Right heart function in obstructive sleep apnea syndrome by three-dimensional echocardiography and speckle tracking echocardiography

Purpose. It is known that obstructive sleep apnea syndrome (OSAS) can affect right ventricular (RV) performance even in the absence of systemic hypertension and other known cardiac or obstructive pulmonary disease. We assessed changes in ventricular parameters determined by three-dimensional echocardiography (3DE) and speckle tracking imaging (STI) before and after continuous positive airway pressure (CPAP) treatment. Methods. We recruited 31 patients with OSAS and 31 healthy subjects without signs of cardiopulmonary dysfunction. OSAS was defined as apnea hypopnea index (AHI) ≥5 events per hour. Twelve patients with severe OSAS (AHI≥30) underwent chronic nocturnal nasal CPAP therapy. RV end-diastolic and end-systolic volumes were measured from three-dimensional echocardiographic datasets and right ventricular ejection fraction (3D-RVEF) was calculated. Pulmonary arterial systolic pressure was obtained by standard Doppler methods. Pulmonary hypertension was defined as a pulmonary artery systolic pressure of 40 mmHg or greater. To assess regional and global RV systolic function in the longitudinal direction using STI, we adopted a 6-segment RV model (basal RV lateral wall, mid RV lateral wall, apical RV wall, apical septum, mid septum, and basal septum). RV peak systolic strain and time to peak-systolic strain from the onset of QRS were recorded for the 6 RV myocardial segments and for the entire RV myocardium (EchoPAC BT09, GE Ultrasound). Global longitudinal strain was calculated by averaging local strains along the entire right ventricle using machine software. RV dyssynchrony (RV-SD6) was defined as the standard deviation of the six time to peak systolic strain values. Results. 3D-RVEF was lower in patients with OSAS and pulmonary hypertension compared to the control group (p<0.001) and compared to patients with OSAS and normal pulmonary pressure (p<0.05). A significant correlation was found between RV-SD6 and pulmonary artery systolic pressure (r = 0.74, p <0.005) and between RV-SD6 and AHI (r = 0.77, p <0.001). The group treated with CPAP had a significant decrease in pulmonary artery systolic pressure, total pulmonary vascular resistance and RV-SD6 as well as significant increase in 3D-RVEF. By multivariate analysis, RV-SD6 (p=0.006) and 3D-RVEF (p=0.03) were predictive of AHI

Left ventricular torsion abnormalities in patients with obstructive sleep apnea syndrome: an early sign of subclinical dysfunction

BACKGROUND: Previous echocardiographic studies using tissue Doppler imaging (TDI) and speckle tracking imaging (STI) have demonstrated that obstructive sleep apnea syndrome (OSAS) patients may develop subclinical left ventricular (LV) systolic and diastolic dysfunction. Our purpose was to evaluate the impact of OSAS on LV torsion dynamics and aortic stiffness by using TDI and STI echocardiography. METHODS: Forty-two patients with OSAS and no comorbidities were studied. They were classified into mild and severe OSAS according to the apnea-hypopnea index (AHI). Thirty-five healthy subjects were selected as controls. Fifteen patients with severe OSAS underwent chronic nocturnal nasal continuous positive airway pressure (CPAP) therapy. Standard echocardiographic parameters were assessed. Global LV longitudinal strain (LS), radial and circumferential strain were determined by STI. Averaged LV rotation and rotational velocities from the base and apex were obtained and used for calculation of LV torsion (LVtor). Mitral annular velocities and aortic wall velocities and strain (AoS) were also obtained by TDI. RESULTS: Severe OSAS had decreased LS compared with control subjects. LVtor increased significantly in severe OSAS compared to normals (p<.001) as a result of a predominant increase in apical rotation and was independently related to AHI and AoS in a multiple stepwise linear regression model. The group treated with CPAP had a significant decrease in LVtor and aortic stiffness index and significant increase in LS and AoS. CONCLUSIONS: LVtor, LS and AoS were identified as parameters demonstrating an association between LV dysfunction, aortic stiffness and severity of OSAS independently of other possible factors or comorbidities