ArticleMedical science monitor : international medical journal of experimental and clinical research2019
Cardiac Sympathetic Afferent Denervation Protects Against Ventricular Arrhythmias by Modulating Cardiac Sympathetic Nerve Activity During Acute Myocardial Infarction.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 32 citations in OpenAlex.
- Trial
- Atrial Fibrillation Risk Management and Emerging Therapies.Journal of clinical medicine · 2026Review
- Cardiac Sympathetic Denervation Mitigated Ischemic Cardiomyopathy Progression in a Rat Model of Sleep Apnea.Journal of the American Heart Association · 2025Article
- Neurocardiology: translational advancements and potential.The Journal of physiology · 2025Review
- Effects and mechanism of renal denervation on ventricular arrhythmia after acute myocardial infarction in rats.BMC cardiovascular disorders · 2022Article
- SGLT2 Inhibitors: New Hope for the Treatment of Acute Myocardial Infarction?American journal of cardiovascular drugs : drugs, devices, and other interventions · 2022Review
- Cardiac sympathetic afferent ablation to prevent ventricular arrhythmia complicating acute myocardial infarction by inhibiting activated astrocytes.Journal of cellular and molecular medicine · 2022Article
- Bilateral Superior Cervical Sympathectomy Activates Signal Transducer and Activator of Transcription 3 Signal to Alleviate Myocardial Ischemia-Reperfusion Injury.Frontiers in cardiovascular medicine · 2022Article
- The connectome from the cerebral cortex to the viscera using viral transneuronal tracers.American journal of translational research · 2021Review
- Long Non-Coding RNA SNHG8 Plays a Key Role in Myocardial Infarction Through Affecting Hypoxia-Induced Cardiomyocyte Injury.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Augmented cardiac sympathetic afferent reflex (CSAR) plays a role in enhanced sympathetic activity. Given that a strategy for abolishing augmented CSAR-induced sympathetic activation may be beneficial for protecting against ventricular arrhythmias (VAs) triggered by acute myocardial infarction (AMI), we investigated whether cardiac sympathetic afferent denervation (CSAD) could protect against VAs by modulating cardiac sympathetic nerve activity in an AMI dog model. MATERIAL AND METHODS Twenty-two anesthetized dogs were assigned to the CSAD group (n=9) and the sham group (n=13) randomly. CSAD was produced by epicardial application of resiniferatoxin. Heart rate variability (HRV), ventricular action potential duration (APD), APD dispersion, beat-to-beat variability of repolarization (BVR), effective refractory period (ERP) of ventricles, ERP dispersion, plasma norepinephrine (NE) concentration, and left stellate ganglion (LSG) neural activity were determined at baseline and after CSAD. We designed an AMI model by occluding the left anterior coronary artery, and performed analysis of VAs for 60 minutes using electrocardiography. Then, levels of c-fos and nerve growth factor (NGF) were determined. RESULTS Relative to baseline values, CSAD prolonged ERP and APD of ventricles, increased HRV, decreased APD dispersion, BVR, ERP dispersion and serum NE concentration, and attenuated LSG activity in the CSAD group. AMI triggered a remarkable increase in LSG activity and function but decreased the HRV of the sham group animals relative to the CSAD group. Moreover, the CSAD group had higher levels of VAs relative to the sham group. This was accompanied by a corresponding decrease in proteins quantities of NGF and c-fos in the CSAD group in the LSG after AMI compared to the sham group. CONCLUSIONS CSAD can suppress LSG neural activity, hence enhance the electrophysiological stability and protect the heart from AMI-triggered VAs.
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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 Socratic graph.