Evidence map›Paper›PMID 32277995›Full record

ReviewProgress in cardiovascular diseases

What do we know about the role of lipoprotein(a) in atherogenesis 57 years after its discovery?

Barbara Cybulska, Longina Kłosiewicz-Latoszek, Peter E Penson, Maciej Banach

Abstract readReview
PubMed Publisher
In one paragraph

Review in Progress in cardiovascular diseases. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.7field-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

32 citing papers in PubMed, 56 citations in OpenAlex.

  1. [Nomogram prediction model for factors associated with vascular plaques in a physical examination population].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
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  13. The Anti-Thrombotic Effects of PCSK9 Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Barbara CybulskaNational Institute of Public Health - National Institute of Hygiene, Warsaw, Poland.
Longina Kłosiewicz-LatoszekNational Institute of Public Health - National Institute of Hygiene, Warsaw, Poland.
Peter E PensonSchool of Pharmacy and Biomolecular Sciences, Liverpool John Moores University, Liverpool, UK; Liverpool Centre For Cardiovascular Science, Liverpool, UK; University of Liverpool, Liverpool, UK.
Maciej BanachDepartment of Hypertension, WAM University Hospital, Lodz, Medical University, Lodz, Poland; Polish Mothers Memorial Hospital Research Institute (PMMHRI), Lodz, Poland. Electronic address: maciejbanach77@gmail.com.
National Institute of Public Health · PLPolish Mother’s Memorial Hospital Research Institute · PLUniversity of Liverpool · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated circulating concentrations of lipoprotein(a) [Lp(a)] is strongly associated with increased risk of atherosclerotic cardiovascular disease (CVD) and degenerative aortic stenosis. This relationship was first observed in prospective observational studies, and the causal relationship was confirmed in genetic studies. Everybody should have their Lp(a) concentration measured once in their lifetime. CVD risk is elevated when Lp(a) concentrations are high i.e. > 50 mg/dL (≥100 mmol/L). Extremely high Lp(a) levels >180 mg/dL (≥430 mmol/L) are associated with CVD risk similar to that conferred by familial hypercholesterolemia. Elevated Lp(a) level was previously treated with niacin, which exerts a potent Lp(a)-lowering effect. However, niacin is currently not recommended because, despite the improvement in lipid profile, no improvements on clinical outcomes have been observed. Furthermore, niacin use has been associated with severe adverse effects. Post hoc analyses of clinical trials with proprotein convertase subtilisin/kexin type-9 (PCSK9) inhibitors have shown that these drugs exert clinical benefits by lowering Lp(a), independent of their potent reduction of low-density lipoprotein cholesterol (LDL-C). It is not yet known whether PCSK9 inhibitors will be of clinical use in patients with elevated Lp(a). Apheresis is a very effective approach to Lp(a) reduction, which reduces CVD risk but is invasive and time-consuming and is thus reserved for patients with very high Lp(a) levels and progressive CVD. Studies are ongoing on the practical application of genetic approaches to therapy, including antisense oligonucleotides against apolipoprotein(a) and small interfering RNA (siRNA) technology, to reduce the synthesis of Lp(a).

Indexed as

Plaque, AtheroscleroticAnimalsAortic ValveAortic Valve StenosisArteriesAtherosclerosisBiomarkersCalcinosisHumansLipoprotein(a)PrognosisRisk FactorsUp-RegulationBiomarkersLipoprotein(a)LPA protein, humanAtherogenesisGenetic studiesLipoprotein(a)ManagementObservational studiesRisk factor

Identifiers

PMID32277995
OpenAlexW3015522882

What OpenQuestion holds

Textmetadata
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.