Evidence map›Paper›PMID 20642543›Full record

ReviewBritish journal of clinical pharmacology2010

Drug- and non-drug-associated QT interval prolongation.

Charlotte van Noord, Mark Eijgelsheim, Bruno H Ch Stricker

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of clinical pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 2 pooled it
7.4field-weighted citation impact, top 2% 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

100 citing papers in PubMed, 2 syntheses or guidelines pooled it, 263 citations in OpenAlex.

  1. Guideline
  2. Risk factors for QTc-prolongation: systematic review of the evidence.International journal of clinical pharmacy · 2017
    Pooled it
  3. Trial
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  12. Article
  13. Article
  14. Activation of Small Conductance CaInternational journal of molecular sciences · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Surveillance of Corrected QT Interval-Prolonging Medications upon Admission throughout Hospitalization in a Tertiary Care Geriatric Ward.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2025
    Article
  19. Curiositas - Teenage Kicks.The Ulster medical journal · 2024
    Article
  20. Review

40 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Charlotte van NoordDepartment of Epidemiology, Erasmus Medical Center, Rotterdam, The Netherlands.
Mark Eijgelsheim
Bruno H Ch Stricker
Erasmus MC · NLMedicines Evaluation Board · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sudden cardiac death is among the most common causes of cardiovascular death in developed countries. The majority of sudden cardiac deaths are caused by acute ventricular arrhythmia following repolarization disturbances. An important risk factor for repolarization disturbances is use of QT prolonging drugs, probably partly explained by gene-drug interactions. In this review, we will summarize QT interval physiology, known risk factors for QT prolongation, including drugs and the contribution of pharmacogenetics. The long QT syndrome can be congenital or acquired. The congenital long QT syndrome is caused by mutations in ion channel subunits or regulatory protein coding genes and is a rare monogenic disorder with a mendelian pattern of inheritance. Apart from that, several common genetic variants that are associated with QT interval duration have been identified. Acquired QT prolongation is more prevalent than the congenital form. Several risk factors have been identified with use of QT prolonging drugs as the most frequent cause. Most drugs that prolong the QT interval act by blocking hERG-encoded potassium channels, although some drugs mainly modify sodium channels. Both pharmacodynamic as well as pharmacokinetic mechanisms may be responsible for QT prolongation. Pharmacokinetic interactions often involve drugs that are metabolized by cytochrome P450 enzymes. Pharmacodynamic gene-drug interactions are due to genetic variants that potentiate the QT prolonging effect of drugs. QT prolongation, often due to use of QT prolonging drugs, is a major public health issue. Recently, common genetic variants associated with QT prolongation have been identified. Few pharmacogenetic studies have been performed to establish the genetic background of acquired QT prolongation but additional studies in this newly developing field are warranted.

Indexed as

Drug InteractionsDeath, Sudden, CardiacHumansLong QT SyndromePotassium Channels, Voltage-GatedRisk FactorsPotassium Channels, Voltage-Gated

Identifiers

PMID20642543
PMCPMC2909803
OpenAlexW2136682738

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.