Evidence map›Paper›PMID 27095708›Full record

ReviewJournal of thrombosis and thrombolysis2016

PCSK9 inhibitors in the prevention of cardiovascular disease.

James Latimer, Jonathan A Batty, R Dermot G Neely, Vijay Kunadian

Erratum issuedOpen access · hybridFull text readReview
In one paragraph

Review in Journal of thrombosis and thrombolysis, 2016. 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 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Residual inflammatory risk after contemporary lipid lowering therapy.European heart journal. Quality of care & clinical outcomes · 2020
    Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Implementing genome-driven personalized cardiology in clinical practice.Journal of molecular and cellular cardiology · 2018
    Review
  15. Observational
  16. Review
  17. PCSK9 as a therapeutic target for cardiovascular disease.Experimental and therapeutic medicine · 2017
    Article
  18. Genes for a 'Wellderly' Life.Trends in molecular medicine · 2016
    Article
  19. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

James LatimerInstitute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, M3.131, 3rd Floor William Leech Building, Newcastle upon Tyne, NE2 4HH, UK.
Jonathan A BattyInstitute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, M3.131, 3rd Floor William Leech Building, Newcastle upon Tyne, NE2 4HH, UK.
R Dermot G NeelyInstitute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, M3.131, 3rd Floor William Leech Building, Newcastle upon Tyne, NE2 4HH, UK.
Vijay KunadianInstitute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, M3.131, 3rd Floor William Leech Building, Newcastle upon Tyne, NE2 4HH, UK. vijay.kunadian@newcastle.ac.uk.
Newcastle University · GBNewcastle upon Tyne Hospitals NHS Foundation Trust · GBRoyal Victoria Infirmary · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reducing plasma levels of low-density lipoprotein cholesterol (LDL-C) remains the cornerstone in the primary and secondary prevention of cardiovascular disease. However, lack of efficacy and adverse effects mean that a substantial proportion of patients fail to achieve acceptable LDL-C levels with currently available lipid-lowering drugs. Over the last decade, inhibition of proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a promising therapeutic strategy to reduce residual cardiovascular disease risk. Binding of PCSK9 to the LDL receptor targets the receptor for lysosomal degradation. The recognition that inhibition of PCSK9 increases LDL receptor activity has led to the development of a number of approaches to directly target PCSK9. Numerous monoclonal antibodies against PCSK9 are currently being evaluated in phase 3 trials, involving various patient categories on different background lipid-lowering therapies. Current evidence shows reductions in LDL-C levels of up to 70 % may be achieved with PCSK9 inhibition, independent of background statin therapy. This review examines the most recent evidence and future prospects for the use of PCSK9 inhibitors in the prevention of cardiovascular disease.

Indexed as

PCSK9 InhibitorsAnticholesteremic AgentsCardiovascular DiseasesCholesterol, LDLHumansProprotein Convertase 9Receptors, LDLAnticholesteremic AgentsCholesterol, LDLLDLR protein, humanPCSK9 InhibitorsPCSK9 protein, humanProprotein Convertase 9Receptors, LDLAlirocumabEvolocumabLow-density lipoproteinMonoclonal antibodyPreventionProprotein convertase subtilisin kexin type 9 (PCSK9)

Identifiers

PMID27095708
PMCPMC5010583
OpenAlexW2337465008

What OpenQuestion holds

Textfull text, public
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.