Background/Objectives Adults with heart failure (HF) have high prevalence of central sleep apnea (CSA). While this has been repeatedly investigated in adults, there is a deficiency of similar research in pediatric populations. The goal of this study was to compare prevalence of CSA in children with and without HF and correlate central apneic events with heart function. Methods Retrospective analysis of data from children with and without HF was conducted. Eligible children were less than 18 years old with echocardiogram and polysomnogram within 6 months of each other. Children were separated into groups with and without HF based on left ventricular ejection fraction (LVEF). Defining CSA as central apnea‐hypopnea index (CAHI) more than 1/hour, the cohort was also classified into children with and without CSA for comparative study. Results A total of 120 children (+HF: 19, −HF: 101) were included. The +HF group was younger, with higher prevalence of trisomy 21, muscular dystrophy, oromotor incoordination, and structural heart disease. The +HF group had lower apnea‐hypopnea index (median: 3/hour vs. 8.6/hour) and lower central apnea index (CAI) (median: 0.2/hour vs. 0.55/hour). Prevalence of CSA was similar in both groups (p = .195). LogCAHI was inversely correlated to age (Pearson correlation coefficient: −0.245, p = .022). Children with CSA were younger and had higher prevalence of prematurity (40% vs. 5.3%). There was no significant difference in LVEF between children with and without CSA. After excluding children with prematurity, relationship between CAHI and age was no longer sustained. Conclusions In contrast to adults, there is no difference in prevalence of CSA in children with and without HF. Unlike in adults, LVEF does not correlate with CAI in children. Overall, it appears that central apneic events may be more a function of age and prematurity rather than of heart function.

Though endogenous S‐nitroso‐l‐cysteine (l‐CSNO) signaling at the level of the carotid body increases minute ventilation (v̇E), neither the background data nor the potential clinical relevance are well‐understood by pulmonologists in general, or by pediatric pulmonologists in particular. Here, we first review how regulation of the synthesis, activation, transmembrane transport, target interaction, and degradation of l‐CSNO can affect the ventilatory drive. In particular, we review l‐CSNO formation by hemoglobin R to T conformational change and by nitric oxide (NO) synthases (NOS), and the downstream effects on v̇E through interaction with voltage‐gated K+ (Kv) channel proteins and other targets in the peripheral and central nervous systems. We will review how these effects are independent of—and, in fact may be opposite to—those of NO. Next, we will review evidence that specific elements of this pathway may underlie disorders of respiratory control in childhood. Finally, we will review the potential clinical implications of this pathway in the development of respiratory stimulants, with a particular focus on potential pediatric applications.

Background/Objectives: Adults with heart failure (HF) have high prevalence of central sleep apnea (CSA). While this has been repeatedly investigated in adults, there is a deficiency of similar research in the pediatric population. The goal of this study was to compare prevalence of CSA in children with and without HF and correlate central apnea events with heart function. Methods: Retrospective analysis of data from children with and without HF was conducted. Eligible children were <18 years old with echocardiogram and polysomnogram within 6 months of each other. Children were separated into groups with and without HF and groups with and without elevated central apnea index (CAI) for comparative study. Results: 120 children (+HF:19, -HF:101) were included. The +HF group was younger, with higher prevalence of trisomy 21, muscular dystrophy, oromotor incoordination, and structural heart disease and lower Apnea Hypopnea Index and lower CAI. Prevalence of CSA was similar in both the groups. LogCAI was inversely correlated to age at time of sleep study. Children with elevated CAI were younger and had higher prevalence of prematurity. There was no difference in left ventricular ejection fraction (LVEF) between groups with and without elevated CAI. Conclusion: In contrast to adults, after adjusting for age, there is no difference in frequency of central apneic events in children with and without heart failure. Unlike in adults, LVEF does not correlate with CAI in children. Overall, it appears that CAI may be more a function of age rather than of heart function in the pediatric population.