Abnormal breathing during sleep and increased central chemoreflex sensitivity in congestive heart failure.

Central Chemoreflex Sensitivity in Congestive Heart Failure To the Editor: The data of Narkiewicz et al1 expand our understanding of the importance of the imbalance between enhanced central versus peripheral chemoreflex sensitivity in the pathophysiology of congestive heart failure. The authors comment on the links between central cardiovascular and respiratory control, but despite this, patients in this study were not assessed for sleep apnea, which may have confounded their study conclusions. It is known that '50% of patients with stable congestive heart failure have associated sleep-disordered breathing, predominantly central sleep apnea (CSA), whereas a minority have obstructive sleep apnea (OSA). We have previously shown that hypercapnic ventilatory responses are increased in patients with CSA and left ventricular dysfunction,2,3 but hypoxic responses are normal. In contrast, patients with OSA have relatively normal central and peripheral chemoreflex responses whether they have congestive heart failure or not.3,4 Increased central chemosensitivity is associated with hypocapnia during the awake state and unstable breathing during sleep. Although the etiology of this enhanced central chemosensitivity is not known, hyperventilation occurs as a consequence of this and is accompanied by increased sympathetic activity. Naughton et al5 reported that treatment of central sleep apnea in congestive cardiac failure with nocturnal continuous positive airway pressure reduced awake sympathetic nerve activity. Thus, it does appear likely that the increased sympathetic efferent activity that characterizes left ventricular systolic dysfunction and congestive heart failure may be due in part to the interaction between abnormal breathing during sleep and increased central chemoreflex sensitivity.