Introduction:
Left stellate ganglion (LSG) and cardiac neural remodeling, which are associated with ventricular arrhythmias (VAs) in post-infarction model, can be attenuated by low-level vagus nerve stimulation. However, whether chronic low-level transcutaneous electrical stimulation at the tragus, where the auricular branch of vagus nerve innervate, can attenuate neural remodeling both in heart and LSG and then reduce VAs is unknown.
Hypothesis:
We hypothesized that chronic low-level tragus stimulation (LL-TS) would attenuate cardiac and LSG nerve remodeling and then reduce inducibility of VAs in a post-infarction model.
Methods:
Twenty beagles after ligating coronary artery were randomly divided into normal control (NC, n=4), MI treated with LL-TS (MI-TS n=8)and MI treated with shame LL-TS (MI-NTS, n=8)groups. LL-TS was performed at 80% below the threshold, at which sinus rate or atrioventricular conduction slowing can be initially induced, for 2 hours a day for 2 months. Left stellate ganglionic nerve activity (SGNA) and left thoracic vagal nerve activity (VNA) was recorded. Slope of ventricular restitution curves (Smax) and programmed ventricular stimulation were performed to evaluate VAs. Nerve sprouting, nerve synaptic density and associated protein expression both in LSG and hearts were evaluated by immunostaining or Western blotting.
Results:
Two months later, the increased SGNA induced by MI was attenuated by LL-TS. However, the increased VNA was strengthened.In the MI-TS group, the number of sympathetic nerves both in peri-infarct zone and LSG were reduced, while the parasympathetic nerve fibers were increased compared to MI-NTS group. Moreover, the expression of synaptophysin, NGF in peri-infarct as well as in LSG in the MI-TS group was significantly lower than the MI-NTS group, while the level of SK2 was much higher.Chronic LL-TS also significantly decreased the Smax, LF/HF ratio and arrhythmia score of programmed ventricular stimulation induced VAs.
Conclusions:
These findings suggested that chronic LL-TS augmented cardiac vagal and reduced sympathetic tone, attenuated cardiac and LSG nerve remodeling, regulated nerve associated protein expression and potentially contributed to reducing vulnerability to VAs.
Myocardial viability as integral part of the diagnostic and therapeutic approach to ischemic heart failure
