Evidence map›Paper›PMID 26108299›Full record

ReviewDrug safety2015

Pharmacogenetics of Drug-Induced QT Interval Prolongation: An Update.

Maartje N Niemeijer, Marten E van den Berg, Mark Eijgelsheim, Peter R Rijnbeek, Bruno H Stricker

Open access · hybridAbstract readReview
In one paragraph

Review in Drug safety, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
5.3field-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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. An Unusual Genetic Variant of Long QT Syndrome with Late Presentation in the Sixth Decade.The Journal of innovations in cardiac rhythm management · 2026
    Article
  5. Review
  6. Article
  7. Observational
  8. Review
  9. Observational
  10. Article
  11. Review
  12. Genetic QT score as a predictor of sudden cardiac death in participants with sleep-disordered breathing in the UK Biobank.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2025
    Article
  13. Article
  14. Observational
  15. Article
  16. Review
  17. Article
  18. Review
  19. 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 at 1 institution in 1 country.

Maartje N NiemeijerDepartment of Epidemiology, Erasmus MC-University Medical Center Rotterdam, PO Box 2040, 3000 CA, Rotterdam, The Netherlands.
Marten E van den BergDepartment of Medical Informatics, Erasmus MC-University Medical Center Rotterdam, Rotterdam, The Netherlands.
Mark EijgelsheimDepartment of Epidemiology, Erasmus MC-University Medical Center Rotterdam, PO Box 2040, 3000 CA, Rotterdam, The Netherlands.
Peter R RijnbeekDepartment of Medical Informatics, Erasmus MC-University Medical Center Rotterdam, Rotterdam, The Netherlands.
Bruno H StrickerDepartment of Epidemiology, Erasmus MC-University Medical Center Rotterdam, PO Box 2040, 3000 CA, Rotterdam, The Netherlands. b.stricker@erasmusmc.nl.
Erasmus MC · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A prolonged QT interval is an important risk factor for ventricular arrhythmias and sudden cardiac death. QT prolongation can be caused by drugs. There are multiple risk factors for drug-induced QT prolongation, including genetic variation. QT prolongation is one of the most common reasons for withdrawal of drugs from the market, despite the fact that these drugs may be beneficial for certain patients and not harmful in every patient. Identifying genetic variants associated with drug-induced QT prolongation might add to tailored pharmacotherapy and prevent beneficial drugs from being withdrawn unnecessarily. In this review, our objective was to provide an overview of the genetic background of drug-induced QT prolongation, distinguishing pharmacokinetic and pharmacodynamic pathways. Pharmacokinetic-mediated genetic susceptibility is mainly characterized by variation in genes encoding drug-metabolizing cytochrome P450 enzymes or drug transporters. For instance, the P-glycoprotein drug transporter plays a role in the pharmacokinetic susceptibility of drug-induced QT prolongation. The pharmacodynamic component of genetic susceptibility is mainly characterized by genes known to be associated with QT interval duration in the general population and genes in which the causal mutations of congenital long QT syndromes are located. Ethnicity influences susceptibility to drug-induced QT interval prolongation, with Caucasians being more sensitive than other ethnicities. Research on the association between pharmacogenetic interactions and clinical endpoints such as sudden cardiac death is still limited. Future studies in this area could enable us to determine the risk of arrhythmias more adequately in clinical practice.

Indexed as

AnimalsBrugada SyndromeCardiac Conduction System DiseaseDrug-Related Side Effects and Adverse ReactionsGenetic VariationHumansLong QT SyndromePharmacogenetics

Identifiers

PMID26108299
PMCPMC4579250
OpenAlexW1160401237

What OpenQuestion holds

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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 OpenQuestion graph.