Abnormal atrial function in hypertensive patients with obstructive sleep apnea assessed by speckle tracking echocardiography

Hypertension is a well-known risk factor for heart remodeling and atrial fibrillation, and there is growing interest in exploring the potential role of the influence of obstructive sleep apnea (OSA) in these mechanisms [1]. OSA is characterized by recurrent upper airway obstructions promoting inspiratory efforts against the occluded pharynx and causing abrupt reductions in intrathoracic pressure, which in turn increase left ventricular transmural pressure. Beyond the mechanical response, OSA also triggers recurrent hypoxia, hypercapnia and sleep fragmentation [2]. These OSA components may contribute to promoting blood pressure instability and have a significant impact on heart remodeling over time [3]. More severe forms of OSA are associated with heart remodeling [4] in patients with hypertension. However, the literature evaluating the impact of OSA on the heart structure has limited their analysis to linear measurements and Dopplerderived indexes in transthoracic echocardiography as well as left atrial diameter or left atrial area calculations [4]. In this study, we tested the hypothesis that OSA patients presented impaired left atrial function (LAF) and diastolic dysfunction among hypertensive adults compared with their counterparts. Therefore, the aim of the present study was to investigate the association of LAF in hypertensive adults with and without OSA using two-dimensional speckle tracking echocardiography (2D-STE), a more robust technique for evaluating early signs of heart remodeling. A total of 65 hypertensive patients aged between 30 and 65 years old were recruited. The local Ethics Committee approved the study (CAAE-64411917.2.0000.5192), and all participants gave written informed consent. We excluded patients on dialysis, those not in sinus rhythm, those with frequent ventricular arrhythmia or premature ventricular beats, those with implanted cardiac devices, those with primary valve diseases, coronary artery disease, or heart failure, those with a limited echocardiographic window, and those using continuous positive airway pressure. All patients underwent a portable overnight sleep recording in the sleep laboratory using a validated device (ApneaLinkTM, ResMed, San Diego, CA, USA) to evaluate OSA [5]. Echocardiography was performed with standard equipment (CX-50 Philips Healthcare, Andover, MA, USA). Images were obtained according to current guidelines [6]. The reservoir function of the LA was analyzed by the expansion index: EI= [left atrial volume maximum (LAVmax)− left atrial volume minimum (LAVmin)/ LAVmin] and the total emptying fraction [TEF= (LAVmax− LAVmin)/LAVmax]. The conduit function was evaluated through the passive emptying fraction [PEF= (LAVmax− LAVpreP)/LAVmax]. The LA pump function was analyzed through the active emptying fraction [AEF= (LAVpreP− LAVmin)/LAVpreP [7]. The volumes and diameters of the left atrium and left ventricle were indexed by the body surface area. Left atrial enlargement was defined as LAVmax index >34 mL/m2. LA strain during systole (LAε-S) was obtained immediately before mitral opening (with the QRS complex as reference), strain during late diastole (LAε-A) was obtained at the onset of the P wave of electrocardiography, and LA strain during early diastole (LAε-E) was defined as LAε-S minus LAε-A values. The peak systolic strain rate (LA-SRS), peak early diastolic strain rate (LA-SRE), and peak late diastolic strain rate (LA-SRA) were obtained for the entire traced contour of * Rodrigo P. Pedrosa rppedrosa@terra.com.br