Evidence map›Paper›PMID 42859724›Full record

ReviewReviews in cardiovascular medicine2026

Lipoprotein(a) Inhibition: Current Evidence, Therapeutic Landscape, and Future Directions.

Pierre Sabouret, Domenico Mario Giamundo, Joanna Popiolek-Kalisz, Luigi Spadafora, Marco Bernardi, Elad Asher, Mamas A Mamas, Dan Atar, Giuseppe Andò

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Reviews in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Pierre SabouretACTION Study Group, Inserm UMRS1166, Heart Institute, Pitié-Salpetriere Hospital, Sorbonne University, 75013 Paris, France.ORCID https://orcid.org/0000-0002-0243-3673
Domenico Mario GiamundoDivision of Cardiology, Policlinico Casilino, 00169 Rome, Italy.ORCID https://orcid.org/0009-0000-2161-3066
Joanna Popiolek-KaliszClinical Dietetics Unit, Department of Bioanalytics, Medical University of Lublin, 20-059 Lublin, Poland.ORCID https://orcid.org/0000-0001-9108-8391
Luigi SpadaforaDepartment of Clinical, Internal Medicine, Anesthesiology and Cardiovascular Sciences, Sapienza University of Rome, 00185 Rome, Italy.ORCID https://orcid.org/0000-0001-6443-4121
Marco BernardiDepartment of Clinical, Internal Medicine, Anesthesiology and Cardiovascular Sciences, Sapienza University of Rome, 00185 Rome, Italy.ORCID https://orcid.org/0000-0001-9269-8829
Elad AsherJesselson Heart Center, Shaare Zedek Medical Center, The Eisenberg R&D Authority, and Faculty of Medicine, Hebrew University of Jerusalem, 9103102 Jerusalem, Israel.ORCID https://orcid.org/0000-0003-3381-605X
Mamas A MamasKeele Cardiac Research Group, Centre for Prognosis Research, Keele University, ST5 5BG Stoke-on-Trent, UK.ORCID https://orcid.org/0000-0001-9241-8890
Dan AtarDepartment of Cardiology, Oslo University Hospital, 0450 Oslo, Norway.ORCID https://orcid.org/0000-0003-1513-8793
Giuseppe AndòDepartment of Clinical and Experimental Medicine, University of Messina and Azienda Ospedaliera Universitaria Policlinico "Gaetano Martino", 98125 Messina, Italy.ORCID https://orcid.org/0000-0001-5552-6382

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipoprotein(a) [Lp(a)] is a genetically determined, apolipoprotein B-containing lipoprotein that contributes to cardiovascular risk through atherogenic, proinflammatory, and potentially antifibrinolytic mechanisms. Genetic, epidemiological, and mechanistic evidence supports a causal role for elevated Lp(a) in atherosclerotic cardiovascular disease and calcific aortic valve disease. In contrast, associations with other cardiovascular phenotypes are less consistent. Since circulating concentrations are largely inherited and only modestly affected by lifestyle measures and conventional lipid-lowering therapies, Lp(a) represents an important component of residual cardiovascular risk. This review summarizes the structural, genetic, and pathogenic characteristics of Lp(a), examines the strength of evidence across coronary artery disease, ischemic stroke, peripheral artery disease, abdominal aortic aneurysm, calcific aortic valve disease, and heart failure, and discusses measurement, clinical interpretation, and potential biomarkers. The therapeutic landscape has expanded rapidly. Antisense oligonucleotides and small interfering RNA agents substantially suppress hepatic apolipoprotein(a) synthesis, oral small-molecule inhibitors prevent Lp(a) particle assembly, and

Indexed as

antisense oligonucleotidesaortic valve stenosisatherosclerosiscardiovascular diseaseslipoprotein(a)small interfering RNA

Identifiers

PMID42859724
PMCPMC13653194

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.