Evidence map›Paper›PMID 27205885›Full record

ReviewCurrent opinion in cardiology2016

Lipoprotein(a) and oxidized phospholipids in calcific aortic valve stenosis.

Calvin Yeang, Michael J Wilkinson, Sotirios Tsimikas

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
6.5field-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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Novel Lipoprotein (a) Therapies: A Comprehensive Review.Current atherosclerosis reports · 2026
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Lipoprotein(a) Lowering with Pelacarsen (TQJ230).Cardiovascular & hematological disorders drug targets · 2026
    Review
  13. Review
  14. Observational
  15. Novel Circulating Biomarkers in Aortic Valve Stenosis.International journal of molecular sciences · 2025
    Review
  16. Review
  17. Article
  18. Atherosclerotic features in patients with heart failure.Archives of medical science : AMS · 2025
    Article
  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

Calvin YeangDivision of Cardiovascular Diseases, Sulpizio Cardiovascular Center, Department of Medicine, University of California San Diego, La Jolla, California, USA.
Michael J Wilkinson
Sotirios Tsimikas
University of California, San Diego · US

Funding

Blood Cells in Hemostasis and ThrombosisT32HL086344 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GINSBERG, MARK HOWARD · 2008 to 2023
$4.4M
Oxidation-specific nanoparticles for imaging atherosclerosisR01HL119828 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TSIMIKAS, SOTIRIOS · 2013 to 2017
$2.0M
NHLBI NIH HHS R01 HL119828NHLBI NIH HHS T32 HL086344
6 · The paper itself

Abstract

purpose of reviewAs the incidence of calcific aortic valve stenosis increases with the aging of the population, improved understanding and novel therapies to reduce its progression and need for aortic valve replacement are urgently needed. RECENT

findingsLipoprotein(a) is the only monogenetic risk factor for calcific aortic stenosis. Elevated levels are a strong, causal, independent risk factor, as demonstrated in epidemiological, genome-wide association studies and Mendelian randomization studies. Lipoprotein(a) is the major lipoprotein carrier of oxidized phospholipids, which are proinflammatory and promote calcification of vascular cells, two key pathophysiological drivers of aortic stenosis. Elevated plasma lipoprotein(a) and oxidized phospholipids predict progression of pre-existing aortic stenosis and need for aortic valve replacement. The failure of statin trials in pre-existing aortic stenosis may be partially due to an increase in lipoprotein(a) and oxidized phospholipid levels caused by statins. Antisense oligonucleotides targeted to apo(a) are in Phase 2 clinical development and shown to lower both lipoprotein(a) and oxidized phospholipids. SUMMARY: Lipoprotein(a) and oxidized phospholipids are key therapeutic targets in calcific aortic stenosis. Strategies aimed at potent lipoprotein(a) lowering to normalize levels and/or to suppress the proinflammatory effects of oxidized phospholipids may prevent progression of this disease.

Indexed as

Aortic ValveAortic Valve StenosisCalcinosisGenome-Wide Association StudyHumansLipoprotein(a)PhospholipidsLipoprotein(a)Phospholipids

Identifiers

PMID27205885
PMCPMC4956483
OpenAlexW2402243097

What OpenQuestion holds

Textmetadata
LicenceTDM
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.