Vagus nerve stimulation in experimental heart failure

Heart Fail Rev. 2011 Mar;16(2):171-8. doi: 10.1007/s10741-010-9209-z.

Abstract

Chronic heart failure (HF) is associated with autonomic dysregulation characterized by a sustained increase in sympathetic drive and by withdrawal of parasympathetic activity. Sympathetic overdrive and increased heart rate are predictors of poor long-term outcome in patients with HF. Considerable evidence exists that supports the use of pharmacologic agents that partially inhibit sympathetic activity as effective long-term therapy for patients with HF; the classic example is the wide use of selective and non-selective beta-adrenergic receptor blockers. In contrast, modulation of parasympathetic activation as potential therapy for HF has received only limited attention over the years given its complex cardiovascular effects. In this article, we review the results of recent experimental animal studies that provide support for the possible use of electrical Vagus nerve stimulation (VNS) as a long-term therapy for the treatment of chronic HF. In addition to exploring the effects of chronic VNS on left ventricular (LV) function, the review will also address the effects of VNS on potential modifiers of the HF state that include cytokine production and nitric oxide elaboration. Finally, we will briefly review other nerve stimulation approaches which is also currently under investigation as potential therapeutic modalities for treating chronic HF.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cytokines / metabolism
  • Disease Models, Animal
  • Heart Failure / therapy*
  • Humans
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase / metabolism*
  • Parasympathetic Nervous System / pathology
  • Stroke Volume
  • Sympathetic Nervous System
  • Vagus Nerve / physiopathology*
  • Vagus Nerve Stimulation*
  • Ventricular Function, Left
  • Ventricular Remodeling

Substances

  • Cytokines
  • Nitric Oxide
  • Nitric Oxide Synthase