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.