title: Continuous positive airway pressure intolerance associated with elevated nasal resistance is possible mechanism of complex sleep apnea syndrome.
abstract: OBJECTIVE
  Complex sleep apnea syndrome (CompSAS) is diagnosed after an elimination of obstructive events with continuous positive airway pressure (CPAP), when a central apnea index ≥5/h or Cheyne-Stokes respiration pattern emerges in patients with obstructive sleep apnea syndrome (OSAS). However, the pathophysiology of CompSAS remains controversial.
  
  
  METHODS
  Of the 281 patients with suspected OSAS, all of whom underwent polysomnography conducted at Nagoya University Hospital, we enrolled 52 patients with apnea-hypopnea index ≥15/h (age 51.4 ± 13.3 years). The polysomnographic findings, left ventricular ejection fraction (LVEF), and nasal resistance were compared between the CompSAS patients and OSAS patients.
  
  
  RESULTS
  Forty-three patients were diagnosed with OSAS and nine patients with central sleep apnea syndrome by natural sleep PSG. Furthermore, 43 OSAS patients were classified into the OSAS patients (OSAS group, n = 38) and the CompSAS patients (CompSAS group, n = 5) by the night on CPAP PSG. The nasal resistance was significantly higher in CompSAS group than in OSAS group (0.30 ± 0.10 vs. 0.19 ± 0.07 Pa/cm(3)/s, P = 0.004). The arousal index, percentage of stage 1 sleep, and oxygen desaturation index were significantly decreased, and the percentage of stage REM sleep was significantly increased in the OSAS group with the initial CPAP treatment, but not in the CompSAS group. In addition, the patients with CompSAS showed normal LVEF.
  
  
  CONCLUSIONS
  CPAP intolerance secondary to an elevated nasal resistance might relate to frequent arousals, which could presumably contribute to an increase in central sleep apnea. Further evaluation in a large study is needed to clarify the mechanism of CompSAS.
authors.affiliation: Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
authors.forename: Chie
authors.initials: C
authors.lastname: Nakazaki
authors.forename: Akiko
authors.initials: A
authors.lastname: Noda
authors.forename: Yoshinari
authors.initials: Y
authors.lastname: Yasuda
authors.forename: Seiichi
authors.initials: S
authors.lastname: Nakata
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Koike
authors.forename: Fumihiko
authors.initials: F
authors.lastname: Yasuma
authors.forename: Toyoaki
authors.initials: T
authors.lastname: Murohara
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Nakashima
mesh_terms: D000328:Adult; D000368:Aged; D000403:Airway Resistance / Q000502:physiology*; D001143:Arousal / Q000502:physiology; D002639:Cheyne-Stokes Respiration / Q000175:diagnosis / Q000503:physiopathology*; D045422:Continuous Positive Airway Pressure / Q000009:adverse effects*; D004452:Echocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015508:Nasal Obstruction / Q000150:complications* / Q000175:diagnosis / Q000503:physiopathology*; D010100:Oxygen / Q000097:blood; D017286:Polysomnography; D012891:Sleep Apnea Syndromes / Q000175:diagnosis / Q000503:physiopathology* / Q000628:therapy*; D020182:Sleep Apnea, Central / Q000175:diagnosis / Q000503:physiopathology*; D020181:Sleep Apnea, Obstructive / Q000175:diagnosis / Q000503:physiopathology* / Q000628:therapy*; D012895:Sleep, REM / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology
chemical_list: D010100:Oxygen