Evidence map›Paper›PMID 37975708›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2024

A comprehensive protocol combining in vivo and ex vivo electrophysiological experiments in an arrhythmogenic animal model.

Mathias Nyman, Tomas O Stølen, Anne Berit Johnsen, Karin Garten, Francis L Burton, Godfrey L Smith, Jan Pål Loennechen

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

7 authors.

Mathias NymanDepartment of Circulation and Medical Imaging, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.ORCID 0000-0001-9618-5107
Tomas O StølenDepartment of Circulation and Medical Imaging, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.ORCID 0000-0002-2190-9948
Anne Berit JohnsenDepartment of Circulation and Medical Imaging, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.
Karin GartenDepartment of Circulation and Medical Imaging, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.
Francis L BurtonSchool of Cardiovascular and Metabolic Health, University of Glasgow, Glasgow, United Kingdom.ORCID 0000-0002-6970-6250
Godfrey L SmithSchool of Cardiovascular and Metabolic Health, University of Glasgow, Glasgow, United Kingdom.ORCID 0000-0003-4821-9741
Jan Pål LoennechenDepartment of Circulation and Medical Imaging, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.

Funding

The Joint Research Committee between St. Olavs hospital and the Faculty of Medicine and Health Science, NTNU 7/38297-99The Liaison Committee for education, research and innovation in Central Norway 2017/38202The Research Council of Norway 241040
6 · The paper itself

Abstract

Ventricular arrhythmias contribute significantly to cardiovascular mortality, with coronary artery disease as the predominant underlying cause. Understanding the mechanisms of arrhythmogenesis is essential to identify proarrhythmic factors and develop novel approaches for antiarrhythmic prophylaxis and treatment. Animal models are vital in basic research on cardiac arrhythmias, encompassing molecular, cellular, ex vivo whole heart, and in vivo models. Most studies use either in vivo protocols lacking important information on clinical relevance or exclusively ex vivo protocols, thereby missing the opportunity to explore underlying mechanisms. Consequently, interpretation may be difficult due to dissimilarities in animal models, interventions, and individual properties across animals. Moreover, proarrhythmic effects observed in vivo are often not replicated in corresponding ex vivo preparations during mechanistic studies. We have established a protocol to perform both an in vivo and ex vivo electrophysiological characterization in an arrhythmogenic rat model with heart failure following myocardial infarction. The same animal is followed throughout the experiment. In vivo methods involve intracardiac programmed electrical stimulation and external defibrillation to terminate sustained ventricular arrhythmia. Ex vivo methods conducted on the Langendorff-perfused heart include an electrophysiological study with optical mapping of regional action potentials, conduction velocities, and dispersion of electrophysiological properties. By exploring the retention of the in vivo proarrhythmic phenotype ex vivo, we aim to examine whether the subsequent ex vivo detailed measurements are relevant to in vivo pathological behavior. This protocol can enhance greater understanding of cardiac arrhythmias by providing a standardized, yet adaptable model for evaluating arrhythmogenicity or antiarrhythmic interventions in cardiac diseases.

Indexed as

Arrhythmias, CardiacMyocardial InfarctionAnimalsAnti-Arrhythmia AgentsHeartModels, AnimalRatsAnti-Arrhythmia Agentsdefibrillationex vivo electrophysiological studyin vivo electrophysiological studyoptical mappingventricular arrhythmia

Identifiers

PMID37975708
PMCPMC11213483

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Registered trials

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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.