Evidence map›Paper›PMID 37078819›Full record

SynthesisCardiovascular research2023

Lipoprotein(a) and calcific aortic valve disease initiation and progression: a systematic review and meta-analysis.

Panteleimon Pantelidis, Evangelos Oikonomou, Stamatios Lampsas, Georgios E Zakynthinos, Antonios Lysandrou, Konstantinos Kalogeras, Efstratios Katsianos, Panagiotis Theofilis, Gerasimos Siasos, Michael Andrew Vavuranakis and 3 more

Open access · hybridAbstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 3 pooled it
13.7field-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.

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

35 citing papers in PubMed, 3 syntheses or guidelines pooled it, 43 citations in OpenAlex.

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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

13 authors at 3 institutions in 2 countries.

Panteleimon Pantelidis3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 152 Mesogeion St, Athens 11527, Greece.ORCID 0000-0001-5394-832X
Evangelos Oikonomou3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 152 Mesogeion St, Athens 11527, Greece.ORCID 0000-0001-8079-0599
Stamatios Lampsas3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 152 Mesogeion St, Athens 11527, Greece.ORCID 0000-0001-6481-0000
Georgios E Zakynthinos3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 152 Mesogeion St, Athens 11527, Greece.
Antonios Lysandrou3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 152 Mesogeion St, Athens 11527, Greece.
Konstantinos Kalogeras3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 152 Mesogeion St, Athens 11527, Greece.
Efstratios Katsianos3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 152 Mesogeion St, Athens 11527, Greece.ORCID 0000-0002-0754-1964
Panagiotis Theofilis3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 152 Mesogeion St, Athens 11527, Greece.ORCID 0000-0001-9260-6306
Gerasimos Siasos3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 152 Mesogeion St, Athens 11527, Greece.
Michael Andrew Vavuranakis3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 152 Mesogeion St, Athens 11527, Greece.
Alexios S AntonopoulosClinical, Experimental Surgery & Translational Research Center, Biomedical Research Foundation of the Academy of Athens, 4 Soranou Ephessiou St, Athens 11527, Greece.
Dimitris Tousoulis1st Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Ippokrateio Hospital, 114 Vasilissis Sofias St, Athina 11527, Greece.ORCID 0000-0001-7492-4984
Manolis Vavouranakis3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 152 Mesogeion St, Athens 11527, Greece.
National and Kapodistrian University of Athens · GRAcademy of Athens · GRBrigham and Women's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although evidence indicates the association of lipoprotein(a) [Lp(a)] with atherosclerosis, the link with calcific aortic valve disease (CAVD) is unclear. This systematic review and meta-analysis explores the connection between Lp(a) and aortic valve calcification and stenosis (AVS). We included all relevant studies, indexed in eight databases, up to February 2023. A total of 44 studies (163 139 subjects) were included, with 16 of them being further meta-analysed. Despite considerable heterogeneity, most studies support the relationship between Lp(a) and CAVD, especially in younger populations, with evidence of early aortic valve micro-calcification in elevated-Lp(a) populations. The quantitative synthesis showed higher Lp(a) levels, by 22.63 nmol/L (95% CI: 9.98-35.27), for patients with AVS, while meta-regressing the data revealed smaller Lp(a) differences for older populations with a higher proportion of females. The meta-analysis of eight studies providing genetic data, revealed that the minor alleles of both rs10455872 and rs3798220 LPA gene loci were associated with higher risk for AVS (pooled odds ratio 1.42; 95% CI: 1.34-1.50 and 1.27; 95% CI: 1.09-1.48, respectively). Importantly, high-Lp(a) individuals displayed not only faster AVS progression, by a mean difference of 0.09 m/s/year (95% CI: 0.09-0.09), but also a higher risk of serious adverse outcomes, including death (pooled hazard ratio 1.39; 95% CI: 1.01-1.90). These summary findings highlight the effect of Lp(a) on CAVD initiation, progression and outcomes, and support the early onset of Lp(a)-related subclinical lesions before clinical evidence.

Indexed as

Aortic Valve StenosisHyperlipidemiasAortic ValveCalcinosisFemaleHumansLipoprotein(a)Risk FactorsLipoprotein(a)LPA protein, humanAortic valve stenosisCalcific aortic valve diseaseLipoprotein(a)Lp(a)Meta-analysis

Identifiers

PMID37078819
PMCPMC10702855
OpenAlexW4366463192

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.