Evidence map›Paper›PMID 35450607›Full record

ArticleJACC. Clinical electrophysiology2022

Proarrhythmic Effects of Sympathetic Activation Are Mitigated by Vagal Nerve Stimulation in Infarcted Hearts.

Jonathan D Hoang, Kentaro Yamakawa, Pradeep S Rajendran, Christopher A Chan, Daigo Yagishita, Keijiro Nakamura, Robert L Lux, Marmar Vaseghi

Open access · greenAbstract read
In one paragraph

Article in JACC. Clinical electrophysiology, 2022. 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
1.5field-weighted citation impact, top 17% 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, 9 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

8 authors at 1 institution in 1 country.

Jonathan D HoangUCLA Cardiac Arrhythmia Center, University of California, Los Angeles, California, USA; UCLA Neurocardiology Program of Excellence, University of California, Los Angeles, California, USA; Molecular, Cellular and Integrative Physiology Interdepartmental Program, University of California, Los Angeles, California, USA.
Kentaro YamakawaUCLA Cardiac Arrhythmia Center, University of California, Los Angeles, California, USA.
Pradeep S RajendranUCLA Cardiac Arrhythmia Center, University of California, Los Angeles, California, USA; UCLA Neurocardiology Program of Excellence, University of California, Los Angeles, California, USA.
Christopher A ChanUCLA Cardiac Arrhythmia Center, University of California, Los Angeles, California, USA; UCLA Neurocardiology Program of Excellence, University of California, Los Angeles, California, USA.
Daigo YagishitaUCLA Cardiac Arrhythmia Center, University of California, Los Angeles, California, USA.
Keijiro NakamuraUCLA Cardiac Arrhythmia Center, University of California, Los Angeles, California, USA.
Robert L LuxUCLA Cardiac Arrhythmia Center, University of California, Los Angeles, California, USA.
Marmar VaseghiUCLA Cardiac Arrhythmia Center, University of California, Los Angeles, California, USA; UCLA Neurocardiology Program of Excellence, University of California, Los Angeles, California, USA; Molecular, Cellular and Integrative Physiology Interdepartmental Program, University of California, Los Angeles, California, USA. Electronic address: mvaseghi@mednet.ucla.edu.
University of California, Los Angeles · US

Funding

Ventricular arrhythmias and mechanisms of parasympathetic dysfunction following myocardial infarctionR01HL148190 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI VASEGHI, MARMAR · 2020 to 2024
$3.2M
NHLBI NIH HHS R01 HL148190
6 · The paper itself

Abstract

objectivesThe goal of this study was to evaluate whether intermittent VNS reduces electrical heterogeneities and arrhythmia inducibility during sympathoexcitation.

backgroundSympathoexcitation increases the risk of ventricular tachyarrhythmias (VT). Vagal nerve stimulation (VNS) has been antiarrhythmic in the setting of ischemia-driven arrhythmias, but it is unclear if it can overcome the electrophysiological effects of sympathoexcitation in the setting of chronic myocardial infarction (MI).

methodsIn Yorkshire pigs after chronic MI, a sternotomy was performed, a 56-electrode sock was placed over the ventricles (n = 17), and a basket catheter was positioned in the left ventricle (n = 6). Continuous unipolar electrograms from sock and basket arrays were obtained to analyze activation recovery interval (ARI), a surrogate of action potential duration. Bipolar voltage mapping was performed to define scar, border zone, or viable myocardium. Hemodynamic and electrical parameters and VT inducibility were evaluated during sympathoexcitation with bilateral stellate ganglia stimulation (BSS) and during combined BSS with intermittent VNS.

resultsDuring BSS, global epicardial ARIs shortened from 384 ± 59 milliseconds to 297 ± 63 milliseconds and endocardial ARIs from 359 ± 36 milliseconds to 318 ± 40 milliseconds. Dispersion in ARIs increased in all regions, with the greatest increase observed in scar and border zone regions. VNS mitigated the effects of BSS on border zone ARIs (from -18.3% ± 6.3% to -2.1% ± 14.7%) and ARI dispersion (from 104 ms

conclusionsAfter chronic MI, VNS overcomes the detrimental effects of sympathoexcitation by reducing electrophysiological heterogeneities exacerbated by sympathetic stimulation, decreasing VT inducibility.

Indexed as

Myocardial InfarctionTachycardia, VentricularVagus Nerve StimulationAnimalsArrhythmias, CardiacCicatrixHeartHeart RateHumansSwinedispersionmyocardial infarctionneuromodulationsympatheticvagal nerve stimulationventricular arrhythmias

Identifiers

PMID35450607
PMCPMC9034056
OpenAlexW4220809307

What OpenQuestion holds

Textmetadata
LicenceTDM
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.