Abstract
Noninvasive magnetic stimulation has been widely used in autonomic disorders in the past few decades, but few studies has been done in cardiac diseases. Recently, studies showed that low-frequency electromagnetic field (LF-EMF) might suppress atrial fibrillation by mediating the cardiac autonomic nervous system. In the present study, the effect of LF-EMF stimulation of left stellate ganglion (LSG) on LSG neural activity and ventricular arrhythmia has been studied in an acute myocardium infarction canine model. It is shown that LF-EMF stimulation leads to a reduction both in the neural activity of LSG and in the incidence of ventricular arrhythmia. The obtained results suggested that inhibition of the LSG neural activity might be the causal of the reduction of ventricular arrhythmia since previous studies have shown that LSG hyperactivity may facilitate the incidence of ventricular arrhythmia. LF-EMF stimulation might be a novel noninvasive substitute for the existing implant device-based electrical stimulation or sympathectomy in the treatment of cardiac disorders.
Highlights
Noninvasive magnetic stimulation has been widely used in autonomic disorders in the past few decades, but few studies has been done in cardiac diseases
The acute myocardial infarction-induced increased neural activity of left stellate ganglion (LSG) was significantly attenuated and the ventricular arrhythmia (VA) was significantly reduced by low-frequency magnetic field (LF-EMF)
These findings suggested that exposure the LSG to low frequency component (LF)-EMF might significantly reduce the neural activity of LSG, reducing the incidence of VAs
Summary
Noninvasive magnetic stimulation has been widely used in autonomic disorders in the past few decades, but few studies has been done in cardiac diseases. The effect of LF-EMF stimulation of left stellate ganglion (LSG) on LSG neural activity and ventricular arrhythmia has been studied in an acute myocardium infarction canine model. Previous studies have demonstrated that the activation and remodeling of left stellate ganglion (LSG) induced by myocardial infarction[1,2] might be the immediate triggering mechanisms of ventricular arrhythmia (VA) and sudden cardiac death[3,4], and suppressing LSG neural activity might be a feasible antiarrhythmic therapy[5]. Yu et al.[9] further demonstrated that LF-EMF stimulation of the vagal trunks or chest might suppress atrial fibrillation by inhibiting the neural activity of atrial ganglionated plexus. We hypothesized that exposure LSG to the LF-EMF might inhibit the LSG neural activity, thereby reducing VAs after acute myocardial infarction[6]
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