title: Vagal nerve stimulation markedly improves long-term survival after chronic heart failure in rats.
abstract: BACKGROUND
  Diminished cardiac vagal activity and higher heart rate predict a high mortality rate of chronic heart failure (CHF) after myocardial infarction. We investigated the effects of chronic electrical stimulation of the vagus nerve on cardiac remodeling and long-term survival in an animal model of CHF after large myocardial infarction.
  
  
  RESULTS
  Two weeks after the ligation of the left coronary artery, surviving rats were randomized to vagal- and sham-stimulated groups. Using an implantable miniature radio-controlled electrical stimulator, we stimulated the right vagal nerve of CHF rats for 6 weeks. The intensity of electrical stimulation was adjusted for each rat, so that the heart rate was lowered by 20 to 30 beats per minute. The treated rats had significantly lower left ventricular end-diastolic pressure (17.1+/-5.9 versus 23.5+/-4.2 mm Hg, P<0.05) and higher maximum dp/dt of left ventricular pressure (4152+/-237 versus 2987+/-192 mm Hg/s, P<0.05) than the untreated rats. Improvement of cardiac pumping function was accompanied by a decrease in normalized biventricular weight (2.75+/-0.25 versus 3.14+/-0.22 g/kg, P<0.01). Although the 140-day survival of the untreated group was only half, vagal stimulation markedly improved the survival rate (86% versus 50%, P=0.008). Vagal stimulation therapy achieved a 73% reduction in a relative risk ratio of death.
  
  
  CONCLUSIONS
  Vagal nerve stimulation markedly improved the long-term survival of CHF rats through the prevention of pumping failure and cardiac remodeling.
authors.affiliation: Department of Cardiovascular Dynamics, Cardiovascular Center Research Institute, Suita, Japan.
authors.forename: Meihua
authors.initials: M
authors.lastname: Li
authors.forename: Can
authors.initials: C
authors.lastname: Zheng
authors.forename: Takayuki
authors.initials: T
authors.lastname: Sato
authors.forename: Toru
authors.initials: T
authors.lastname: Kawada
authors.forename: Masaru
authors.initials: M
authors.lastname: Sugimachi
authors.forename: Kenji
authors.initials: K
authors.lastname: Sunagawa
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D006333:Heart Failure / Q000209:etiology / Q000401:mortality / Q000503:physiopathology* / Q000628:therapy; D006339:Heart Rate / Q000502:physiology; D006352:Heart Ventricles / Q000473:pathology; D008297:Male; D009203:Myocardial Infarction / Q000097:blood / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D020097:Natriuretic Peptide, Brain / Q000097:blood; D009638:Norepinephrine / Q000097:blood; D009929:Organ Size; D011379:Prognosis; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D014630:Vagus Nerve / Q000502:physiology*; D017725:Ventricular Pressure / Q000502:physiology; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D020097:Natriuretic Peptide, Brain; D009638:Norepinephrine