title: Augmented peripheral chemosensitivity as a potential input to baroreflex impairment and autonomic imbalance in chronic heart failure.
abstract: BACKGROUND
  The precise mechanisms responsible for the sympathetic overactivity and blunted baroreflex control in chronic heart failure (CHF) remain obscure. Augmented peripheral chemosensitivity has recently been demonstrated in CHF. We evaluated the relation between peripheral chemoreflex sensitivity and autonomic activity in patients with CHF.
  
  
  RESULTS
  We studied in 26 stable patients with CHF the peripheral chemosensitivity (ventilatory response to hypoxia using transient inhalations of pure nitrogen), autonomic balance (spectral analysis of heart rate variability [HRV]), and baroreflex sensitivity (bolus phenylephrine method and alpha index). To determine whether transient inactivation of peripheral chemoreceptors might influence autonomic balance, 12 patients underwent a second study during which they breathed 100% O2. Peripheral chemosensitivity correlated inversely with HRV power within the low-frequency band (0.04 to 0.15 Hz) (r=-.52, P=.006) and inversely with baroreflex sensitivity (r=-.60, P=.005). When the patients were divided into two groups according to the chemosensitivity of age-matched normal controls (above and below mean+2 SDs of chemosensitivity of control subjects), those above the normal range revealed more impaired autonomic balance, ie, lower baroreflex sensitivity (1.4 +/- 1.3 versus 5.0 +/- 1.5 ms/mm Hg, P<.0001) and depressed values of low-frequency power (2.5 +/- 1.8 versus 4.1 +/- 0.8 ln ms2, P<.005) compared with those with normal chemosensitivity. Transient hyperoxia did not alter heart rate or systolic pressure but resulted in an increase in HRV and an improvement in baroreflex sensitivity.
  
  
  CONCLUSIONS
  A link between increased peripheral chemosensitivity and impaired autonomic control, including baroreflex inhibition, is demonstrated. The clinical importance of this phenomenon warrants further investigation.
authors.affiliation: Department of Cardiac Medicine, Imperial College School of Medicine, National Heart and Lung Institute, London, UK.
authors.forename: P
authors.initials: P
authors.lastname: Ponikowski
authors.forename: T P
authors.initials: TP
authors.lastname: Chua
authors.forename: M
authors.initials: M
authors.lastname: Piepoli
authors.forename: D
authors.initials: D
authors.lastname: Ondusova
authors.forename: K
authors.initials: K
authors.lastname: Webb-Peploe
authors.forename: D
authors.initials: D
authors.lastname: Harrington
authors.forename: S D
authors.initials: SD
authors.lastname: Anker
authors.forename: M
authors.initials: M
authors.lastname: Volterrani
authors.forename: R
authors.initials: R
authors.lastname: Colombo
authors.forename: G
authors.initials: G
authors.lastname: Mazzuero
authors.forename: A
authors.initials: A
authors.lastname: Giordano
authors.forename: A J
authors.initials: AJ
authors.lastname: Coats
mesh_terms: D000368:Aged; D001341:Autonomic Nervous System / Q000503:physiopathology*; D017704:Baroreflex; D001794:Blood Pressure; D002311:Cardiomyopathy, Dilated / Q000150:complications / Q000503:physiopathology*; D002628:Chemoreceptor Cells / Q000503:physiopathology*; D005260:Female; D006339:Heart Rate; D006801:Humans; D018496:Hyperoxia / Q000150:complications / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000150:complications / Q000503:physiopathology*