Evidence map›Paper›PMID 35057907›Full record

ArticleJournal of the American College of Cardiology2022

Association of Lipoprotein(a) With Atherosclerotic Plaque Progression.

Yannick Kaiser, Marwa Daghem, Evangelos Tzolos, Mohammed N Meah, Mhairi K Doris, Alistair J Moss, Jacek Kwiecinski, Jeffrey Kroon, Nick S Nurmohamed, Pim van der Harst and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of the American College of Cardiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 3 pooled it
35.7field-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

92 citing papers in PubMed, 3 syntheses or guidelines pooled it, 183 citations in OpenAlex.

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32 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 10 institutions in 5 countries.

Yannick KaiserDepartment of Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Marwa DaghemBritish Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, United Kingdom.
Evangelos TzolosBritish Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, United Kingdom.
Mohammed N MeahBritish Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, United Kingdom.
Mhairi K DorisBritish Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, United Kingdom.
Alistair J MossDepartment of Cardiovascular Science, National Institute of Health Research Biomedical Research Centre Leicester, University of Leicester, Leicester, United Kingdom.
Jacek KwiecinskiDepartment of Interventional Cardiology and Angiology, Institute of Cardiology, Warsaw, Poland.
Jeffrey KroonDepartment of Experimental Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Nick S NurmohamedDepartment of Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands; Department of Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit, Amsterdam, the Netherlands.
Pim van der HarstDepartment of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands.
Philip D AdamsonBritish Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, United Kingdom; Christchurch Heart Institute, University of Otago, Christchurch, New Zealand.
Michelle C WilliamsBritish Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, United Kingdom.
Damini DeyBiomedical Imaging Research Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA.
David E NewbyBritish Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, United Kingdom.
Erik S G StroesDepartment of Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Kang H ZhengDepartment of Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands. Electronic address: https://twitter.com/Zheng_KH.
Marc R DweckBritish Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, United Kingdom. Electronic address: marc.dweck@ed.ac.uk.
University of Edinburgh · GBAmsterdam University Medical Centers · NLBritish Heart Foundation · GBUniversity of Amsterdam · NLCedars-Sinai Medical Center · USInstitute of Cardiology · PLNew Zealand Brain Research Institute · NZUniversity Medical Center Utrecht · NLUniversity of Leicester · GBVrije Universiteit Amsterdam · NL

Funding

Integrated prediction of cardiovascular events by automated coronary plaque and pericoronary adipose tissue quantification from CT AngiographyR01HL148787 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI DEY, DAMINI · 2020 to 2023
$3.0M
Effect of Intensive Medical Treatment on Quantified Coronary Artery Plaque Components with Serial Coronary CTA in Women with Non-Obstructive CADR01HL151266 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI DEY, DAMINI, TAMARAPPOO, BALAJI K. · 2020 to 2023
$1.6M
British Heart Foundation CH/09/002/26360British Heart Foundation FS/14/78/31020British Heart Foundation FS/17/79/33226British Heart Foundation FS/19/46/34445British Heart Foundation FS/CRTF/20/24086British Heart Foundation FS/ICRF/20/26002NHLBI NIH HHS R01 HL148787
6 · The paper itself

Abstract

backgroundLipoprotein(a) [Lp(a)] is associated with increased risk of myocardial infarction, although the mechanism for this observation remains uncertain.

objectivesThis study aims to investigate whether Lp(a) is associated with adverse plaque progression.

methodsLp(a) was measured in patients with advanced stable coronary artery disease undergoing coronary computed tomography angiography at baseline and 12 months to assess progression of total, calcific, noncalcific, and low-attenuation plaque (necrotic core) in particular. High Lp(a) was defined as Lp(a) ≥ 70 mg/dL. The relationship of Lp(a) with plaque progression was assessed using linear regression analysis, adjusting for body mass index, segment involvement score, and ASSIGN score (a Scottish cardiovascular risk score comprised of age, sex, smoking, blood pressure, total and high-density lipoprotein [HDL]-cholesterol, diabetes, rheumatoid arthritis, and deprivation index).

resultsA total of 191 patients (65.9 ± 8.3 years of age; 152 [80%] male) were included in the analysis, with median Lp(a) values of 100 (range: 82 to 115) mg/dL and 10 (range: 5 to 24) mg/dL in the high and low Lp(a) groups, respectively. At baseline, there was no difference in coronary artery disease severity or plaque burden. Patients with high Lp(a) showed accelerated progression of low-attenuation plaque compared with low Lp(a) patients (26.2 ± 88.4 mm

conclusionsAmong patients with advanced stable coronary artery disease, Lp(a) is associated with accelerated progression of coronary low-attenuation plaque (necrotic core). This may explain the association between Lp(a) and the high residual risk of myocardial infarction, providing support for Lp(a) as a treatment target in atherosclerosis.

Indexed as

Disease ProgressionAgedBiomarkersComputed Tomography AngiographyCoronary AngiographyCoronary Artery DiseaseFemaleHumansLipoprotein(a)MalePlaque, AtheroscleroticBiomarkersLipoprotein(a)coronary computed tomography angiographylipoprotein(a)low-attenuation plaque

Identifiers

PMID35057907
PMCPMC8784819
OpenAlexW4206473131

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Registered trials

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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.