Obstructive Sleep Apnea and Heart Failure: Pathophysiologic and Therapeutic Implications

• Published in: Journal of the American College of Cardiology Vol. 57; no. 2; pp. 119 - 127
• Main Authors: KASAI, Takatoshi, BRADLEY, T. Douglas
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier 11.01.2011; Elsevier Limited
• Subjects: Biological and medical sciences; Cardiology; Cardiology. Vascular system; Disease Progression; Heart; Heart failure; Heart Failure - etiology; Heart Failure - physiopathology; Heart Failure - prevention & control; Heart failure, cardiogenic pulmonary edema, cardiac enlargement; Humans; Legs; Medical sciences; Morbidity; Mortality; Myocardial Contraction - physiology; Pneumology; Positive-Pressure Respiration - methods; Respiratory system : syndromes and miscellaneous diseases; Sleep apnea; Sleep Apnea, Obstructive - complications; Sleep Apnea, Obstructive - physiopathology; Sleep Apnea, Obstructive - therapy; Sleep disorders; Sympathetic Nervous System - physiopathology; Systole; Ventricular Function, Left; Heart failure; Nervous system diseases; Sleep apnea syndrome; Treatment; Respiratory disease; Heart disease; Cardiovascular disease; Circulatory system; Cardiology
• ISSN: 0735-1097; 1558-3597; 1558-3597
• DOI: 10.1016/j.jacc.2010.08.627

Obstructive sleep apnea (OSA) exposes the cardiovascular system to intermittent hypoxia, oxidative stress, systemic inflammation, exaggerated negative intrathoracic pressure, sympathetic overactivation, and elevated blood pressure (BP). These can impair myocardial contractility and cause development and progression of heart failure (HF). Epidemiological studies have shown significant independent associations between OSA and HF. On the other hand, recent prospective observational studies reported a significant association between the presence of moderate to severe OSA and increased risk of mortality in patients with HF. In randomized trials, treating OSA with continuous positive airway pressure suppressed sympathetic activity, lowered BP, and improved myocardial systolic function in patients with HF. These data suggest the potential for treatment of OSA to improve clinical outcomes for patients with HF. However, large-scale randomized trials with sufficient statistical power will be needed to ascertain whether treatment of OSA will prevent development of, or reduce morbidity and mortality from HF.