Evidence map›Paper›PMID 29878063›Full record

SynthesisCardiovascular research2018

Role of genetics in the prediction of statin-associated muscle symptoms and optimization of statin use and adherence.

Liam R Brunham, Steven Baker, Andrew Mammen, G B John Mancini, Robert S Rosenson

Abstract readSystematic Review
In one paragraph

Synthesis in Cardiovascular research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

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

  1. Pooled it
  2. Trial
  3. Review
  4. Genetic Biomarkers for Statin-Induced Myopathy.International journal of molecular sciences · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Adverse drug reactions of statin therapy in China from 1989 to 2019: a national database analysis.European journal of hospital pharmacy : science and practice · 2023
    Article
  14. Predictive Value ofGenes · 2023
    Article
  15. Pharmacotherapy of the Lipid-Lowering Drugs: Update on Efficacy and Risk.International journal of molecular sciences · 2023
    Article
  16. Article
  17. Statins Neuromuscular Adverse Effects.International journal of molecular sciences · 2022
    Review
  18. A Cost-Consequence Analysis of PreemptiveJournal of personalized medicine · 2021
    Article
  19. Statin-Associated Myopathy: Emphasis on Mechanisms and Targeted Therapy.International journal of molecular sciences · 2021
    Review
  20. Review
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

5 authors.

Liam R BrunhamDepartment of Medicine, Centre for Heart Lung Innovation, University of British Columbia, St. Paul's Hospital, Rm 166 - 1081 Burrard St., Vancouver, British Columbia V6Z 1Y6, Canada.
Steven BakerDepartment of Medicine, Neuromuscular Disease Clinic, McMaster University, Hamilton, Ontario, Canada.
Andrew MammenMuscle Disease Unit, National Institutes of Health, Bethesda, MD, USA.
G B John ManciniDepartment of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
Robert S RosensonMount Sinai Heart, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Funding

Clinical Support Services for the NIAMS Intramural Research ProgramZIDAR041180 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI COLBERT, ROBERT · 2009 to 2025
$119.2M
CIHR
6 · The paper itself

Abstract

Statin therapy reduces cardiovascular events in patients with, or at risk of, atherosclerotic cardiovascular disease. However, statins are underutilized in patients for whom they are indicated and are frequently discontinued. Discontinuation may be the result of statin-associated muscle symptoms (SAMS), which encompass a broad spectrum of clinical phenotypes from myalgia to severe myopathy. As with many adverse drug reactions (ADRs), inter-individual variability in susceptibility to SAMS is due, at least in part, to differences in host genetics. The genetic basis for SAMS has been investigated in candidate gene studies, genome-wide association studies, and, more recently, studies of multi-omic networks, including at the transcriptome level. In this article, we provide a systematic review of the pharmacogenetic basis of SAMS, focusing on how an understanding of the genetic and molecular determinants of SAMS can be considered in a personalized approach to reduce the incidence of this ADR, optimize statin adherence, and reduce the risk for cardiovascular events.

Indexed as

Medication AdherencePharmacogenomic VariantsClinical Decision-MakingGenetic Predisposition to DiseaseHumansHydroxymethylglutaryl-CoA Reductase InhibitorsMuscular DiseasesPatient SelectionPharmacogeneticsPhenotypePrecision MedicineRisk AssessmentRisk FactorsHydroxymethylglutaryl-CoA Reductase Inhibitors

Identifiers

PMID29878063
PMCPMC6014181

What OpenQuestion holds

Textmetadata
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.