Published ahead of print on March 2, 2006, doi:10.1164/rccm.200503-320OC Am. J. Respir. Crit. Care Med., Volume 173, Number 10, May 2006, 1170-1175 A more recent version of this article appeared on May 15, 2006
Submitted on March 1, 2005 Left Ventricular Structural Adaptations to Obstructive Sleep Apnea in Dilated CardiomyopathyKengo Usui1,1 Sleep Research Laboratory, Toronto Rehabilitation Institute, Toronto, ON, Canada, 2 University Health Network, Toronto General Hospital, Toronto, ON, Canada; Mount Sinai Hospital, Harrowston Heart Failure Clinic, Toronto, ON, Canada, 3 University Health Network, Toronto General Hospital, Toronto, ON, Canada, 4 Sleep Research Laboratory, Toronto Rehabilitation Institute, Toronto, ON, Canada; University Health Network, Toronto General Hospital, Toronto, ON, Canada; Centre for Sleep Medicine and Circadian Biology, University of Toronto, Toronto, ON, Canada * To whom correspondence should be addressed. E-mail: douglas.bradley{at}utoronto.ca.
Rationale and Objectives: 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 non-ischemic 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 ( Key words: heart failure, obstructive sleep apnea, left ventricular hypertrophy
This article has been cited by other articles:
|
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
12 mm), and greater septal thickness than those without obstructive sleep apnea.
Methods and Results: We performed echocardiography and polysomnography in 47 patients with non-ischemic dilated cardiomyopathy. Obstructive sleep apnea was present in 45%. The prevalence of left ventricular hypertrophy was greater in those with, than in those without obstructive sleep apnea (47.6% versus 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 non-ischemic 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.
