Evidence map›Paper›PMID 24496483›Full record

ReviewHerzschrittmachertherapie & Elektrophysiologie2014

[New developments in the antiarrhythmic therapy of atrial fibrillation].

Ursula Ravens

Abstract readReview
PubMed Publisher
In one paragraph

Review in Herzschrittmachertherapie & Elektrophysiologie, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 99% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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.

Ursula RavensMedizinische Fakultät Carl Gustav Carus, Institut für Pharmakologie und Toxikologie, Technische Universität Dresden, Fetscherstraße 74, 01307, Dresden, Deutschland, ravens@rcs.urz.tu-dresden.de.
TU Dresden · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial fibrillation often affects elderly people with cardiovascular disease and takes a progressive course with increasing resistance to treatment. For the latter, electrical and structural changes (remodelling) seem to be responsible that are directly related to the high excitatory rate in the atria. Therapeutic strategies for atrial fibrillation consist of (i) treating the underlying cardiovascular disease, (ii) re-establishing sinus rhythm and (iii) reducing ventricular rate. Rapid pharmacological or electrical cardioversion is expected to prevent remodelling. Classical antiarrhythmic drugs are notoriously ineffective and burdened with serious cardiac and extracardiac side effects so that there is an urgent need for effective and safe novel compounds. In this review the three recently introduced drugs dronedarone, vernakalant and ranolazine are discussed with respect to the use in atrial fibrillation. Other new antiarrhythmic agents are still in the developmental phase and aim at atria-selective mechanisms thereby excluding ventricular proarrhythmic effects. The mechanisms of action will be discussed in the context of the present understanding of the pathophysiology of onset and maintenance of atrial fibrillation.

Indexed as

AcetanilidesAmiodaroneAnisolesAnti-Arrhythmia AgentsAtrial FibrillationDose-Response Relationship, DrugDronedaroneDrug Therapy, CombinationEvidence-Based MedicineHumansPiperazinesPyrrolidinesRanolazineSodium Channel BlockersTreatment OutcomeAcetanilidesAmiodaroneAnisolesAnti-Arrhythmia AgentsDronedaronePiperazinesPyrrolidinesRanolazineSodium Channel Blockersvernakalant

Identifiers

PMID24496483
OpenAlexW204887492

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.