Abstract
The main purpose of this manuscript is to introduce the reader to the present “state of the art” in experimental Low Level Magnetic Fields nerve stimulation approaches to improve chaotic cardiac arrhythmias and muscle contractions. The area addressed in this paper is the transcutaneous application of Low Level Magnetic Fields to a branch of the vagus nerve. Cardiac Arrhythmias such as Atrial Fibrillation, as well as and muscle contractility were reversed by Low Level Transcutaneous Stimulation (LL-TS) of the Auricular Branch of the Vagus Nerve (ABVN). This treatment has been successfully reported in humans as well as in awaken and anesthetized animals such as rodents and dogs. The functional improvement has been attributed to a reversal of cardiac myocytes remodeling (reversal of fibrosis) resulting from experimentally provoking induced rapid heartbeats. The prolonged duration of a tachycardia state induces intracellular accumulation of glycogen leading into fibrosis, this in turn is hypothesized to impede the intercellular electrical communications of the specialized cardiac cells. It also reduces the functional ability of the main pumping chamber (Left Ventricle).
Highlights
The purpose of this manuscript is to propose a mechanism for the effect on specialized muscle cells by Low Level Electrical Transcutaneous Stimulation (LL-TS) of the auricular branch of the vagus nerve (ABVN)
Fibrosis has been identified as a factor for arrhythmia, which is a group of conditions where the heartbeat is irregular; it sometimes could lead into severe symptoms requiring medial care
We know that by definition myocytes remodeling entails an accumulation of interstitial fibrosis, linked to intramyocyte glycogen accumulation
Summary
The purpose of this manuscript is to propose a mechanism (based on published data) for the effect on specialized muscle cells (cardiac myocytes) by Low Level Electrical Transcutaneous Stimulation (LL-TS) of the auricular branch of the vagus nerve (ABVN). The LL-TS stimulation has been reported to attenuate unwanted interstitial fibrosis and collagen degradation in the atria and ventricle myocytes [3,4,5]. Fibrosis has been identified as a factor for arrhythmia, which is a group of conditions where the heartbeat is irregular; it sometimes could lead into severe symptoms requiring medial care. Atrial remodeling is defined as any change in atrial structure or function that promotes atrial arrhythmias. In the ventricles, remodeling is defined as any change in structure that decreases muscle performance. Preliminary results of LL-TS of the ABVN are encouraging in the atria and left ventricle. The mechanism causing this improvement is unknown at present
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