Evidence map›Paper›PMID 23108433›Full record

ReviewCardiovascular drugs and therapy2013

Role of late sodium channel current block in the management of atrial fibrillation.

Alexander Burashnikov, Charles Antzelevitch

Abstract readReview
In one paragraph

Review in Cardiovascular drugs and therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Local Anesthetic Like Inhibition of the Cardiac NaJournal of experimental pharmacology · 2022
    Article
  6. Article
  7. Phospho-ablation of cardiac sodium channel NaInternational journal of obesity (2005) · 2021
    Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Homocysteine-induced electrical remodeling via the mediation of IPAmerican journal of translational research · 2020
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Short-course of ranolazine prevents postoperative atrial fibrillation following coronary artery bypass grafting and valve surgeries.Clinical research in cardiology : official journal of the German Cardiac Society · 2015
    Article
  20. 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

2 authors at 1 institution in 1 country.

Alexander BurashnikovMasonic Medical Research Laboratory, 2150 Bleecker Street, Utica, NY 13501, USA. sasha@mmrl.edu
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
ELECTRICAL HETEROGENEITY AND CARDIAC ARRHYTHMIASR55HL047678 · NHLBI · MASONIC MEDICAL RESEARCH LABORATORY, INC · PI ANTZELEVITCH, CHARLES · 1992 to 1992
–
NHLBI NIH HHS HL 47678NHLBI NIH HHS R01 HL047678
6 · The paper itself

Abstract

The anti-arrhythmic efficacy of the late sodium channel current (late I(Na)) inhibition has been convincingly demonstrated in the ventricles, particularly under conditions of prolonged ventricular repolarization. The value of late I(Na) block in the setting of atrial fibrillation (AF) remains poorly investigated. All sodium channel blockers inhibit both peak and late I(Na) and are generally more potent in inhibiting late vs. early I(Na). Selective late I(Na) block does not prolong the effective refractory period (ERP), a feature common to practically all anti-AF agents. Although the late I(Na) blocker ranolazine has been shown to be effective in suppression of AF, it is noteworthy that at concentrations at which it blocks late I(Na) in the ventricles, it also potently blocks peak I(Na) in the atria, thus causing rate-dependent prolongation of ERP due to development of post-repolarization refractoriness. Late I(Na) inhibition in atria is thought to suppress intracellular calcium (Ca(i))-mediated triggered activity, secondary to a reduction in intracellular sodium (Na(i)). However, agents that block late I(Na) (ranolazine, amiodarone, vernakalant, etc) are also potent atrial-selective peak I(Na) blockers, so that the reduction of Na(i) loading in atrial cells by these agents can be in large part due to the block of peak I(Na). The impact of late I(Na) inhibition is reduced by the abbreviation of the action potential that occurs in AF patients secondary to electrical remodeling. It stands to reason that selective late I(Na) block may contribute more to inhibition of Ca(i)-mediated triggered activity responsible for initiation of AF in clinical pathologies associated with a prolonged atrial APD (such as long QT syndrome). Additional studies are clearly needed to test this hypothesis.

Indexed as

Action PotentialsAnimalsAnti-Arrhythmia AgentsAtrial FibrillationHumansMyocytes, CardiacSodium Channel BlockersSodium ChannelsTreatment OutcomeAnti-Arrhythmia AgentsSodium Channel BlockersSodium Channels

Identifiers

PMID23108433
PMCPMC3557765
OpenAlexW1984915521

What OpenQuestion holds

Textmetadata
LicenceTDM
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.