Evidence map›Paper›PMID 19880073›Full record

ReviewHeart rhythm2009

Inward rectifier potassium channels control rotor frequency in ventricular fibrillation.

José Jalife

Open access · greenAbstract readReview
In one paragraph

Review in Heart rhythm, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Rotor mechanism and its mapping in atrial fibrillation.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 · 2023
    Review
  3. Article
  4. Tetramisole is a new IPharmacology research & perspectives · 2022
    Review
  5. The Challenges of Predicting Drug-Induced QTc Prolongation in Humans.Toxicological sciences : an official journal of the Society of Toxicology · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Flecainide increases Kir2.1 currents by interacting with cysteine 311, decreasing the polyamine-induced rectification.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
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

1 author at 1 institution in 1 country.

José JalifeUniversity of Michigan, Ann Arbor, Michigan 48108, USA. jjalife@umich.edu
University of Michigan–Ann Arbor · US

Funding

THREE DIMENSIONAL VORTEX LIKE REENTRY IN CORONARY PERFUSED VENTRICULAR WALLP01HL039707 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI JALIFE, JOSE S · 1990 to 2010
$19.0M
P3: Biophysical Mechanisms in two Arhythmogenic DiseasesP01HL087226 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI JALIFE, JOSE S · 2007 to 2012
$10.3M
Molecular Mechanisms of Ventricular FibrillationR01HL070074 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI JALIFE, JOSE S · 2002 to 2007
$1.7M
Role of Potassium Channels in Fibrillatory ConductionR01HL080159 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI JALIFE, JOSE S · 2006 to 2009
$1.5M
NHLBI NIH HHS P01 HL039707NHLBI NIH HHS P01-HL039707NHLBI NIH HHS P01 HL087226NHLBI NIH HHS P01-HL087226NHLBI NIH HHS R01 HL070074NHLBI NIH HHS R01 HL080159NHLBI NIH HHS R01-HL080159
6 · The paper itself

Abstract

Ventricular fibrillation (VF) is the most important cause of sudden cardiac death. While traditionally thought to result from random activation of the ventricles by multiple independent wavelets, recent evidence suggests that VF may be determined by the sustained activation of a relatively small number of reentrant sources. In addition, recent experimental data in various species as well as computer simulations have provided important clues about its ionic and molecular mechanisms, particularly in regards to the role of potassium currents in such mechanisms. The results strongly argue that the inward rectifier current, I(K1,) is an important current during functional reentry because it mediates the electrotonic interactions between the unexcited core and its immediate surroundings. In addition, I(K1) is a stabilizer of reentry due to its ability to shorten action potential duration and reduce conduction velocity near the center of rotation. Increased I(K1) prevents wave front-wave tail interactions and thus averts rotor destabilization and breakup. Other studies have shown that while the slow component of the delayed rectifier potassium current I(Ks) does not significantly modify rotor frequency or stability, it plays a major role in postrepolarization refractoriness and wave break formation. Therefore, the interplay between I(K1) and the rapid sodium inward current (I(Na)) is a major factor in the control of cardiac excitability and thus the stability and frequency of reentry, while I(Ks) is an important determinant of fibrillatory conduction.

Indexed as

AnimalsDeath, Sudden, CardiacHeart Conduction SystemHumansPotassium Channels, Inwardly RectifyingVentricular FibrillationPotassium Channels, Inwardly Rectifying

Identifiers

PMID19880073
PMCPMC2782423
OpenAlexW2010326652

What OpenQuestion holds

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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.