ABC | Volume 111, Nº3, September 2018

Original Article Medeiros et al Obstructive sleep apnea in chagas disease Arq Bras Cardiol. 2018; 111(3):364-372 from August 2013 to August 2014. Chagas cardiomyopathy was diagnosed in patients with serological evidence of antibodies to T. cruzi and evidence of Chagas heart disease who may or may not have cardiac symptoms (such as dyspnea, edema, and chest pain). The indeterminate form of CD was diagnosed in patients with serological and/or parasitological evidence of T. cruzi infection who lacked symptoms, physical signs, electrocardiographic abnormalities and any radiographic evidence (on chest radiography, barium-contrast esophageal, or colon radiography) of cardiac or gastrointestinal involvement. 9 Patients with cardiac pacemakers, manifest or suspected coronary disease; decompensated heart failure requiring hospital admission, predominant central sleep apnea (>50% of events scored as central), or renal disease (serum creatinine >2mg/dL), as well as those with a previous stroke were excluded. Patients were invited to undergo the sleep study in the week after they underwent all examinations, including echocardiography, Ambulatory Blood Pressure Monitoring (ABPM) and 24-hour Holter monitoring as described below. Sleep Study All patients underwent portable sleep monitoring in the sleep laboratory using a validated device (Embletta Gold, PDS; Medcare, Reykjavik, Iceland) 10 to evaluate oxygen saturation, body position, nasal flow measurements (pressure cannula), and respiratory effort measurements using two respiratory inductance plethysmography belts. All exams were scored by an experienced physician. Apnea was defined as total absence (>90%) and hypopneas as a decrease (>30%) in nasal flow for ≥ 10 seconds, followed by a 4% desaturation (in hypopneas), respectively. 11 The apnea-hypopnea index (AHI) was calculated by dividing the total number of apnea and hypopnea events by the total hours in bed. 11,12 Mild OSA was defined by an AHI between 5 and 14.9 events/h and moderate to severe OSA was considered when the AHI was ≥ 15 events/h. The oxygen desaturation index (ODI) was calculated as the total number of desaturations, divided by the total time in bed. Excessive daytime sleepiness was evaluated using the Epworth Sleepiness Scale. A total score > 10 was considered excessive daytime somnolence. 13 Office blood pressure Blood pressure (BP) was measured after 5 min of rest using standard protocols. 14 The average of two readings was obtained at 5 min intervals with an automatic digital sphygmomanometer (Omron BP742). Ambulatory Blood Pressure Monitoring (ABPM) All participants underwent blood pressure monitoring for 24 hours, using SpaceLabs equipment (model 90207; SpaceLabs, Redmond, WA). The BP reading was taken every 10 minutes during the day and every 20 minutes at night, using an appropriate cuff placed on the non-dominant arm. Participants were instructed to perform their ordinary daily activities and not to move their arm during the ongoing measurement. Activity, bedtime, and time on awakening from sleep were recorded by participants in diaries. 15 The normal BP dip was defined separately for systolic and diastolic BP as a ≥ 10% reduction in BP during sleep compared with the awake period. Nondipping was defined as a decrease of < 10%. Holter monitoring Holter monitoring (Cardios®, Cardio Systems, São Paulo, Brazil) was performed in all patients for 24 hours. The following characteristics of the ECGwere analyzed: baseline heart rhythm, heart rate, ventricular and atrial arrhythmias, and breaks. The complexities of the arrhythmias were described as follows: isolated, paired, or tachycardia. 16 Patients were instructed to keep a diary with their symptoms during the exam. The Holter analysis was performed by an experienced observer, who was blinded to the presence or absence of OSA. Echocardiogram A transthoracic echocardiogram was performed using a Philips IE33 S5-1 device. Conventional M-mode echocardiography was used to measure cavity dimensions (diastolic and systolic diameters, wall thickness, and aorta and left atrial size). 17 Left atrial volumes were indexed by body surface area according to the American Society of Echocardiography. 18 Using two-dimensional echocardiography, segmental and global contractility were assessed, and the left ventricular ejection fraction (LVEF) was calculated using Simpson's formula. Ventricular dysfunction was considered when LVEF <50%. 18 Le ft ventricular longitudinal strain with speckle-tracking was calculated and values below –16% were considered abnormal. 19 The Echocardiographic evaluation was performed by the same experienced observer, who was blinded to the presence or absence of OSA. Statistical analysis Normality distribution was evaluated with the Kolmogorov- Smirnov test. For the categorical variables, the Chi-square test of Pearson was used. Quantitative variables with a normal distribution were presented as mean and standard deviation and the ANOVA test was used, whereas the variables without normal distribution were presented as median and percentiles (P25; P75) and the Kruskal-Wallis was used, with Bonferroni post‑hoc test, when appropriate. A multiple linear regression analysis was performed to evaluate independent predictors of left atrial dimensions. The independent variables of the left atrial dimensions were age, 24-hour systolic BP, body mass index (BMI), and AIH. Due to the non-normality of the AHI, a log-transformed version of this variable was used in the multivariate model. To analyze the predictors of ventricular dysfunction, a multiple logistic regression analysis was performed with the following variables: age, BMI, male gender, 24-hour systolic BP, diabetes mellitus diagnosis, AHI ≥15 events/h, ODI, and saturation < 90%. The data were analyzed with SPSS 21.0 statistical software (IBM Corporation) and a value of p < 0.05 was considered significant. 365