Evidence mapPaperPMID 38892807Full record

ReviewJournal of clinical medicine2024

Role of Lipid-Lowering and Anti-Inflammatory Therapies on Plaque Stabilization.

Krzysztof L Bryniarski, Wijnand den Dekker, Jacek Legutko, Pawel Gasior, Jeroen Tahon, Roberto Diletti, Jeroen M Wilschut, Rutger-Jan Nuis, Joost Daemen, Pawel Kleczynski and 2 more

Abstract readReview
In one paragraph

Review in Journal of clinical medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
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

7 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Ten Years After.Maedica · 2024
    Article
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

12 authors.

Krzysztof L BryniarskiDepartment of interventional Cardiology, Thoraxcenter, Cardiovascular Institute, Erasmus University Medical Center, 3000 CA Rotterdam, The Netherlands.
Wijnand den DekkerDepartment of interventional Cardiology, Thoraxcenter, Cardiovascular Institute, Erasmus University Medical Center, 3000 CA Rotterdam, The Netherlands.
Jacek LegutkoDepartment of Interventional Cardiology, Jagiellonian University Medical College, Institute of Cardiology, St. John Paul II Hospital, 31-202 Krakow, Poland.
Pawel GasiorDivision of Cardiology and Structural Heart Diseases, Medical University of Silesia in Katowice, 40-055 Katowice, Poland.ORCID 0000-0001-8564-7257
Jeroen TahonDepartment of interventional Cardiology, Thoraxcenter, Cardiovascular Institute, Erasmus University Medical Center, 3000 CA Rotterdam, The Netherlands.
Roberto DilettiDepartment of interventional Cardiology, Thoraxcenter, Cardiovascular Institute, Erasmus University Medical Center, 3000 CA Rotterdam, The Netherlands.
Jeroen M WilschutDepartment of interventional Cardiology, Thoraxcenter, Cardiovascular Institute, Erasmus University Medical Center, 3000 CA Rotterdam, The Netherlands.
Rutger-Jan NuisDepartment of interventional Cardiology, Thoraxcenter, Cardiovascular Institute, Erasmus University Medical Center, 3000 CA Rotterdam, The Netherlands.
Joost DaemenDepartment of interventional Cardiology, Thoraxcenter, Cardiovascular Institute, Erasmus University Medical Center, 3000 CA Rotterdam, The Netherlands.
Pawel KleczynskiDepartment of Interventional Cardiology, Jagiellonian University Medical College, Institute of Cardiology, St. John Paul II Hospital, 31-202 Krakow, Poland.ORCID 0000-0002-8591-8739
Nicolas M Van MieghemDepartment of interventional Cardiology, Thoraxcenter, Cardiovascular Institute, Erasmus University Medical Center, 3000 CA Rotterdam, The Netherlands.
Ik-Kyung JangCardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02115, USA.ORCID 0000-0002-5796-3006

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is the predominant underlying etiopathology of coronary artery disease. Changes in plaque phenotype from stable to high risk may spur future major adverse cardiac events (MACE). Different pharmacological therapies have been implemented to mitigate this risk. Over the last two decades, intravascular imaging modalities have emerged in clinical studies to clarify how these therapies may affect the composition and burden of coronary plaques. Lipid-lowering agents, such as statins, ezetimibe, and proprotein convertase subtilisin/kexin type 9 inhibitors, were shown not only to reduce low-density lipoprotein levels and MACE but also to directly affect features of coronary plaque vulnerability. Studies have demonstrated that lipid-lowering therapy reduces the percentage of atheroma volume and number of macrophages and increases fibrous cap thickness. Future studies should answer the question of whether pharmacological plaque stabilization may be sufficient to mitigate the risk of MACE for selected groups of patients with atherosclerotic coronary disease.

Indexed as

coronary artery diseaselipid-lowering therapyplaque vulnerability

Identifiers

PMID38892807
PMCPMC11172633

What Socratic holds

Textmetadata
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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 Socratic graph.