title: Provocation of ventricular ectopy by cheyne-stokes respiration in patients with heart failure.
abstract: OBJECTIVE
  Previous reports have suggested an association between Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) and ventricular ectopy, but there has been relatively little evidence of a cause-effect relationship. The objective of this study was to determine whether CSR-CSA directly provokes ventricular ectopy and, if so, whether it is associated with any particular phase of the CSR-CSA breathing cycle.
  
  
  METHODS
  We compared the frequency of ventricular premature beats (1) between the apneic and hyperpneic phases of CSR-CSA, (2) between periods of CSR-CSA and periods of regular breathing during sleep, and (3) in response to the elimination of CSR-CSA by administration of a low concentration of inhaled CO2.
  
  
  METHODS
  Hospital-based cardiopulmonary sleep laboratory.
  
  
  METHODS
  Twenty-three patients with heart failure and CSR-CSA.
  
  
  RESULTS
  Ventricular premature beats were found to occur 40% more frequently during the hyperpneic phase than the apneic phase of CSR-CSA (mean+/-SD, 7.0+/-7.4 versus 4.9+/-5.7 ventricular premature beats per minute, P = .003). Ventricular premature beat frequency was also found to be higher during periods of CSR-CSA than during periods of regular breathing occurring either spontaneously (median [25th, 75th percentile], 2.2 [1.2, 6.5] versus 1.1 [0.8, 2.0] ventricular premature beats per minute, P = .027), or induced through inhalation of CO2 (from 4.7+/-3.8 to 3.3+/-4.0 ventricular premature beats per minute, P = .048).
  
  
  CONCLUSIONS
  CSR-CSA provokes ventricular ectopy that is most pronounced during the hyperpneic phase. Such an increase in ventricular premature beats might contribute to the higher mortality rates reported in heart failure patients with CSR-CSA.
authors.affiliation: University of Toronto Centre for Sleep Medicine and Circadian Biology, Ontario, Canada.
authors.forename: Richard S T
authors.initials: RS
authors.lastname: Leung
authors.forename: Tung M
authors.initials: TM
authors.lastname: Diep
authors.forename: Michael E
authors.initials: ME
authors.lastname: Bowman
authors.forename: Geraldo
authors.initials: G
authors.lastname: Lorenzi-Filho
authors.forename: T Douglas
authors.initials: TD
authors.lastname: Bradley
mesh_terms: D000368:Aged; D001143:Arousal / Q000502:physiology; D002245:Carbon Dioxide / Q000097:blood; D002423:Cause of Death; D002639:Cheyne-Stokes Respiration / Q000150:complications / Q000401:mortality / Q000503:physiopathology; D004562:Electrocardiography; D005260:Female; D006333:Heart Failure / Q000150:complications* / Q000401:mortality / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010102:Oxygen Inhalation Therapy; D017286:Polysomnography; D012307:Risk Factors; D012894:Sleep Stages / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000401:mortality / Q000503:physiopathology; D018879:Ventricular Premature Complexes / Q000209:etiology* / Q000401:mortality / Q000503:physiopathology
chemical_list: D002245:Carbon Dioxide