Evidence map›Paper›PMID 36113961›Full record

ArticleRMD open2022

Serum cholesterol loading capacity on macrophages is linked to coronary atherosclerosis and cardiovascular event risk in rheumatoid arthritis.

George Athanasios Karpouzas, Bianca Papotti, Sarah Ormseth, Marcella Palumbo, Elizabeth Hernandez, Maria Pia Adorni, Francesca Zimetti, Matthew Budoff, Nicoletta Ronda

Open access · goldAbstract read
In one paragraph

Article in RMD open, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Observational
  2. Observational
  3. Myocardial infarction in rheumatic diseases.Rheumatology international · 2025
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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

9 authors at 2 institutions in 2 countries.

George Athanasios KarpouzasInternal Medicine-Rheumatology, Lundquist Institute, Torrance, California, USA gkarpouzas@lundquist.org.ORCID 0000-0003-1065-1563
Bianca PapottiDepartment of Food and Drug, University of Parma, Parma, Italy.
Sarah OrmsethInternal Medicine-Rheumatology, Lundquist Institute, Torrance, California, USA.
Marcella PalumboDepartment of Food and Drug, University of Parma, Parma, Italy.
Elizabeth HernandezInternal Medicine, Lundquist Institute, Torrance, California, USA.
Maria Pia AdorniUniversity of Parma, Parma, Emilia-Romagna, Italy.
Francesca ZimettiDepartment of Pharmacy, University of Parma, Parma, Emilia-Romagna, Italy.
Matthew BudoffInternal Medicine, Lundquist Institute, Torrance, California, USA.
Nicoletta RondaDepartment of Pharmacy, University of Parma, Parma, Emilia-Romagna, Italy.
University of Parma · ITUCLA Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesCholesterol loading capacity (CLC) describes the ability of serum to deliver cholesterol to cells. It is linked to foam cell formation, a pivotal step in atherosclerotic plaque development. We evaluate the associations of CLC with coronary atherosclerosis presence, burden and cardiovascular risk in patients with rheumatoid arthritis (RA).

methodsCoronary atherosclerosis (any, high-risk low-attenuation plaque and obstructive plaque) was evaluated with CT angiography in 141 patients. Participants were prospectively followed for 6.0±2.4 years and cardiovascular events including cardiac death, myocardial infarction, unstable angina, stroke, claudication, revascularisation and hospitalised heart failure were recorded. CLC was quantified as intracellular cholesterol in human macrophages after incubation with patient serum.

resultsCLC was not linked to overall plaque presence or burden after adjustments for atherosclerotic cardiovascular disease (ASCVD) score, statin use and low-density lipoprotein cholesterol. However, CLC associated with presence and numbers of any, low-attenuation and obstructive plaques exclusively in biologic disease-modifying antirheumatic drugs (bDMARD) non-users (p for interaction ≤0.018). CLC associated with cardiovascular event risk overall after adjustments for ASCVD and number of segments with plaque (HR=1.76 (95% CI 1.16 to 2.67) per 1 SD increase in CLC, p=0.008). Additionally, bDMARD use modified the impact of CLC on event risk; CLC associated with events in bDMARD non-users (HR=2.52 (95% CI 1.36 to 4.65) per 1SD increase in CLC, p=0.003) but not users.

conclusionCLC was linked to long-term cardiovascular event risk in RA and associated with high-risk low attenuation and obstructive coronary plaque presence and burden in bDMARD non-users. Its prospective validation as a predictive biomarker may be, therefore, warranted.

Indexed as

Arthritis, RheumatoidCholesterolCoronary Artery DiseaseMacrophagesPlaque, AtheroscleroticAntirheumatic AgentsBiological ProductsBiomarkersHumansHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteins, LDLAntirheumatic AgentsBiological ProductsBiomarkersCholesterolHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteins, LDLarthritis, rheumatoidatherosclerosislipids

Identifiers

PMID36113961
PMCPMC9486392
OpenAlexW4296073436

What OpenQuestion holds

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LicenceCC BY-NC
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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.