Abstract 15578: Effects of Low-Intensity Atrial Ganglionated Plexi Stimulation on Ventricular Electrophysiology in Normal Heart and after Acute Myocardial Ischemia
Background: Atrial ganglionated plexus (GP) has been shown to modulate sinus rate, atrioventricular conduction and atrial electrophysiology. The aim of this study was to investigate the effect of low-intensity GP stimulation (LIGPS) on ventricular electrophysiological properties in normal heart and on ventricular arrhythmogenesis after acute myocardial ischemia (AMI) in canine.
Methods: Thirty-nine dogs were assigned into the normal heart group (n=12) and the AMI group (n=27, 12 in control and 15 in LIGPS). In the normal heart, ventricular effective refractory period (ERP), action potential duration (APD), electrical alternans, dynamic APD restitution and serum levels of norepinephrine (NE) and acetylcholine (Ach) were measured at baseline and after 6-hour LIGPS (the strength for LIGPS was set at the voltage level causing a 10% decrease of sinus rate). In the AMI heart, LIGPS was performed 1 hour before coronary artery ligation and the incidence and duration of ventricular arrhythmias were determined during 1-hour ligation.
Results: In the normal heart, 6-hour LIGPS significantly prolonged ventricular ERP and APD at each site (P<0.05 for all) but did not change their spatial dispersion when compared with baseline. LIGPS also caused an upward shift of ventricular restitution curves in each site but the slope of restitution curves was not affected. APD alternans occurred at longer pacing cycle length at each site when compared with baseline (P<0.05). Both NE and Ach levels were significantly increased after 6-hour LIGPS (NE 1192.27 ± 71.31 ng/L, Ach 302.15 ± 11.02 pmol/L) when compared with baseline (NE 1032.68 ± 50.06 ng/L, Ach 265.41 ± 18.87 pmol/L, both P<0.05). In the AMI heart, ventricular premature contraction (VPC) episodes, ventricular tachycardia (VT) duration and the incidence of spontaneous ventricular fibrillation (VF) in LIGPS group (VPC: 68 ± 36, VT: 0.8 ± 0.2 s and VF: 13.3%) were significantly lower than that in control group (VPC: 124 ± 54, VT: 1.9 ± 0.8 s and VF: 58.3%, all P<0.05).
Conclusions: LIGPS induces no increase in the risk of ventricular arrhythmias in normal heart as well as protects against ventricular arrhythmogenesis during AMI.
- © 2012 by American Heart Association, Inc.