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Adaptive servo‐ventilation in heart failure associated with central sleep apnoea. Is it effective in both acute and chronic setting?

Chronic heart failure (CHF) is a highly prevalent disease associated with repeated hospitalisations, and high morbidity and mortality. Patients with CHF often have sleep-disordered breathing (SDB) characterized by either obstructive sleep apnoea (OSA) or central sleep apnoea (CSA). Due to the fact that in these patients the classic breathing Cheyne2Stokes respiration (CSR) often occurs, CSA is called CSR-CSA. Both types, OSA and CSR-CSA, contribute to the progression of CHF and are associated with an increased mortality in patients with CHF. When using the apnoea2hyperpnoea index of .15/h for the diagnosis of SDB, the reported prevalence is 50% in patients with CHF. Although the pathophysiologies of OSA and CSR-CSA are different, the continuous exposure of the heart to nocturnal stress by repeated episodes of apnoea, hypoxia, and arousal from sleep result in a cascade of phenomena including activation of the sympathetic nervous system leading to increased pre-load and afterload and impaired cardiac contractility. Cheyne2Stokes respiration-central sleep apnoea is more common in heart failure patients, but mixed patterns exist. However, OSA may expose the failing heart to greater stress than CSR-CSA because of a different pathophysiology. In short, the generation of negative intrathoracic pressure during obstructive apnoea increases left ventricular (LV) transmural pressure and afterload. Increased venous return contributes to right ventricular distension compromising LV filling by displacement of the interventricular septum during diastole. This results in reduced stroke volume and cardiac output. Cheyne2Stokes respiration-central sleep apnoea is associated with chronic hypocapnia which is related to stimulation of pulmonary vagal irritant receptors by elevated LV filling pressures and volumes. The pulmonary congestion in heart failure contributes to augmented CO2-chemoreceptor sensitivity resulting in chronic hyperventilation which leads by definition to a reduction in PaCO2. This may bring the PaCO2 below the apnoeic threshold resulting in an apnoea. Before starting specific therapy for SDB in patients with CHF, pharmacological treatment for CHF should be optimized. Improvements in cardiac performance have been associated with an improvement of CSR-CSA suggesting that congestive heart failure is a contributing factor for breathing abnormalities. Among the many therapies that have been shown to improve the severity of SDB, only positive pressure ventilation is associated with an improvement in cardiac function. Sleep-disordered breathing can be effectively treated with various forms of positive-pressure ventilation therapy. Adaptive Servo-Ventilation (ASV) has been shown to be more effective than continuous positive airway pressure (CPAP) in reducing CSR-CSA in patients with CHF, while Philippe et al. showed that ASV led to better compliance. Other studies showed improvements in laboratory data (decreased N-terminal prohormone of brain natriuretic peptide), clinical parameters (decreased apnoea2 hypopnoea index, improved daytime sleepiness, improved quality of life), and functional parameters (LV ejection fraction). –11 However, the mechanism of how ASV improves cardiac function in CHF remains unclear. In the current issue of the European Journal of Heart Failure, Haruki et al. evaluate in CHF patients with CSAwhether the impact of ASV on left chamber geometry and function differs in the acute and chronic setting. For the acute setting (30 min after the initiation of ASV therapy) they demonstrated a significant increase in stroke volume and cardiac output at a lower heart rate in conjunction with a reduction of systemic vascular resistance (SVR). Left ventricular end-diastolic volume or echocardiographic parameters of diastolic function including E/e′ remained unchanged. The authors also investigated the impact of chronic ASV therapy on cardiac performance and geometry. Of the 30 patients included in this study, 15 patients tolerated ASV therapy and were compared with 11 patients in the withdrawal group due to poor tolerance (four patients were lost to follow-up). These patients were included in the chronic study and were followed up for a period