Obstructive Sleep Apnea in Heart Failure: Review of Prevalence, Treatment with Continuous Positive Airway Pressure, and Prognosis

Abstract

Obstructive sleep apnea is a sleep-related breathing disorder that has a major impact on cardiovascular function. It has been associated with hypertension, coronary artery disease, cardiac arrhythmias, sudden cardiac death, and heart failure. This review focuses on the relationship between obstructive sleep apnea and heart failure with either reduced or preserved ejection fraction. We discuss the pathophysiology of obstructive sleep apnea, as well as its prevalence, treatment outcomes with continuous positive airway pressure, and prognosis in these 2 distinct types of heart failure. We also identify areas in which further work is needed to improve our understanding of this association in heart failure patients.

Keywords: Continuous positive airway pressure/methods; heart diseases/epidemiology/etiology; heart failure/complications/therapy; prevalence; risk factors; sleep apnea syndromes/classification/physiopathology; sleep apnea, obstructive/complications/prevention & control/therapy; treatment outcome; ventricular function.

Fig. 1

Diagram shows pathophysiologic mechanisms by which obstructive sleep apnea affects cardiovascular function and heart failure. Modified with permission from Mann DL. Heart failure: a companion to Braunwald's heart disease. Philadelphia: Elsevier; 2011. p. 484. BP = blood pressure; HF = heart failure; HR = heart rate; LV = left ventricular; LVH = left ventricular hypertrophy; PNA = parasympathetic nervous system activity; RV = right ventricular; RVH = right ventricular hypertrophy; SNA = sympathetic nervous system activity; SV = stroke volume; VR = venous return

Fig. 2

Graph shows prevalence of obstructive sleep apnea (OSA) in studies of patients with heart failure and reduced ejection fraction. Authors used Apnea-Hypopnea Index (AHI) cutoffs of ≥15 events/hr (Yumino D, et al.; Vazir A,* et al.; Javaheri S, et al.; and Sin DD, et al.37), ≥10 events/hr (Ferrier K, et al.; and Schulz R, et al.39), and ≥5 events/hr (Herrscher T, et al.; and Oldenburg O, et al.42). Unattended overnight cardiorespiratory polygraphy was used in hospital, and home sleep studies; otherwise, overnight-attended polysomnography was used. One study was retrospective; the others were prospective. Because of patient overlap between 2 studies,, one is not included here. Figure adapted with permission from Kasai T, Bradley TD. J Am Coll Cardiol 2011;57(2):119–27. *Vazir A, et al. inconsistently refer to >15 and ≥15 AHI cutoffs.