Evidence map›Paper›PMID 34327467›Full record

ArticleAmerican journal of preventive cardiology2020

C-reactive protein levels and plaque regression with evolocumab: Insights from GLAGOV.

Adam J Nelson, Rishi Puri, Danielle M Brennan, Todd J Anderson, Leslie Cho, Christie M Ballantyne, John Jp Kastelein, Wolfgang Koenig, Helina Kassahun, Ransi M Somaratne and 3 more

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Article in American journal of preventive cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Adam J NelsonSouth Australian Health & Medical Research Institute, Adelaide, Australia.
Rishi PuriDepartment of Cardiovascular Medicine, Cleveland Clinic Coordinating Center for Clinical Research (C5Research), Cleveland Clinic, Cleveland, OH, USA.
Danielle M BrennanDepartment of Cardiovascular Medicine, Cleveland Clinic Coordinating Center for Clinical Research (C5Research), Cleveland Clinic, Cleveland, OH, USA.
Todd J AndersonLibin Cardiovascular Institute, Cumming School of Medicine, University of Calgary, Canada.
Leslie ChoDepartment of Cardiovascular Medicine, Cleveland Clinic Coordinating Center for Clinical Research (C5Research), Cleveland Clinic, Cleveland, OH, USA.
Christie M BallantyneSection of Cardiovascular Research, Baylor College of Medicine and the Methodist DeBakey Heart and Vascular Center, Houston, TX, USA.
John Jp KasteleinDepartment of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Wolfgang KoenigDeutsches Herzzentrum München, Technische Universität München, Munich, DZHK (German Centre for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany.
Helina KassahunAmgen Inc., Thousand Oaks, CA, USA.
Ransi M SomaratneAmgen Inc., Thousand Oaks, CA, USA.
Scott M WassermanAmgen Inc., Thousand Oaks, CA, USA.
Steven E NissenDepartment of Cardiovascular Medicine, Cleveland Clinic Coordinating Center for Clinical Research (C5Research), Cleveland Clinic, Cleveland, OH, USA.
Stephen J NichollsMonash Cardiovascular Research Centre, Victorian Heart Institute, Monash University, Melbourne, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveOn-treatment levels of high sensitivity C-reactive protein (hsCRP) in statin-treated patients predict plaque progression and the prospective risk of atherosclerotic cardiovascular events. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors produce additional LDL-C lowering, reduce plaque burden and improve cardiovascular outcomes in statin-treated patients. It is unknown whether residual systemic inflammation attenuates their favorable effects on plaque burden.

methodsGLAGOV compared the effects of treatment for 78 weeks with evolocumab or placebo on progression of coronary atherosclerosis in statin-treated patients with coronary artery disease.Clinical demographics, biochemistry and changes in both the burden (percentage atheroma volume (PAV), total atheroma volume (TAV), n ​= ​413) and composition (n ​= ​162) of coronary plaque were evaluated in evolocumab-treated patients according to baseline hsCRP strata (<1, 1-3, >3 ​mg/L).

resultsThe study cohort comprised 413 evolocumab-treated patients (32% low [<1 ​mg/L], 41% intermediate [1-3 ​mg/L] and 27% high [>3 ​mg/L] baseline hsCRP levels). Patients in the highest hsCRP stratum were more likely to be female and had a higher prevalence of diabetes, hypertension, and the metabolic syndrome. LDL-C levels were similar across the groups, however participants with higher hsCRP levels had higher triglyceride and lower HDL-C levels at baseline. At follow-up, the change in PAV from baseline (-0.87% [low] vs. -0.84% [intermediate] vs. -1.22% [high], p ​= ​0.46) and the proportion of patients experiencing any degree of regression (65.9% vs. 63.5% vs. 63.1%, p ​= ​0.88) was similar across hsCRP strata and when evaluated by levels of achieved LDL-C. There were no serial differences in plaque composition by hsCRP strata.

conclusionThe ability of evolocumab to induce regression in statin-treated patients is not attenuated by the presence of enhanced systemic inflammation. This underscores the potential benefits of intensive lipid lowering, even in the presence of heightened inflammatory states.

Indexed as

AtherosclerosisC-reactive proteinIntravascular imagingIVUSPCSK9 inhibitor

Identifiers

PMID34327467
PMCPMC8315612

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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.