title: Parasympathetic withdrawal is an integral component of autonomic imbalance in congestive heart failure: demonstration in human subjects and verification in a paced canine model of ventricular failure.
abstract: Although enhanced sympathetic tone is a well recognized component of the autonomic profile characteristic of congestive heart failure, the contribution of parasympathetic withdrawal to this autonomic imbalance is less well described. The technique of spectral analysis of heart rate variability provides a dynamic map of sympathetic and parasympathetic tone and was thus used to define the nature of sympathetic-parasympathetic interactions in humans with idiopathic dilated cardiomyopathy and in a paced canine model of congestive heart failure. Humans with cardiomyopathy were found to have an augmentation of the sympathetically mediated low frequency area of the power density spectrum. Parasympathetic withdrawal was demonstrated by significant reductions in the parasympathetically mediated high frequency area (p less than 0.05) and the ratio of high to low frequency areas (p less than 0.01). Administration of atropine to normal subjects resulted in a significant reduction in the high frequency area (p less than 0.05) and the high/low frequency area ratio, both of which decreased within the range noted in patients with congestive heart failure. Administration of isoproterenol in normal subjects led to an augmentation of the low frequency area but to only a small decrease in the high/low frequency area ratio. Induction of congestive heart failure in a paced canine model resulted in alterations in the autonomic profile that resembled those seen in humans with ventricular failure. The prominent high frequency region of the spectrum at baseline, indicating a predominance of parasympathetic tone, was absent after the evolution of congestive heart failure, and there was a marked augmentation of the low frequency region of the spectrum.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Medicine, Ohio State University, Columbus 43210.
authors.forename: P F
authors.initials: PF
authors.lastname: Binkley
authors.forename: E
authors.initials: E
authors.lastname: Nunziata
authors.forename: G J
authors.initials: GJ
authors.lastname: Haas
authors.forename: S D
authors.initials: SD
authors.lastname: Nelson
authors.forename: R J
authors.initials: RJ
authors.lastname: Cody
mesh_terms: D000328:Adult; D000818:Animals; D001285:Atropine; D002304:Cardiac Pacing, Artificial; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology*; D004285:Dogs; D004562:Electrocardiography; D005260:Female; D006333:Heart Failure / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D007545:Isoproterenol; D008297:Male; D008875:Middle Aged; D010275:Parasympathetic Nervous System / Q000503:physiopathology*; D012815:Signal Processing, Computer-Assisted; D013564:Sympathetic Nervous System / Q000503:physiopathology*
chemical_list: D001285:Atropine; D007545:Isoproterenol