathophysiology and Treatment Perspectives.International journal of environmental research and public health · 2023
    Review

3 more citing papers are in PubMed but not listed here.

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 at 6 institutions in 2 countries.

Anja LaschkolnigDivision of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Schöpfstr. 41, A-6020 Innsbruck, Austria.
Barbara KolleritsDivision of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Schöpfstr. 41, A-6020 Innsbruck, Austria.
Claudia LaminaDivision of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Schöpfstr. 41, A-6020 Innsbruck, Austria.
Christa MeisingerHelmholtz Zentrum München - German Research Center for Environmental Health (GmbH), Institute of Epidemiology II, Neuherberg, Germany.
Barbara RantnerDivision of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Schöpfstr. 41, A-6020 Innsbruck, Austria Department of Vascular Surgery, Innsbruck Medical University, Innsbruck, Austria.
Marietta StadlerThird Medical Department of Metabolic Diseases and Nephrology, Hietzing Hospital, Vienna, Austria.
Annette PetersHelmholtz Zentrum München - German Research Center for Environmental Health (GmbH), Institute of Epidemiology II, Neuherberg, Germany.
Wolfgang KoenigDepartment of Internal Medicine II - Cardiology, University of Ulm Medical Center, Ulm, Germany.
Andrea StöcklDivision of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Schöpfstr. 41, A-6020 Innsbruck, Austria.
Doreen DähnhardtDivision of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Schöpfstr. 41, A-6020 Innsbruck, Austria.
Carsten A BögerDepartment of Internal Medicine II, University Medical Center Regensburg, Regensburg, Germany.
Bernhard K KrämerVth Department of Medicine, University Medicine Mannheim, Medical Faculty Mannheim of the University of Heidelberg, Mannheim, Germany.
Gustav FraedrichDepartment of Vascular Surgery, Innsbruck Medical University, Innsbruck, Austria.
Konstantin StrauchHelmholtz Zentrum München - German Research Center for Environmental Health (GmbH), Institute of Genetic Epidemiology, Neuherberg, Germany Biometry and Epidemiology, Chair of Genetic Epidemiology, Ludwig-Maximilians-Universität, Institute of Medical Informatics, Munich, Germany.
Florian KronenbergDivision of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Schöpfstr. 41, A-6020 Innsbruck, Austria florian.kronenberg@i-med.ac.at.
Innsbruck Medical University · ATHeidelberg University · DEKlinik Hietzing · ATLudwig-Maximilians-Universität München · DEUniversität Ulm · DEUniversity Hospital Regensburg · DE

Funding

Austrian Science Fund FWF P 26660
6 · The paper itself

Abstract

aimsThe relevance of lipoprotein(a) [Lp(a)] concentrations and low-molecular-weight (LMW) apo(a) phenotypes in peripheral arterial disease (PAD) has only been investigated by few studies. Therefore, we analysed this association in three independent cohorts and performed a Mendelian Randomization approach using instrumental variable regression. METHODS AND

resultsLp(a) concentrations, apo(a) phenotypes, and one SNP in the LPA gene (rs10455872) were measured in the CAVASIC study, including 241 male patients with intermittent claudication and 246 age- and diabetes-matched controls as well as in the two population-based studies KORA F3 (n = 3184) and KORA F4 (n = 3080). In KORA F3/F4, 109/80 persons suffered from intermittent claudication, 200/144 from PAD, and 128/103 showed an ankle-brachial index (ABI) <0.9. In CAVASIC, adjusted logistic regression analyses revealed significant associations between an increase of log-Lp(a) per one standard deviation (SD) (OR = 1.28, P = 0.02) as well as LMW apo(a) phenotypes and symptomatic PAD (OR = 1.65, P = 0.03). Linear regression models with continuous ABI showed a significant association in the combined analyses of KORA F3/F4: an increase in log-Lp(a) per one SD (β = -0.006, P = 0.005) and the presence of LMW apo(a) phenotypes (β = -0.011, P = 0.02) or the minor allele of rs10455872 (ß = -0.016, P = 0.03) were associated with a decrease in ABI in the fully adjusted linear and instrumental variable regression models.

conclusionAnalyses in three independent populations showed significant associations of Lp(a) concentrations, LMW apo(a) phenotypes, and rs10455872 with PAD. This points to a causal relationship between Lp(a) and PAD since the genetically determined apo(a) phenotypes and SNP alleles are indeed associated with PAD.

Indexed as

AdultAgedAnkle Brachial IndexApoprotein(a)Cohort StudiesFemaleGenetic Predisposition to DiseaseHumansIntermittent ClaudicationLinear ModelsLipoprotein(a)MaleMiddle AgedMolecular WeightPeripheral Arterial DiseasePhenotypeApoprotein(a)Lipoprotein(a)Ankle-brachial indexApolipoprotein(a) phenotypesCausalityLp(a) concentrationsMendelian randomizationPeripheral arterial disease

Identifiers

PMID24760552
PMCPMC4065111
OpenAlexW2144046999

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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.