Evidence map›Paper›PMID 22005044›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2012

Atrial-selective sodium channel block strategy to suppress atrial fibrillation: ranolazine versus propafenone.

Alexander Burashnikov, Luiz Belardinelli, Charles Antzelevitch

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.9field-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

16 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Ranolazine depresses conduction of rapid atrial depolarizations in a beating rabbit heart model.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2021
    Article
  3. New Strategies for the Treatment of Atrial Fibrillation.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Frontiers in physiology · 2018
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. 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

3 authors at 1 institution in 1 country.

Alexander BurashnikovMasonic Medical Research Laboratory, 2150 Bleecker Street, Utica, NY 13501, USA. sasha@mmrl.edu
Luiz Belardinelli
Charles Antzelevitch
Masonic Medical Research Laboratory · US

Funding

ELECTRICAL HETEROGENEITY AND CARDIAC ARRHYTHMIASR01HL047678 · NHLBI · MASONIC MEDICAL RESEARCH LABORATORY, INC · PI ANTZELEVITCH, CHARLES · 1993 to 2014
$5.7M
SMALL INSTRUMENTATION GRANTS15HL047687 · NHLBI · UNIVERSITY OF WASHINGTON · PI HOLBROOK, KAREN A. · 1991 to 1991
–
NHLBI NIH HHS HL-47687NHLBI NIH HHS R01 HL047678
6 · The paper itself

Abstract

Ranolazine has been shown to produce atrial-selective depression of sodium channel-dependent parameters and suppress atrial fibrillation (AF) in a variety of experimental models. The present study contrasts the effects of ranolazine and those of a clinically used anti-AF class IC agent, propafenone. Electrophysiological and anti-AF effects of propafenone and ranolazine were compared at clinically relevant concentrations (i.e., 0.3-1.5 and 1-10 μM, respectively) in canine isolated coronary-perfused atrial and ventricular preparations. Transmembrane action potential and pseudo-ECG were recorded. Both ranolazine and propafenone produced atrial-selective prolongation of action potential duration. Propafenone depressed sodium channel-mediated parameters [maximum rate of rise of the action potential upstroke (V(max)), conduction time, and diastolic threshold of excitation] and induced postrepolarization refractoriness to a greater degree than ranolazine, and these effects, unlike those induced by ranolazine, were not or only mildly atrial-selective at normal rates (cycle length 500 ms). At fast pacing rates, however, the effects of propafenone on V(max) and conduction time became atrial-selective, because of the elimination of diastolic interval in atria, but not in ventricles. Propafenone (1.5 μM) and ranolazine (10.0 μM) were effective in preventing the initiation of persistent acetylcholine-mediated AF (6/7 and 9/11 atria, respectively), its termination (8/10 and 8/12 atria, respectively), and subsequent reinduction (8/8 and 7/8 atria, respectively). Thus, propafenone and ranolazine both suppress AF, but ranolazine, unlike propafenone, does it with minimal effects on ventricular myocardium, suggesting a reduced potential for promoting ventricular arrhythmias.

Indexed as

AcetanilidesAction PotentialsAnimalsAnti-Arrhythmia AgentsAtrial FibrillationDiastoleDogsElectrophysiological PhenomenaHeart AtriaHeart Conduction SystemHeart VentriclesKineticsPiperazinesPropafenoneRanolazineRefractory Period, ElectrophysiologicalAcetanilidesAnti-Arrhythmia AgentsPiperazinesPropafenoneRanolazineSodium Channel Blockers

Identifiers

PMID22005044
PMCPMC3251016
OpenAlexW2105597458

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.