|
|
||||||||
1 Pulmonary Dept, Athens University Medical School, 2 Nuclear Medicine Dept, and 3 Cardiology Department, "Sotiria" Hospital for Chest Diseases, Athens, Greece
CORRESPONDENCE: M. Alchanatis, 10 Mpakopoulou Str., 15451, Athens, Greece. Fax: 30 107770423. E-mail: enkosmas@mland.gr
Keywords: cardiovascular disease, continuous positive airway pressure, ejection fraction, left ventricular function, obstructive sleep apnoea
Received: September 6, 2001
Accepted June 11, 2002
There is limited information on the development of left ventricular (LV) dysfunction in patients with obstructive sleep apnoea (OSA) in the absence of lung and cardiac comorbidity. This study aimed to investigate whether OSA patients without heart morbidity develop LV dysfunction, and to assess the effect of continuous positive airway pressure (CPAP) on LV function.
Twenty-nine OSA patients and 12 control subjects were studied using technetium-99m ventriculography to estimate LV ejection fraction (LVEF), LV peak emptying rate (LVPER), time to peak emptying rate (TPER), peak filling rate (LVPFR) and time to peak filling rate (TPFR) before and after 6 months of treatment with CPAP.
A significantly lower LVEF was found in OSA patients, compared to control subjects, (53±7 versus 61±6%) along with a reduced LVPER (2.82±0.58 versus 3.82±0.77 end-diastolic volumes·s1). Furthermore, OSA patients had significantly lower LVPFR (2.67±0.71 versus 3.93±0.58 end-diastolic volumes·s1) and delayed TPFR (0.19±0.04 versus 0.15±0.03 s) in comparison with the control group. Six-months of CPAP treatment was effective in significantly improving LVEF, LVPER, LVPFR and TPFR.
In conclusion, obstructive sleep apnoea patients without any cardiovascular disease seem to develop left ventricular systolic and diastolic dysfunction, which may be reversed, either partially or completely, after 6 months of continuous positive airway pressure treatment.
This article has been cited by other articles:
![]() |
J. A. Simpson, K. R. Brunt, and S. Iscoe Repeated inspiratory occlusions acutely impair myocardial function in rats J. Physiol., May 1, 2008; 586(9): 2345 - 2355. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Hayashi, C. Yamashita, C. Matsumoto, C.-J. Kwak, K. Fujii, T. Hirata, M. Miyamura, T. Mori, A. Ukimura, Y. Okada, et al. Role of gp91phox-containing NADPH oxidase in left ventricular remodeling induced by intermittent hypoxic stress Am J Physiol Heart Circ Physiol, May 1, 2008; 294(5): H2197 - H2203. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. Parati, C. Lombardi, and K. Narkiewicz Sleep apnea: epidemiology, pathophysiology, and relation to cardiovascular risk Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2007; 293(4): R1671 - R1683. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Alonso-Fernandez, F. Garcia-Rio, M. A. Arias, O. Mediano, J. M. Pino, I. Martinez, and J. Villamor Obstructive sleep apnoea-hypoapnoea syndrome reversibly depresses cardiac response to exercise Eur. Heart J., January 2, 2006; 27(2): 207 - 215. [Abstract] [Full Text] [PDF] |
||||
![]() |
L J Cormican and A Williams Sleep disordered breathing and its treatment in congestive heart failure Heart, October 1, 2005; 91(10): 1265 - 1270. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. A. Arias, F. Garcia-Rio, A. Alonso-Fernandez, O. Mediano, I. Martinez, and J. Villamor Obstructive Sleep Apnea Syndrome Affects Left Ventricular Diastolic Function: Effects of Nasal Continuous Positive Airway Pressure in Men Circulation, July 19, 2005; 112(3): 375 - 383. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. R. Mansfield, N. C. Gollogly, D. M. Kaye, M. Richardson, P. Bergin, and M. T. Naughton Controlled Trial of Continuous Positive Airway Pressure in Obstructive Sleep Apnea and Heart Failure Am. J. Respir. Crit. Care Med., February 1, 2004; 169(3): 361 - 366. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |