Evidence map›Paper›PMID 19633207›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2009

K+ current changes account for the rate dependence of the action potential in the human atrial myocyte.

Mary M Maleckar, Joseph L Greenstein, Wayne R Giles, Natalia A Trayanova

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
–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

74 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Human atrial fibrillation and genetic defects in transient outward currents: mechanistic insights from multi-scale computational models.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Article
  7. Article
  8. Atrial fibrillation driver identification through regional mutual information networks: a modeling perspective.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2022
    Article
  9. Frontiers in physiology · 2022
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Calibration of ionic and cellular cardiac electrophysiology models.Wiley interdisciplinary reviews. Systems biology and medicine · 2020
    Review
  17. Article
  18. Article
  19. Ultrarapid Delayed Rectifier KFrontiers in cell and developmental biology · 2020
    Article
  20. Article

14 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

4 authors.

Mary M MaleckarDepartment of Biomedical Engineering and Institute for Computational Medicine, Johns Hopkins University, Baltimore,Maryland, USA. mmaleck@simula.no
Joseph L Greenstein
Wayne R Giles
Natalia A Trayanova

Funding

Virtual Electrode Polarization Hypothesis of DefibrillationR01HL067322 · NHLBI · WASHINGTON UNIVERSITY · PI EFIMOV, IGOR R · 2001 to 2010
$3.7M
Defibrillation Mechanisms in Infarcted HeartsR01HL082729 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TRAYANOVA, NATALIA A. · 2007 to 2010
$2.1M
CARDIAC TISSUE STRUCTURE IN THE DEFIBRILLATION PROCESSR01HL063195 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI TRAYANOVA, NATALIA A. · 1999 to 2008
$1.4M
NHLBI NIH HHS R01-HL-063195NHLBI NIH HHS R01-HL-067322NHLBI NIH HHS R01 HL082729NHLBI NIH HHS R01-HL-082729
6 · The paper itself

Abstract

Ongoing investigation of the electrophysiology and pathophysiology of the human atria requires an accurate representation of the membrane dynamics of the human atrial myocyte. However, existing models of the human atrial myocyte action potential do not accurately reproduce experimental observations with respect to the kinetics of key repolarizing currents or rate dependence of the action potential and fail to properly enforce charge conservation, an essential characteristic in any model of the cardiac membrane. In addition, recent advances in experimental methods have resulted in new data regarding the kinetics of repolarizing currents in the human atria. The goal of this study was to develop a new model of the human atrial action potential, based on the Nygren et al. model of the human atrial myocyte and newly available experimental data, that ensures an accurate representation of repolarization processes and reproduction of action potential rate dependence and enforces charge conservation. Specifically, the transient outward K(+) current (I(t)) and ultrarapid rectifier K(+) current (I(Kur)) were newly formulated. The inwardly recitifying K(+) current (I(K1)) was also reanalyzed and implemented appropriately. Simulations of the human atrial myocyte action potential with this new model demonstrated that early repolarization is dependent on the relative conductances of I(t) and I(Kur), whereas densities of both I(Kur) and I(K1) underlie later repolarization. In addition, this model reproduces experimental measurements of rate dependence of I(t), I(Kur), and action potential duration. This new model constitutes an improved representation of excitability and repolarization reserve in the human atrial myocyte and, therefore, provides a useful computational tool for future studies involving the human atrium in both health and disease.

Indexed as

Computer SimulationModels, CardiovascularAction PotentialsCalcium SignalingHeart AtriaHumansKineticsMyocytes, CardiacPotassiumPotassium ChannelsPotassium Channels, Inwardly RectifyingPotassiumPotassium ChannelsPotassium Channels, Inwardly Rectifying

Identifiers

PMID19633207
PMCPMC2770776

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.