Evidence map›Paper›PMID 20126530›Full record

ArticlePLoS computational biology2010

Acute effects of sex steroid hormones on susceptibility to cardiac arrhythmias: a simulation study.

Pei-Chi Yang, Junko Kurokawa, Tetsushi Furukawa, Colleen E Clancy

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

43 citing papers in PubMed, 74 citations in OpenAlex.

  1. Gender-specific cardiac features in Andersen-Tawil syndrome: a comprehensive meta-analysis of case reports and series.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2026
    Article
  2. Sex-specific virtual population for the prediction and assessment of arrhythmia risk.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026
    Article
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  7. Guidelines for mechanistic modeling and analysis in cardiovascular research.American journal of physiology. Heart and circulatory physiology · 2024
    Review
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  9. Article
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  12. When it comes to the heart, age, and sex matter (sometimes).American journal of physiology. Heart and circulatory physiology · 2023
    Article
  13. Review
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  19. Gender Differences in Arrhythmias: Focused on Atrial Fibrillation.Journal of cardiovascular translational research · 2020
    Review
  20. A Bitter Taste in Your Heart.Frontiers in physiology · 2020
    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

4 authors at 2 institutions in 2 countries.

Pei-Chi YangDepartment of Pharmacology, University of California, Davis, Davis, California, United States of America.
Junko Kurokawa
Tetsushi Furukawa
Colleen E Clancy
Tokyo Medical and Dental University · JPUniversity of California, Davis · US

Funding

Pharmacogenomics and antiarrhythmic therapy: An in silico investigationR01HL085592 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CLANCY, COLLEEN E · 2007 to 2011
$1.8M
NHLBI NIH HHS R01 HL085592NHLBI NIH HHS R01-HL-085592
6 · The paper itself

Abstract

Acute effects of sex steroid hormones likely contribute to the observation that post-pubescent males have shorter QT intervals than females. However, the specific role for hormones in modulating cardiac electrophysiological parameters and arrhythmia vulnerability is unclear. Here we use a computational modeling approach to incorporate experimentally measured effects of physiological concentrations of testosterone, estrogen and progesterone on cardiac ion channel targets. We then study the hormone effects on ventricular cell and tissue dynamics comprised of Faber-Rudy computational models. The "female" model predicts changes in action potential duration (APD) at different stages of the menstrual cycle that are consistent with clinically observed QT interval fluctuations. The "male" model predicts shortening of APD and QT interval at physiological testosterone concentrations. The model suggests increased susceptibility to drug-induced arrhythmia when estradiol levels are high, while testosterone and progesterone are apparently protective. Simulations predict the effects of sex steroid hormones on clinically observed QT intervals and reveal mechanisms of estrogen-mediated susceptibility to prolongation of QT interval. The simulations also indicate that acute effects of estrogen are not alone sufficient to cause arrhythmia triggers and explain the increased risk of females to Torsades de Pointes. Our results suggest that acute effects of sex steroid hormones on cardiac ion channels are sufficient to account for some aspects of gender specific susceptibility to long-QT linked arrhythmias.

Indexed as

Computer SimulationDisease SusceptibilityAction PotentialsAnimalsAnti-Arrhythmia AgentsArrhythmias, CardiacCells, CulturedElectrocardiographyEstrogensFemaleGonadal Steroid HormonesGuinea PigsMaleMarkov ChainsMenstrual CycleMyocytes, CardiacAnti-Arrhythmia AgentsE 4031EstrogensGonadal Steroid HormonesPiperidinesPotassium ChannelsProgesteronePyridinesTestosterone

Identifiers

PMID20126530
PMCPMC2813260
OpenAlexW2140307760

What OpenQuestion holds

Textmetadata
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.