Left Ventricular Systolic and Diastolic Function in Obstructive Sleep Apnea: Impact of Continuous Positive Airway Pressure Therapy
Background—Previous studies in obstructive sleep apnoea (OSA) were limited by study cohorts with co-morbidities which confound assessment of left ventricular (LV) systolic and diastolic function. We comprehensively evaluated LV function using two dimensional echocardiography (2DE), tissue Doppler imaging (TDI) and three dimensional echocardiography (3DE) in subjects moderate-severe OSA, who were compared to 'disease' (patients with hypertension, no OSA) and 'healthy' controls.
Methods and Results—A total of 120 subjects (n=40 each of matched OSA, hypertension and healthy cohorts) underwent echocardiographic examination for the assessment of septal and posterior wall thickness, LV mass index, LV volumes and ejection fraction, mitral valve inflow indices (E, A), mitral annular velocity (S, E') and left atrial volume index (LAVI). OSA subjects were treated with CPAP (mean duration of 26 weeks) following which the echocardiographic parameters were reassessed. Posterior wall thickness and LV mass index were significantly higher in OSA and hypertensive groups compared to healthy. Systolic 'S' velocity was reduced in OSA and hypertensive compared to healthy (P<0.05). Diastolic function (E/A, IVRT and E/E') was impaired in both OSA and hypertensive groups. On 3DE, mean LAVI was significantly greater in OSA and hypertensive compared to healthy. In OSA patients, CPAP therapy resulted in reduction of the posterior wall thickness (p=0.02) and improvement in LV ejection fraction (p<0.05), systolic 'S' velocity (p<0.05) and diastolic LV impairment parameters.
Conclusions—Moderate to severe OSA causes structural and functional changes in LV function and are comparable to that seen in hypertension. These abnormalities significantly improve following CPAP therapy.
- systolic function
- continuous positive airway pressure
- diastolic function
- left ventricle
- obstructive sleep apnea
- Received August 1, 2011.
- Accepted January 11, 2012.
- Copyright © 2012, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited