Abstract 19921: Influence of Obstructive Sleep Apnea in the Clinical Presentation of Acute Coronary Syndrome: Bedside Polysomnography Study
Introduction: Obstructive Sleep Apnea (OSA) is characterized by sleep fragmentation and repetitive hypoxia during sleep and has been associated with arterial hypertension, atrial fibrillation, coronary artery disease, and cardiovascular mortality. OSA has also been extensively linked with atherogenesis.
Hypothesis: We sought to evaluate the role of OSA on clinical and angiographic patterns in patients admitted with acute coronary syndrome (ACS).
Methods: Patients who were admitted with ACS in intensive care unit (ICU), aged over 20 years old, and with no previous diagnosis or treatment for OSA were consecutively selected between June 2013 and June 2014. A bedside overnight full polysomnography (PSG) was performed using an EMBLA digital system® within second day of admission. All patients underwent transthoracic echocardiogram. The time between pain onset and treatment (TPT) were obtained for all patients. The sample was divided into 3 groups: G1: non OSA; G2: mild to moderate OSA and G3: severe OSA according to the apnea/hypopnea index (AHI) obtained by PSG recordings. All patients signed an informed consent form. ANOVA and GLM followed by Bonferroni test were used, p<0.05.
Results: One hundred twenty ACS patients, 58 ± 12 y were included. Seventy-seven% underwent pharmacoinvasive strategy and 23% to primary percutaneous coronary angioplasty. Age and BMI were higher in G3 (p<0.05). The TPT and left ventricle ejection fraction were different between G1, G2 and G3 [(241.44±186.43; 202.13±132.54; 400.5±469.01), p=0.02] and [(51.29±8.95; 50.82±10.57; 45.25±7.44), p=0.04], respectively. After controlling for potential confounder, AHI was independently associated with delay in the onset treatment (p=0.004). The Syntax score was higher in G3 compared with G2 and G1 [(14.15±10.19; 14.46±11.09; 21.33±10.42), p=0.03], respectively.
Conclusion: In ACS patients, severe OSA was associated with more complex coronary artery disease at hospital presentation, lower left ventricle ejection fraction., as well as in the delay of onset of treatment.
Author Disclosures: F.D. Cintra: None. F.U. Maroja: None. A. de Paola: None. L. Storti: None. A.M. Caixeta: None. A.G. Leoncio: None. A.C. Carvalho: None. S. Tufik: None. D. Poyares: None.
- © 2015 by American Heart Association, Inc.