Evidence map›Paper›PMID 28183512›Full record

ReviewJournal of the American College of Cardiology2017

A Test in Context: Lipoprotein(a): Diagnosis, Prognosis, Controversies, and Emerging Therapies.

Sotirios Tsimikas

3 registry-linked trialsOpen access · hybridAbstract readReview
PubMed Publisher
In one paragraph

Review in Journal of the American College of Cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 3 registered trials, which are not on this map. Cited by 536 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
536citing papers in PubMed, 7 pooled it
72.2field-weighted citation impact, top 1% 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.

NCT04613167 naunknown statusstarted 2020, after this paper: background citation

Genetic, Biochemical and Functional Markers of Cardiovascular Risk in Patients With Premature Coronary Artery Disease and Treatment Options

Ran2020Enrolled70Registered outcomes3Posted comparisons0ConditionsAcute Coronary Syndrome, Genetic Polymorphisms, Inflammation, LipoproteinemiaArmsAlirocumab, Control group, Evolocumab
PMID 30995439PMID 30838555PMID 31061262PMID 32453609PMID 14064818PMID 18775538PMID 20032323PMID 23594558PMID 25120086PMID 26002446PMID 26428312PMID 26637278other papers from this trial
Open the trial in the graph
NCT04993664 nawithdrawnnot on this mapstarted 2021, after this paper: background citation

Influence of Pelacarsen on Arterial Wall Properties and Risk Factors in Patients After Myocardial Infarction With High Lp(a) Values

TypeinterventionalSponsorUniversity Medical Centre LjubljanaRan2021 to 2022Enrolled0ConditionsAcute Coronary Syndrome, Lipoproteinemia, Inflammation, Genetic PolymorphismsArmsPelacarsen (TQJ230), Placebo
NCT07184034 not yet recruitingnot on this mapstarted 2025, after this paper: background citation

Assessment of the Correlation Between Lipoprotein (a) Levels and Coronary Artery Findings on Multislice Computed Tomography

Typeobservational_patient_registrySponsorAssiut UniversityRan2025 to 2026Enrolled150ConditionsCoronary Artery Disease (CAD)
3 · Its place in the literature

Who cites it

536 citing papers in PubMed, 7 syntheses or guidelines pooled it, 1,063 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Pooled it
  8. Trial
  9. Lipoprotein(a), remote ischemic conditioning, and stroke recurrence in patients with symptomatic intracranial atherosclerotic stenosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Trial
  10. Trial
  11. Trial
  12. Review
  13. Article
  14. Review
  15. Features of Lipid Disorders in Cardiovascular-Kidney-Metabolic Syndrome.International journal of molecular sciences · 2026
    Review
  16. Article
  17. Lipoprotein(a) and premature myocardial infarction: Mechanistic insights and implications for PCI-era residual risk.International journal of cardiology. Cardiovascular risk and prevention · 2026
    Review
  18. Article
  19. [EJNMMI research · 2026
    Review
  20. Review

476 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

1 author at 1 institution in 1 country.

Sotirios TsimikasDivision of Cardiovascular Medicine, Sulpizio Cardiovascular Center, University of California San Diego, La Jolla, California. Electronic address: stsimikas@ucsd.edu.
University of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evidence that elevated lipoprotein(a) (Lp[a]) levels contribute to cardiovascular disease (CVD) and calcific aortic valve stenosis (CAVS) is substantial. Development of isoform-independent assays, in concert with genetic, epidemiological, translational, and pathophysiological insights, have established Lp(a) as an independent, genetic, and likely causal risk factor for CVD and CAVS. These observations are consistent across a broad spectrum of patients, risk factors, and concomitant therapies, including patients with low-density lipoprotein cholesterol <70 mg/dl. Statins tend to increase Lp(a) levels, possibly contributing to the "residual risk" noted in outcomes trials and at the bedside. Recently approved proprotein convertase subtilisin/kexin-type 9 inhibitors and mipomersen lower Lp(a) 20% to 30%, and emerging RNA-targeted therapies lower Lp(a) >80%. These approaches will allow testing of the "Lp(a) hypothesis" in clinical trials. This review summarizes the current landscape of Lp(a), discusses controversies, and reviews emerging therapies to reduce plasma Lp(a) levels to decrease risk of CVD and CAVS.

Indexed as

Cardiovascular DiseasesHumansLipoprotein(a)PrognosisRisk FactorsLipoprotein(a)aortic stenosiscardiovascular diseasegenome-wide association studiestherapy

Identifiers

PMID28183512
OpenAlexW2586892149

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.