Evidence map›Paper›PMID 32090368›Full record

SynthesisBritish journal of clinical pharmacology2020

CYP2D6 polymorphism and its impact on the clinical response to metoprolol: A systematic review and meta-analysis.

Maxime Meloche, Michael Khazaka, Imad Kassem, Amina Barhdadi, Marie-Pierre Dubé, Simon de Denus

Open access · bronzeAbstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in British journal of clinical pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 3 pooled it
5.5field-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

32 citing papers in PubMed, 3 syntheses or guidelines pooled it, 56 citations in OpenAlex.

  1. Guideline
  2. Pooled it
  3. Pooled it
  4. Association of prior beta-blocker treatment and outcome in patients with out-of-hospital cardiac arrest.Clinical research in cardiology : official journal of the German Cardiac Society · 2026
    Observational
  5. Review
  6. CYP2D6 Metabolizer Status and Mortality in Metoprolol Users.Clinical and translational science · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Comparison between the ECG Outcomes of Metoprolol and Bisoprolol.Cardiovascular & hematological agents in medicinal chemistry · 2024
    Article
  18. Observational
  19. Article
  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

6 authors at 3 institutions in 1 country.

Maxime MelocheFaculty of Pharmacy, Université de Montréal, Montreal, Quebec, Canada.ORCID 0000-0002-5857-5515
Michael KhazakaFaculty of Pharmacy, Université de Montréal, Montreal, Quebec, Canada.
Imad KassemFaculty of Pharmacy, Université de Montréal, Montreal, Quebec, Canada.
Amina BarhdadiFaculty of Pharmacy, Université de Montréal, Montreal, Quebec, Canada.
Marie-Pierre DubéUniversité de Montréal Beaulieu-Saucier Pharmacogenomics Centre, Montreal, Quebec, Canada.
Simon de DenusFaculty of Pharmacy, Université de Montréal, Montreal, Quebec, Canada.
Montreal Heart Institute · CAUniversité de Montréal · CACentre Hospitalier de l’Université de Montréal · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsCYP2D6 genetic polymorphisms are associated with metoprolol pharmacokinetics. Whether the clinical response to metoprolol is also affected remains uncertain.

methodsWe conducted a systematic review on the effects of CYP2D6 polymorphism on the clinical response to metoprolol. Searches were conducted using MEDLINE. Meta-analyses were performed on the impact of CYP2D6-inferred phenotypes on heart rate (HR) reduction, diastolic (DBP) and systolic (SBP) blood pressure reduction, average daily doses, all-type adverse events and bradycardia.

resultsOur qualitative assessment indicated inconsistent results in individual studies and endpoints, but CYP2D6 poor metabolizers (PM) generally presented a greater reduction in HR. The meta-analysis of 15 studies, including a total of 1146 individuals, found a reduction in HR of 3 beats/min (P = .017), and of SBP and DBP by 3 mmHg (P = .0048) for PM compared to non-PM individuals using similar metoprolol doses. Bradycardia appeared more frequent by 4-fold for PM, although significant heterogeneity was observed regarding bradycardia, which limits the scope of this finding.

conclusionPatients without any CYP2D6 metabolic capacities appear to have increased reduction in DBP, HR and SBP during metoprolol treatment and may be at a higher risk of bradycardia compared to patients with active CYP2D6 phenotypes. Further prospective data are required to determine whether CYP2D6 is associated with clinical events in patients treated with metoprolol, as well as to demonstrate the clinical utility of an individualized approach of prescribing metoprolol using CYP2D6-inferred phenotypes.

Indexed as

Cytochrome P-450 CYP2D6MetoprololGenotypeHumansPhenotypePolymorphism, GeneticCytochrome P-450 CYP2D6Metoprololcytochrome P450 enzymesgenetic polymorphismmeta-analysispharmacogenomicssystematic review

Identifiers

PMID32090368
PMCPMC7256128
OpenAlexW3007489417

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.