ArticleJCI insight2017
Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04359004 (A Study to Evaluate the Effect of Vagus Nerve Stimulation in Patients Undergoing Ventricular Tachycardia), which is not on this map. Cited by 68 papers, 2 of them syntheses that pooled 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.
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.
A Study to Evaluate the Effect of Vagus Nerve Stimulation in Patients Undergoing Ventricular Tachycardia (VT) Ablation
Who cites it
68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 92 citations in OpenAlex.
- Cardioneuroablation for the treatment of reflex syncope and functional bradyarrhythmias: A Scientific Statement of the European Heart Rhythm Association (EHRA) of the ESC, the Heart Rhythm Society (HRS), the Asia Pacific Heart Rhythm Society (APHRS) and the Latin American Heart Rhythm Society (LAHRS).Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2024Guideline
- Cardiac sympathetic hyperinnervation after myocardial infarction: a systematic review and qualitative analysis.Annals of medicine · 2023Pooled it
- BDNF/TrkB Signaling in Intracardiac Ganglia Modulates Cardiac Parasympathetic Tone.International journal of molecular sciences · 2026Article
- Prediabetic cardiomyopathy is attenuated by hypothalamic PVN oxytocin neuron activation.The Journal of physiology · 2026Article
- Spinal nociceptive denervation impedes subsequent chronic autonomic remodeling after myocardial infarction in male swine.Nature communications · 2026Article
- Role of Exercise in Modulating the Brain-Heart Axis in Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- Article
- Selected Large-Animal Models of Ventricular Arrhythmias.Biology · 2026Review
- Chemogenetic activation of cholinergic intrinsic cardiac ganglia improves border zone oxygenation and reduces arrhythmias during acute local ischemia.Frontiers in cardiovascular medicine · 2026Article
- Transcutaneous auricular vagus nerve stimulation for disorders of consciousness: a narrative review of neurophysiological mechanisms, clinical evidence, and future directions.Frontiers in human neuroscience · 2026Review
- Autonomic nervous system modulation in arrhythmias: mechanisms and therapeutic advances.Frontiers in physiology · 2026Review
- Development and modeling of cardiac autonomic innervation.Nature cardiovascular research · 2025Review
- Sympathovagal crosstalk: Y2-receptor blockade enhances vagal effects which in turn reduce NPY levels via muscarinic receptor activation.Cardiovascular research · 2025Article
- Brain‑heart axis: Neurostimulation techniques in ischemic heart disease (Review).International journal of molecular medicine · 2025Review
- Tyrosine Hydroxylase-Expressing Neurons in the Vagal Ganglia: Characterization and Implications.Biomedicines · 2025Article
- Biophysical modelling of intrinsic cardiac nervous system neuronal electrophysiology based on single-cell transcriptomics.The Journal of physiology · 2025Article
- Computational modelling of cardiac control following myocardial infarction using an in silico patient cohort.The Journal of physiology · 2025Article
- Bioelectronic block of stellate ganglia mitigates pacing-induced heterogeneous release of catecholamine and neuropeptide Y in the infarcted pig heart.The Journal of physiology · 2025Article
- Article
- Blocking NaBMC cardiovascular disorders · 2024Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Myocardial infarction causes sympathetic activation and parasympathetic dysfunction, which increase risk of sudden death due to ventricular arrhythmias. Mechanisms underlying parasympathetic dysfunction are unclear. The aim of this study was to delineate consequences of myocardial infarction on parasympathetic myocardial neurotransmitter levels and the function of parasympathetic cardiac ganglia neurons, and to assess electrophysiological effects of vagal nerve stimulation on ventricular arrhythmias in a chronic porcine infarct model. While norepinephrine levels decreased, cardiac acetylcholine levels remained preserved in border zones and viable myocardium of infarcted hearts. In vivo neuronal recordings demonstrated abnormalities in firing frequency of parasympathetic neurons of infarcted animals. Neurons that were activated by parasympathetic stimulation had low basal firing frequency, while neurons that were suppressed by left vagal nerve stimulation had abnormally high basal activity. Myocardial infarction increased sympathetic inputs to parasympathetic convergent neurons. However, the underlying parasympathetic cardiac neuronal network remained intact. Augmenting parasympathetic drive with vagal nerve stimulation reduced ventricular arrhythmia inducibility by decreasing ventricular excitability and heterogeneity of repolarization of infarct border zones, an area with known proarrhythmic potential. Preserved acetylcholine levels and intact parasympathetic neuronal pathways can explain the electrical stabilization of infarct border zones with vagal nerve stimulation, providing insight into its antiarrhythmic benefit.
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Registered trials
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.