Abstract 16272: Intermittent Vagal Nerve Stimulation Reduces VT Inducibility and Dispersion of Repolarization in a Chronic Infarct Model
BACKGROUND: Vagal nerve stimulation has been shown to reduce infarct size and ventricular tachyarrhythmias (VT) during ischemia. The benefits of vagal nerve stimulation in the setting of a remodeled chronic infarct are unknown. The purpose of this study was to evaluate the effects of intermittent vagal stimulation on VT inducibility, dispersion of repolarization (DOR), and during sympathetic activation.
METHODS: Porcine heart (n=6) underwent percutaneous myocardial infarction (MI). Four to eight weeks post MI, the chest was opened, a 56 sock electrode placed on the heart, and bilateral stellate ganglia (BSG) and cervical vagal nerves were isolated. Activation recovery interval (ARI), a validated marker of action potential duration, and VT inducibility were assessed at baseline, during BSG, intermittent bilateral vagal nerve, and simultaneous BSG and intermittent bilateral vagal nerve stimulation (coactivation).
RESULTS: Bilateral vagal nerve stimulation reduced heart rate and systolic blood pressure while BSG stimulation increased both. Vagal nerve stimulation during BSG stimulation lead to a blunted hemodynamic response compared to BSG stimulation alone. VT was inducible in 4 of 6 animals at baseline and during BSG stimulation. Only one animal was inducible for VT during vagal stimulation, and 2 animals were inducible during coactivation. Vagal stimulation increased the global mean ARI (341±18 ms vs. 397±10ms, P<0.05) and decreased DOR (from 781±156 to 582±143 ms2, P<0.05). Intermittent vagal nerve stimulation reduced the global ARI shortening effects of BSG stimulation (254±34 ms during BSG stimulation vs. 317±35 ms during coactivation, P<0.05) and reversed the effects of BSG stimulation on DOR (an increase in DOR during BSG of 193±130ms2 vs. a decrease in DOR during coactivation of 123±157 ms2, P<0.05).
CONCLUSIONS: Vagal stimulation was able to reduce VT inducibility and DOR in a chronic infarct model, even during concomitant sympathetic activation.
- © 2013 by American Heart Association, Inc.