Left atrial dysfunction in patients with obstructive sleep apnea: A combined assessment by speckle tracking and real-time three-dimensional echocardiography

Abstract

Background: At present, little research concerning the assessment of left atrial (LA) dysfunction in patients with obstructive sleep apnea (OSA) using a combined assessment by speckle tracking (STE) and real-time three-dimensional echocardiography (RT3DE) is available. The objective of this study was to evaluate the LA volume and function by STE and RT3DE in patients with OSA. Methods: In our cohort study, ninety-two OSA patients and 50 healthy individuals were enrolled. According to the apnea hypopnea index (AHI), patients (AHI >15/h) classified as having moderate and severe OSA were included. The patients were divided into 2 subgroups according to the left ventricular mass index (LVMI): the left ventricular hypertrophy (LVH) group in which patients had LVH (n=30), and the non-LVH group in which patients did not have LVH (n=62). All subjects underwent LA function assessment by conventional techniques and the combination of STE and RT3DE. Results: OSA patients showed impaired LA global longitudinal strain during early diastole (LA S-E) and systole (LA S-S) but increased LA global longitudinal strain during late diastole (LA S-A) compared with controls (all P<0.05). In addition, OSA patients with LVH had lower LA S-S and LA S-E than patients without LVH (all P<0.05). With regard to parameters obtained from RT3DE, indexed LA maximum, minimum, and preatrial contraction volumes (LAVi-max, LAVi-min, LAVi-preA) and the LA active emptying fraction (LAAEF) were significantly higher, whereas the LA passive emptying fraction (LVPEF) was significantly lower in OSA patients in comparison with controls (all P<0.05). The LA total emptying fraction (LVTEF) and the LA expansion index were significantly lower in OSA patients with LVH than in controls (all P<0.05). Additionally, OSA patients with LVH had higher LAVi-min, LAVi-preA and LAAEVi but lower LAPEF than patients without LVH (all P<0.05). Conclusions: OSA is associated with LA remodeling and dysfunction that occurs in the subclinical stage before the development of LVH and left ventricular diastolic dysfunction, and it will be further aggravated along with the development of LVH and OSA severity. The process can be detected with a detailed evaluation of active and passive functions of the LA using the STE and RT3DE method.