ArticleJournal of molecular and cellular cardiology2018
Autonomic conflict exacerbates long QT associated ventricular arrhythmias.
Article in Journal of molecular and cellular cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Sleep, Neural Circulatory Control, and Cardiovascular Disease: A Mechanistic Review.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- The interactive effect of long nighttime sleep and daytime napping on QTc prolongation in hypertensive adults.BMC cardiovascular disorders · 2026Article
- Case Report: Association of a rare single nucleotide variant in the KCNH2 gene with drug-induced QT prolongation.Frontiers in genetics · 2026Article
- Cholinergic suppression of heart rate acceleration during intrinsic optogenetic activation of sympathetic cardiac neurons in perfused hearts.American journal of physiology. Heart and circulatory physiology · 2025Article
- Recent updates on cold adaptation in population and laboratory studies, including cross-adaptation with nonthermal factors.Journal of physiological anthropology · 2025Review
- Cardiovascular safety pharmacology: beyond arrhythmic risk assessment.Frontiers in cardiovascular medicine · 2025Review
- Drowning incidents precipitated by unusual causes (DIPUCs): A narrative review of their diagnoses, evaluation and management.Resuscitation plus · 2024Review
- Remodeling of the Intracardiac Ganglia During the Development of Cardiovascular Autonomic Dysfunction in Type 2 Diabetes: Molecular Mechanisms and Therapeutics.International journal of molecular sciences · 2024Review
- Long QT Syndrome and WPW Syndrome: A Very Rare Association between Two Causes of Sudden Cardiac Death in a Young Patient.Journal of clinical medicine · 2024Article
- Cardiopulmonary nerve stimulation as a novel therapy for cardiac autonomic nervous system modulation.Frontiers in neuroscience · 2024Article
- Fir(e)ing the Rhythm: Inflammatory Cytokines and Cardiac Arrhythmias.JACC. Basic to translational science · 2023Review
- Vagus Nerve Stimulation and Its Cardioprotective Abilities: A Systematic Review.Journal of clinical medicine · 2023Review
- Article
- Declining Levels and Bioavailability of IGF-I in Cardiovascular Aging Associate With QT Prolongation-Results From the 1946 British Birth Cohort.Frontiers in cardiovascular medicine · 2022Article
- QT Interval Dynamics and Cardiovascular Outcomes: A Cohort Study in an Integrated Health Care Delivery System.Journal of the American Heart Association · 2021Article
- Development and Validation of a Risk Prediction Model for Ventricular Arrhythmia in Elderly Patients with Coronary Heart Disease.Cardiology research and practice · 2021Article
- Age-Related Changes in Cardiac Autonomic Modulation and Heart Rate Variability in Mice.Frontiers in neuroscience · 2021Article
- Head-up tilt test induces T-wave alternans in long QT syndrome with KCNQ1 gene mutation: Case report CARE-compliant article.Medicine · 2020Article
- Vagus Nerve Stimulation and the Cardiovascular System.Cold Spring Harbor perspectives in medicine · 2020Review
- Dynamic monitoring of single-terminal norepinephrine transporter rate in the rodent cardiovascular system: A novel fluorescence imaging method.Autonomic neuroscience : basic & clinical · 2020Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
This study tested the hypothesis that concomitant sympathetic and parasympathetic stimulation ("autonomic conflict") may act as a trigger for arrhythmias in long QT syndrome (LQTS). Studies were performed in isolated innervated rabbit hearts treated with clofilium (100 nmol/L); a potassium channel blocker. The influence of vagus nerve stimulation (VNS) on spontaneous ventricular arrhythmias was assessed in the absence/presence of sustained noradrenaline perfusion (100 nmol/L) and with sudden adrenergic stress (injections of noradrenaline into the perfusion line). Hearts were instrumented for a pseudo-electrocardiogram and monophasic action potential recordings. VNS, which slows heart rate, was associated with a stimulation frequency-dependent incidence of spontaneous early after-depolarisations (EADs) and ventricular tachycardia (VT), best predicted by the duration of the electrocardiographic T-wave and by triangulation of the ventricular action potential. In the presence of sustained (steady-state) noradrenaline perfusion, the incidence of EADs and VT with VNS was decreased from 73/55% to 45/27%, respectively. However, sudden adrenergic stress, imposed during periods of sustained VNS, was associated with a transient increase in the incidence of severity of observed arrhythmias, as indicated by an increase in the average arrhythmias score (1.6 ± 0.4 vs. 2.1 ± 0.7, p = .01). Analysis of electrophysiological parameters suggests that sudden adrenergic stress is associated with a transient prolongation, and increased triangulation, of the ventricular action potential, which may predispose to triggered activity. This study demonstrates that autonomic conflict is a pro-arrhythmic stimulus in LQTS. However, combined adrenergic and parasympathetic stimulation has a complex relationship with arrhythmogenicity, with differences in the effects of steady-state adrenergic activation vs. sudden adrenergic stress.
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