Evidence map›Paper›PMID 27844147›Full record

ArticleHeart and vessels2017

Acute ivabradine treatment reduces heart rate without increasing atrial fibrillation inducibility irrespective of underlying vagal activity in dogs.

Kazunori Uemura, Masashi Inagaki, Can Zheng, Toru Kawada, Meihua Li, Masafumi Fukumitsu, Masaru Sugimachi

Abstract read
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In one paragraph

Article in Heart and vessels, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.3field-weighted citation impact, top 16% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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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

7 authors at 1 institution in 1 country.

Kazunori UemuraDepartment of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center, 5-7-1 Fujishirodai, Suita, 565-8565, Japan. kuemura@ncvc.go.jp.ORCID http://orcid.org/0000-0003-2900-4702
Masashi InagakiDepartment of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center, 5-7-1 Fujishirodai, Suita, 565-8565, Japan.
Can ZhengDepartment of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center, 5-7-1 Fujishirodai, Suita, 565-8565, Japan.
Toru KawadaDepartment of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center, 5-7-1 Fujishirodai, Suita, 565-8565, Japan.
Meihua LiDepartment of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center, 5-7-1 Fujishirodai, Suita, 565-8565, Japan.
Masafumi FukumitsuDepartment of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center, 5-7-1 Fujishirodai, Suita, 565-8565, Japan.
Masaru SugimachiDepartment of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center, 5-7-1 Fujishirodai, Suita, 565-8565, Japan.
National Cerebral and Cardiovascular Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ivabradine, a bradycardic agent, has been shown to stably reduce patient's heart rate (HR) in the setting of acute cardiac care. However, an association between atrial fibrillation (AF) risk and acute ivabradine treatment remains a controversial clinical issue, and has not been thoroughly investigated. Bradycardia and abnormal atrial refractoriness induced by ivabradine treatment may enhance vulnerability to AF induction, especially when vagal nerve is concurrently activated. We aimed to experimentally investigate the effects of acute ivabradine treatment with/without concurrent vagal activation on AF inducibility. In 16 anesthetized dogs, cervical vagal nerves were prepared for electrical stimulation (VS). AF induction rate (AFIR) was determined by atrial burst pacing. HR, atrial action potential duration (APD), atrial effective refractory period (ERP), and AFIR were obtained consecutively at baseline, during delivery of VS (VS alone), after intravenous injection of ivabradine 0.5 mg/kg (n = 8, ivabradine group) or saline (n = 8, saline group), and again during VS delivery (drug+VS). In the ivabradine group, ivabradine alone significantly lowered HR compared to baseline, while ivabradine+VS significantly lowered HR compared to VS alone. Contrary to expectations, there were no significant differences in trends of APD, temporal dispersion of APD, ERP, and AFIR between ivabradine and saline groups. Irrespective of whether ivabradine or saline was injected, VS significantly shortened APD and ERP, and increased AFIR. Interestingly, although bradycardia in response to ivabradine injection was more intense than that to VS alone, AFIR was significantly lower after ivabradine injection than during VS alone. We conclude that, despite its intense bradycardic effect, acute ivabradine treatment does not increase AF inducibility irrespective of underlying vagal activity. This study may constitute support for the safety of using ivabradine in the setting of acute cardiac care.

Indexed as

AnimalsAtrial FibrillationBenzazepinesCardiovascular AgentsDogsElectric StimulationElectrophysiological PhenomenaFemaleHeart AtriaHeart RateIvabradineMaleVagus NerveBenzazepinesCardiovascular AgentsIvabradineAcute cardiac careAtrial fibrillationEffective refractory periodIvabradineVagal nerve

Identifiers

PMID27844147
OpenAlexW2551843737

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.