Sleep apnea syndrome (SAS) in patients with chronic heart failure (CHF) increases the risk of death. SAS was divided into 4 types: obstructive sleep apnea-hypopnea syndrome (OSAHS), upper airways resistance syndrome (UARS), central sleep apnea syndrome (CSAS), and sleep hypoventilation syndrome (SHVS). CSAS is caused by temporary cessation of central drive to respiratory muscles, OSAHS results from partial or complete collapse of the pharynx, UARS have typical symptoms of OSAHS and no changes on polysomnography, whereas SHVS results from pathological PCO2 increase with subsequent hypoxemia. Increase in sympathetic activity, renin-angiotensin-aldosterone activation, impaired baroreflex and tonic vagal heart rate control are markers of increased risk of sudden death. CSAS is frequent in patients with CHF. Decreased cardiac output causes delayed transmission of changes in arterial blood gas tensions from the lungs to the chemoreceptors. Increase chemoreceptor sensitivity results from hypoxia and pulmonary congestion. Both types of apneas (OSAHS and CSAS) may occur in the same patient. Periodic cessation in central drive to respiratory muscles (CSAS) causes obstructive apneas/hypopneas by decreased tone of pharyngeal muscles and their collapse. Obstructive apneas (OSAHS) may lead to central apneas by frequent arousals, decreased left ventricular function and prolongation of circulation. Treatment of SAS is based on improvement of cardiovascular function, nocturnal supplementation of O2 and various forms of noninvasive positive airway pressure (i.e. CPAP).