Evidence map›Paper›PMID 25708587›Full record

ArticleClinical research in cardiology supplements2015

Lipoprotein(a) hyperlipidemia as cardiovascular risk factor: pathophysiological aspects.

Gerd Schmitz, Evelyn Orsó

Open access · hybridAbstract read
In one paragraph

Article in Clinical research in cardiology supplements, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Atherosclerosis and Its Related Laboratory Biomarkers.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Article
  8. Article
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  13. Article
  14. Observational
  15. Review
  16. Effect of 405 nm low intensity irradiation on the absorption spectrum of in-vitro hyperlipidemia blood.Technology and health care : official journal of the European Society for Engineering and Medicine · 2018
    Article
  17. Article
  18. Review
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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

2 authors at 1 institution in 1 country.

Gerd SchmitzInstitute for Laboratory Medicine and Transfusion Medicine, University Hospital of Regensburg, Franz-Josef-Strauss-Allee 11, 93053, Regensburg, Germany, gerd.schmitz@klinik.uni-regensburg.de.
Evelyn Orsó
University Hospital Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipoprotein (a) [Lp(a)] is a modified LDL particle with an additional apolipoprotein [apo(a)] protein covalently attached by a thioester bond. Multiple isoforms of apo(a) exist that are genetically determined by differences in the number of Kringle-IV type-2 repeats encoded by the LPA gene. Elevated plasma Lp(a) is an independent risk factor for cardiovascular disease.The phenotypic diversity of familial Lp(a) hyperlipidemia [Lp(a)-HLP] and familial hypercholesterolemia [FH], as defined risks with genetic background, and their frequent co-incidence with additional cardiovascular risk factors require a critical revision of the current diagnostic and therapeutic recommendations established for isolated familial Lp(a)-HLP or FH in combination with elevated Lp(a) levels.Lp(a) assays still suffer from poor standardization, comparability and particle variation. Further evaluation of the current biomarkers and establishment of novel comorbidity biomarkers are necessary for extended risk assessment of cardiovascular disease in FH or Lp(a)-HLP and to better understand the pathophysiology and to improve patient stratification of the Lp(a) syndrome complex.Lp(a) promotes vascular remodeling, increased lesion progression and intima media thickening through induction of M1-macrophages, antiangiogenic effects (e.g. vasa vasorum) with secretion of the antiangiogenic chemokine CXCL10 (IP10) and CXCR3 mediated activation of Th1- and NK-cells.In addition inhibition of serine proteases causing disturbances of thrombosis/ hemostasis/ fibrinolysis, TGFb-activation and acute phase response (e.g. CRP, anti-PL antibodies) are major features of Lp(a) pathology. Anti-PL antibodies (EO6 epitope) also bind to oxidized Lp(a).Lipoprotein apheresis is used to reduce circulating lipoproteins in patients with severe FH and/or Lp(a)-HLP, particularly with multiple cardiovascular risks who are intolerant or insufficiently responsive to lipid-lowering drugs.

Indexed as

Blood Component RemovalCardiovascular DiseasesChronic DiseaseHumansHyperlipoproteinemiasLipoprotein(a)Patient SelectionRisk FactorsTreatment OutcomeLipoprotein(a)

Identifiers

PMID25708587
PMCPMC4361722
OpenAlexW2002436594

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.