Cheyne-Stokes respiration can appear during sleep in patients with chronic heart failure and is generally attributed to a tendency to hyperventilate causing PCO2 to fall below the apnea threshold. We recorded sleep pattern and nocturnal arterial oxygen desaturation during Cheyne-Stokes respiration and correlated those with hemodynamic alterations, in order to investigate their possible role in the evolution of chronic heart failure. Sixty chronic heart failure patients, after optimization of therapy, underwent a polysomnographic study and hemodynamic and echocardiographic evaluations within a few days. The patients were then enrolled in the follow-up of our pre-transplantation program. Only slight alterations of sleep architecture were detected. During sleep, Cheyne-Stoke respiration was present in 50% and arterial oxygen desaturations in 54% of patients. An increased pulmonary wedge pressure (24.7 +/- 8.3 vs 16.7 +/- 8.9 mmHg, p < 0.000) was significantly correlated with the presence of nocturnal Cheyne-Stokes episodes, while cardiac index was not (1.9 +/- 0.6 vs 2.0 +/- 0.5 l m-2 min-1, p = 0.42). In a multivariate analysis of hemodynamic and polysomnographic data, mortality or heart transplantation in status 1 was predicted at the two year follow-up only by an increased pulmonary wedge pressure. In conclusion, in advanced chronic heart failure, with optimized therapy, nocturnal Cheyne-Stokes respiration is present in half of the cases, with concomitant falls in arterial oxygen desaturation. These events were not independently predictive of mortality. The strong correlation found between increased left ventricular filling pressure and presence of Cheyne Stokes respiration and the lack of correlation with cardiac index suggest that other hemodynamic mechanisms besides reduced cardiac output are responsible for this respiratory abnormality.