Abstract 5392: Chronic Cervical Vagus Nerve Stimulation Attenuates Systemic Inflammation and Heart Failure Progression in a Canine Rapid Ventricular Pacing Model
Autonomic dysfunction, characterized by sympathetic activation and vagal (parasympathetic) withdrawal, contributes to the progression of congestive heart failure (CHF). Although the therapeutic benefits of sympathetic inhibition with β-blockers in CHF are clear, the role of increased vagal tone in this setting has been less studied. We have investigated the effects of improving vagal tone by chronic cervical vagus nerve stimulation (VNS) on development of CHF in a canine rapid ventricular pacing model. 15 dogs were randomized into control (n=7) and VNS (n=8) groups; all dogs were implanted with an RV pacemaker. A right cervical vagus nerve stimulator was implanted in VNS group dogs. All dogs underwent 8 weeks of rapid ventricular pacing (220 bpm at first 4 weeks to develop CHF and another 4 weeks at 180 bpm to maintain CHF). Concomitant VNS (at an intensity reducing sinus rate by 20 bpm) was delivered together with the ventricular pacing in the VNS group. Cardiac function was determined by echocardiography in sinus rhythm by temporarily stopping the rapid ventricular pacing and blood samples were obtained before (baseline), and at 4 weeks and 8 weeks of ventricular pacing. After 4 and 8 weeks of ventricular pacing, both left ventricular end diastolic (LVEDV) and systolic (LVESV) volumes were lower and LV ejection fraction (LVEF) was higher in the VNS group than in the control group (table⇓). Plasma C-reactive protein (CRP, an inflammatory marker) increased significantly following rapid ventricular pacing. VNS therapy dramatically attenuated plasma CRP changes. Chronic cervical vagus nerve stimulation significantly attenuates CHF progression in the canine rapid ventricular pacing model. The therapeutic benefit of VNS is independent of heart rate slowing, and is associated with pronounced anti-inflammatory effects. VNS is a novel and potentially useful therapy for treating CHF.
This research has received full or partial funding support from the American Heart Association, AHA Great Rivers Affiliate (Delaware, Kentucky, Ohio, Pennsylvania & West Virginia).