Evidence map›Paper›PMID 36147731›Full record

ArticleFrontiers in synaptic neuroscience2022

Vagally-mediated heart block after myocardial infarction associated with plasticity of epicardial neurons controlling the atrioventricular node.

John D Tompkins, Una Buckley, Siamak Salavatian, Kalyanam Shivkumar, Jeffrey L Ardell

Open access · goldAbstract read
In one paragraph

Article in Frontiers in synaptic neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. 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

5 authors at 1 institution in 1 country.

John D TompkinsNeurocardiology Research Program of Excellence, Cardiac Arrhythmia Center, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
Una BuckleyNeurocardiology Research Program of Excellence, Cardiac Arrhythmia Center, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
Siamak SalavatianNeurocardiology Research Program of Excellence, Cardiac Arrhythmia Center, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
Kalyanam ShivkumarNeurocardiology Research Program of Excellence, Cardiac Arrhythmia Center, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
Jeffrey L ArdellNeurocardiology Research Program of Excellence, Cardiac Arrhythmia Center, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
University of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Imbalances in the opposing actions of sympathetic and parasympathetic nerves controlling the heart enhance risk for arrhythmia and sudden cardiac death after myocardial infarction (MI). Plasticity in peripheral neuron function may underlie the observed changes in cardiomotor nerve activity. We studied vagal control of the heart in pigs after chronic infarction of the left ventricle. Stimulation of the cervical vagus nerve produced greater bradycardic responses 8-weeks after MI. Recordings of epicardial electrocardiograms demonstrate increased severity and duration of atrioventricular (AV) block in MI-pigs during 20 Hz vagal stimulation. Intracellular voltage recordings from isolated neurons of the inferior vena cava-inferior left atrium (IVC-ILA) ganglionated plexus, a cluster of epicardial neurons receiving innervation from the vagus known to regulate the AV node, were used to assess plasticity of membrane and synaptic physiology of intrinsic cardiac neurons (ICNs) after MI. Changes to both passive and active membrane properties were observed, including more negative resting membrane potentials and greater input resistances in MI-pig ICNs, concomitant with a depression of neuronal excitability. Immunoreactivity to pituitary adenylate cyclase-activating polypeptide (PACAP), a cardiotropic peptide known to modulate cardiac neuron excitability, was localized to perineuronal varicosities surrounding pig IVC-ILA neurons. Exogenous application of PACAP increased excitability of control but not MI-ICNs. Stimulation (20 Hz) of interganglionic nerves in the

Indexed as

atrioventricular blockautonomic ganglionelectrophysiologyintrinsic cardiac neuronsvagus nerveYorkshire pig

Identifiers

PMID36147731
PMCPMC9488518
OpenAlexW4291787607

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.