title: Left ventricular structural adaptations to obstructive sleep apnea in dilated cardiomyopathy.
abstract: OBJECTIVE
  Obstructive sleep apnea is common among patients with heart failure and exposes the left ventricle to trophic mechanical and adrenergic stimuli. We hypothesized that in heart failure patients with nonischemic dilated cardiomyopathy (a condition characterized by eccentric hypertrophy), those with obstructive sleep apnea would have a higher prevalence of left ventricular hypertrophy by wall thickness criteria (> or = 12 mm), and greater septal thickness than those without obstructive sleep apnea.
  
  
  RESULTS
  We performed echocardiography and polysomnography in 47 patients with nonischemic dilated cardiomyopathy. Obstructive sleep apnea was present in 45% of these patients. The prevalence of left ventricular hypertrophy was greater in those with than in those without obstructive sleep apnea (47.6 vs. 15.4%, p = 0.016). Interventricular septal thickness (p < 0.001) and relative wall thickness (p = 0.011) were significantly greater in those with than in those without obstructive sleep apnea. However, there was no significant difference in posterior wall thickness between the groups. The frequency of obstructive apneas and hypopneas during sleep was the only significant independent correlate of septal thickness (p = 0.001).
  
  
  CONCLUSIONS
  In patients with nonischemic dilated cardiomyopathy, the presence of obstructive sleep apnea is associated with an increased prevalence of left ventricular hypertrophy. The higher relative wall thickness and interventricular septal thickness in patients with obstructive sleep apnea indicate that the left ventricle is relatively less eccentric than in patients without obstructive sleep apnea, and that such remodeling affects mainly the septum. These structural adaptations may reflect unique nocturnal mechanical and adrenergic stimuli associated with obstructive sleep apnea.
authors.affiliation: Toronto General Hospital/UHN, 9N-943, 200 Elizabeth Street, Toronto, ON, M5G 2C4 Canada. douglas.bradley@utoronto.ca.
authors.forename: Kengo
authors.initials: K
authors.lastname: Usui
authors.forename: John D
authors.initials: JD
authors.lastname: Parker
authors.forename: Gary E
authors.initials: GE
authors.lastname: Newton
authors.forename: John S
authors.initials: JS
authors.lastname: Floras
authors.forename: Clodagh M
authors.initials: CM
authors.lastname: Ryan
authors.forename: T Douglas
authors.initials: TD
authors.lastname: Bradley
mesh_terms: D000222:Adaptation, Physiological; D000328:Adult; D017677:Age Distribution; D000368:Aged; D002311:Cardiomyopathy, Dilated / Q000000981:diagnostic imaging* / Q000453:epidemiology*; D016022:Case-Control Studies; D015897:Comorbidity; D015150:Echocardiography, Doppler; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000453:epidemiology*; D015994:Incidence; D008297:Male; D008875:Middle Aged; D017286:Polysomnography; D015995:Prevalence; D011336:Probability; D011379:Prognosis; D011446:Prospective Studies; D012016:Reference Values; D018570:Risk Assessment; D012720:Severity of Illness Index; D017678:Sex Distribution; D020181:Sleep Apnea, Obstructive / Q000175:diagnosis* / Q000453:epidemiology*