Prognosis and sleep disordered breathing in heart failure.

Abnormal breathing in heart failure as originally described by Cheyne and subsequently by Stokes was observed in apparently awake patients as an agonal breathing pattern. “. . . The only peculiarity in the last period of his illness was in the state of the respiration. For several days his breathing was irregular, then it would become perceptible, though very low, then by degrees it became heaving and quick, and then it would cease again: this revolution in the state of his breathing occupied about a minute, during which there were about 30 acts of respiration (Cheyne, 1818) . . .” The patient described in this report was an obese, elderly, alcoholic who had suVered a substantial, and ultimately, fatal stroke. He probably had obstructive sleep apnoea prior to the stroke and developed central apnoea subsequently. In the literature subsequent to these reports periodic respiration associated with central apnoeas was believed to be a terminal consequence of end stage heart failure. More recently it has been recognised that central apnoeas occur commonly in heart failure, especially during sleep, being reported in 40–50% of patients, predominantly men, with stable, medically treated congestive heart failure. This sleep breathing abnormality leads to sleep fragmentation, alterations in sleep architecture—with relative increases in stage 1 and 2 sleep and reduction in REM sleep—and a clinical sleep disorder with symptoms of tiredness and sleepiness in some patients. The sleep disorder in central sleep apnoea is a consequence of the development of congestive heart failure. Although the pathophysiology is not completely understood, hyperventilation, increased chemoreceptor drive, and increased circulation time 10 11 are all believed to be important factors promoting this sleep disorder. Identification of obstructive sleep apnoea (OSA) in patients with primarily left ventricular (LV) dysfunction and clinical heart failure is a more recent observation. Pulmonary hypertension and consequent right heart failure (cor pulmonale) is well recognised to be part of the combination of obesity, hypoventilation, and severe obstructive sleep apnoea. Malone et al reported a group of patients with a clinical presentation with dilated cardiomyopathy and obstructive sleep apnoea in whom treatment with nasal continuous positive airway pressure (CPAP) was associated with improvements in symptoms of dyspnoea and left ventricular ejection fraction. These, and subsequent observations, have suggested that OSA and heart failure is an adverse combination in which OSA causes or exacerbates left ventricular dysfunction. The disease process responsible for congestive heart failure has been reported to vary, with valvular and hypertensive heart disease being more common in earlier reports. Currently, dilated cardiomyopathy and coronary heart disease account, in approximately equal proportions, for most of the patients with end stage heart failure awaiting cardiac transplantation. The survival of patients who present with congestive heart failure is poor, with reported mortality rates of 50% at 12 months in those with severe symptoms and 50% at 3–4 years in those with less severe heart failure, a prognosis which is similar to that of many patients with malignancy. Prognostic factors in patients with end stage congestive heart failure include haemodynamic (cardiac output, pulmonary vascular resistance), neurohumoral (increased sympathetic nerve activity), electrophysiological (spontaneous ventricular tachycardia), and treatment factors (converting enzyme inhibitors, â blockers). Sleep disordered breathing has not been regarded as a prognostic factor in heart failure previously, although there is increasing evidence to suggest that it may be (table 1).