INTRODUCTION
In adults with heart failure (HF), central sleep apnea (CSA) is highly prevalent and associated with higher mortality rates1,2. HF is defined as the insufficiency of the heart to pump adequate blood to the organs of the body. The etiology of HF in children often differs from adults3. In adults, coronary heart disease, hypertension, acquired valvular defects, arrhythmias and myocardial infarction are the leading causes of HF. In children, however, congenital heart defects and the sequelae of time and surgical intervention, and less commonly, cardiomyopathy are the main causes of HF4. While the relationship between HF and CSA has been well studied in adults, there is a lack of similar data in children5. Sleep apnea is obstructive (due to airway obstruction) or central in nature (lack of drive to breathe)6. The increased risk of CSA in HF is theorized to be due to hemodynamic and autonomic mechanisms involving the sympathetic nervous system’s upregulated response to periods of hypoxemia and hypercapnia7. While both obstructive sleep apnea (OSA) and CSA can present with increased apneic events, the physiology of OSA and CSA are different, hence treatments differ. In OSA, occlusion of airflow increases cardiac afterload and decreases stroke volume8. Relative hypotension triggers baroreceptors to increase sympathetic tone9. CSA occurs when partial pressure of CO2 falls below apneic threshold, a level of CO2 below which the nervous system fails to trigger breathing7. Patients with HF have a higher ventilatory response due to altered chemosensitivity to increased levels of CO210. Furthermore, decreased cardiac output creates a delay in detection of changes in CO2 levels which exacerbates apnea/hyperventilation cycles11. By treating sleep apnea in children and thereby reducing sympathetic output, these adverse effects can be mitigated. However, the link between CSA and HF in children has not been described. This is important to know, as CSA is a potentially reversible condition with which appropriate treatment may improve morbidity and mortality in children with HF.
CSA in infants with congenital heart disease is associated with a fourfold increase in mortality12. However, the study describing these findings did not report prevalence of HF or its association with CSA. In children with HF due to dilated cardiomyopathy, CSA was noted in 19% of the studied population5. No correlation was noted between CSA and heart function. In another prospective uncontrolled case series, there was a high prevalence of CSA with significant correlation between left ventricular end diastolic index, left ventricular end systolic index, and central apnea index13. However, this study focused on comparing polysomnogram (PSG) indices with heart function based on the nature of cardiomyopathy but did not compare prevalence of CSA in children with and without HF. While there is a known high prevalence of OSA and CSA in adults with HF, this has not been well studied in children. Moreover, no study has been done to correlate central apnea events with heart function, in children with HF. We hypothesized that the prevalence of CSA will be different in children with HF compared to children without HF.