Evidence map›Paper›PMID 24456882›Full record

ArticleInternational journal of cardiology2014

Cardiac contractility modulation increases action potential duration dispersion and decreases ventricular fibrillation threshold via β1-adrenoceptor activation in the crystalloid perfused normal rabbit heart.

James Winter, Kieran E Brack, John H Coote, G André Ng

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

James WinterCardiology Group, Department of Cardiovascular Sciences, University of Leicester, UK.
Kieran E BrackCardiology Group, Department of Cardiovascular Sciences, University of Leicester, UK.
John H CooteSchool of Clinical and Experimental Medicine, University of Birmingham, UK.
G André NgCardiology Group, Department of Cardiovascular Sciences, University of Leicester, UK; NIHR Leicester Cardiovascular Biomedical Research Unit, Leicester, UK; University Hospitals of Leicester NHS Trust, Leicester, UK. Electronic address: gan1@le.ac.uk.
University of Leicester · GBUniversity of Birmingham · GB

Funding

British Heart Foundation FS/12/2/29300British Heart Foundation PG/08/039
6 · The paper itself

Abstract

BACKGROUND/

objectivesCardiac contractility modulation (CCM) is a new treatment being developed for heart failure (HF) involving application of electrical current during the absolute refractory period. We have previously shown that CCM increases ventricular force through β1-adrenoceptor activation in the whole heart, a potential pro-arrhythmic mechanism. This study aimed to investigate the effect of CCM on ventricular fibrillation susceptibility.

methodsExperiments were conducted in isolated New Zealand white rabbit hearts (2.0-2.5 kg, n=25). The effects of CCM (± 20 mA, 10 ms phase duration) on the left ventricular basal and apical monophasic action potential duration (MAPD) were assessed during constant pacing (200 bpm). Ventricular fibrillation threshold (VFT) was defined as the minimum current required to induce sustained VF with rapid pacing (30 × 30 ms). Protocols were repeated during perfusion of the β1-adrenoceptor antagonist metoprolol (1.8 μM). In separate hearts, the dynamic and spatial electrophysiological effects of CCM were assessed using optical mapping with di-4-ANEPPS.

resultsCCM significantly shortened MAPD close to the stimulation site (Basal: 102 ± 5 [CCM] vs. 131 ± 6 [Control] ms, P<0.001). VFT was reduced during CCM (2.6 ± 0.6 [CCM] vs. 6.1 ± 0.8 [Control] mA, P<0.01) and was correlated (r(2)=0.40, P<0.01) with increased MAPD dispersion (26 ± 4 [CCM] vs. 5 ± 1 [Control] ms, P<0.01) (n=8). Optical mapping revealed greater spread of CCM induced MAPD shortening during basal vs. apical stimulation. CCM effects were abolished by metoprolol and exogenous acetylcholine. No evidence for direct electrotonic modulation of APD was found, with APD adaptation occurring secondary to adrenergic stimulation.

conclusionsCCM decreases VFT in a manner associated with increased MAPD dispersion in the crystalloid perfused normal rabbit heart.

Indexed as

AcetylcholineAction PotentialsAdrenergic beta-1 Receptor AntagonistsAnimalsAutonomic Nervous SystemCardiac Pacing, ArtificialCholinergic AgonistsElectrophysiologic Techniques, CardiacGanglia, AutonomicHeartMaleMetoprololMyocardial ContractionPerfusionPotassium CompoundsRabbitsAcetylcholineAdrenergic beta-1 Receptor AntagonistsCholinergic AgonistsMetoprololpotassium cardioplegic solutionPotassium CompoundsReceptors, Adrenergic, beta-1Action potential duration dispersionCardiac contractility modulationNon-excitatory stimulation (NES)Ventricular arrhythmiaVentricular fibrillation

Identifiers

PMID24456882
PMCPMC3978661
OpenAlexW2134897733

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.