Evidence map›Paper›PMID 33239979›Full record

ArticleEuropean heart journal supplements : journal of the European Society of Cardiology2020

Lipoprotein(a) and PCSK9 inhibition: clinical evidence.

Massimiliano Ruscica, Maria Francesca Greco, Nicola Ferri, Alberto Corsini

Open access · hybridAbstract read
In one paragraph

Article in European heart journal supplements : journal of the European Society of Cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
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  5. Observational
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  16. Lipoprotein(a): Insights for the Practicing Clinician.Journal of clinical medicine · 2022
    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

4 authors at 2 institutions in 1 country.

Massimiliano RuscicaDipartimento di Science Farmacologiche e Biomolecolari, Università degli Studi di Milano, Milan, Italy.
Maria Francesca GrecoDipartimento di Science Farmacologiche e Biomolecolari, Università degli Studi di Milano, Milan, Italy.
Nicola FerriDipartimento di Scienze del Farmaco, Università degli Studi di Padova, Padua, Italy.
Alberto CorsiniDipartimento di Science Farmacologiche e Biomolecolari, Università degli Studi di Milano, Milan, Italy.
University of Milan · ITUniversity of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Compelling evidence has emerged from epidemiological and Mendelian randomization analyses relative to the causality of lipoprotein(a) [Lp(a)] in atherosclerotic cardiovascular diseases (ASCVD), being elevated Lp(a) a strong risk factor regardless of the reduction of LDL-C achieved by statins. So far, no specific available agent can lower Lp(a) to the extent required to achieve a cardiovascular (CV) benefit, i.e. approximately 100 mg/dL. The most recent outcomes trial FOURIER with evolocumab showed that a 25 nmol/L (12 mg/dL) reduction in Lp(a) corresponded to a 15% decrement in the relative risk of cardiovascular disease. The ODYSSEY OUTCOMES trial with alirocumab has been the first demonstrating that a reduction in Lp(a) associates with less major adverse cardiovascular events (MACE), i.e. hazard ratio: 0.994 per 1 mg/dL decrement in Lp(a). The Lp(a) lowering effect driven by PCSK9 inhibition was confirmed in carriers of

Indexed as

FOURIERLipoprotein(a)ODYSSEY OUTCOMESPCSK9

Identifiers

PMID33239979
PMCPMC7673619
OpenAlexW3106160899

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.