Evidence map›Paper›PMID 30478197›Full record

ArticleThorax2019

Reduced plasma levels of small HDL particles transporting fibrinolytic proteins in pulmonary arterial hypertension.

Lars Harbaum, Pavandeep Ghataorhe, John Wharton, Beatriz Jiménez, Luke S G Howard, J Simon R Gibbs, Jeremy K Nicholson, Christopher J Rhodes, Martin R Wilkins

Open access · hybridAbstract read
In one paragraph

Article in Thorax, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Review
  7. [Research progress on bioinformatics in pulmonary arterial hypertension].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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  15. Review
  16. Promises and Pitfalls of Multiomics Approaches to Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2022
    Article
  17. Review
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Lars Harbaum *Department of Medicine, Imperial College London, London, UK.
Pavandeep Ghataorhe *Department of Medicine, Imperial College London, London, UK.
John WhartonDepartment of Medicine, Imperial College London, London, UK.
Beatriz JiménezImperial Clinical Phenome Centre, Department of Surgery and Cancer, Imperial College London, London, UK.
Luke S G HowardNational Heart and Lung Institute, Imperial College London, London, UK.ORCID 0000-0003-2822-210X
J Simon R GibbsNational Heart and Lung Institute, Imperial College London, London, UK.
Jeremy K NicholsonDivision of Computational Systems Medicine, Department of Surgery and Cancer, and Centre for Digestive and Gut Health, Imperial College London, London, UK.
Christopher J Rhodes *Department of Medicine, Imperial College London, London, UK.
Martin R Wilkins *Department of Medicine, Imperial College London, London, UK.
Imperial College London · GBImperial College Healthcare NHS Trust · GB

Funding

ANTIARRHYTHMIC MECHANISMS IN ISCHEMIC MYOCARDIUMK11HL001559 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI HURWITZ, JODIE L · 1985 to 1990
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British Heart Foundation FS/15/59/31839British Heart Foundation RG/10/16/28575Wellcome Trust
6 · The paper itself

Abstract

backgroundAberrant lipoprotein metabolism has been implicated in experimental pulmonary hypertension, but the relevance to patients with pulmonary arterial hypertension (PAH) is inconclusive.

objectiveTo investigate the relationship between circulating lipoprotein subclasses and survival in patients with PAH.

methodsUsing nuclear magnetic resonance spectroscopy, 105 discrete lipoproteins were measured in plasma samples from two cohorts of patients with idiopathic or heritable PAH. Data from 1124 plasma proteins were used to identify proteins linked to lipoprotein subclasses. The physical presence of proteins was confirmed in plasma lipoprotein subfractions separated by ultracentrifugation.

resultsPlasma levels of three lipoproteins from the small high-density lipoprotein (HDL) subclass, termed HDL-4, were inversely related to survival in both the discovery (n=127) and validation (n=77) cohorts, independent of exercise capacity, comorbidities, treatment, N-terminal probrain natriuretic peptide, C reactive protein and the principal lipoprotein classes. The small HDL subclass rich in apolipoprotein A-2 content (HDL-4-Apo A-2) exhibited the most significant association with survival. None of the other lipoprotein classes, including principal lipoprotein classes HDL and low-density lipoprotein cholesterol, were prognostic. Three out of nine proteins identified to associate with HDL-4-Apo A-2 are involved in the regulation of fibrinolysis, namely, the plasmin regulator, alpha-2-antiplasmin, and two major components of the kallikrein-kinin pathway (coagulation factor XI and prekallikrein), and their physical presence in the HDL-4 subfraction was confirmed.

conclusionReduced plasma levels of small HDL particles transporting fibrinolytic proteins are associated with poor outcomes in patients with idiopathic and heritable PAH.

Indexed as

AdultAgedBiomarkersCohort StudiesFemaleFibrinolysisHemodynamicsHumansHypertension, PulmonaryKallikrein-Kinin SystemKaplan-Meier EstimateLipoproteinsLipoproteins, HDLMagnetic Resonance SpectroscopyMaleMetabolomicsBiomarkersLipoproteinsLipoproteins, HDLProteomeprimary pulmonary hypertension

Identifiers

PMID30478197
PMCPMC6475111
OpenAlexW2903389211

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.