Cardiovascular Complications of Obstructive Sleep Apnea Syndrome: Evidence from Children
Section snippets
Pathophysiology of OSAS in Childhood
Transition to the sleep state will normally result in elevations of upper airway resistance,17, 18 primarily linked to reductions in airway diameter resulting from reduced tone of the pharyngeal dilator and constrictor muscles.19, 20, 21 In children, the cardinal abnormality associated with increased probability of OSAS is the presence of adenotonsillar hypertrophy. This is not surprising because anatomical impingement of the upper airway by the enlarged upper airway lymphoid tissue will
Genetic Influences of OSAS in Childhood
Genetic and ethnic factors have been identified in the pathogenesis of OSAS.39, 40, 41, 42, 43, 44, 45, 46 For example, African Americans are at higher risk than whites when controlling for age, sex, and body mass index.47 Although no specific genes have been thus far identified for OSAS, it has become apparent that OSAS is likely a polygenic disease and that specific genes impacting on factors such as oral mucosa thickness and facial structure will play a deterministic role in OSAS. The
Treatment of OSAS in Childhood
As could be deduced from the pathophysiology of OSAS in childhood, surgical removal of enlarged adenotonsillar tissues constitutes the initial treatment approach to most children diagnosed with the disease. Although studies have yet to demonstrate the efficacy and overall outcomes of this approach in pediatric OSAS, the published evidence suggests that this intervention will lead to significant improvements in most cases, as recently reported from a meta-analysis.48 More recent studies however,
Noncardiovascular Morbidity of OSAS in Childhood
As mentioned above, the peak prevalence of OSAS in childhood occurs in the preschool and early school years.13, 66 During the early years after the initial description of OSAS in childhood,2 failure to thrive was extremely frequent and attributed to increased metabolic expenditure caused by the elevated work of breathing during sleep, reduced nutrient intake due to tonsillar hypertrophy, and most likely to disrupted growth hormone–insulin growth factor pathways in the presence of recurrent
Cardiovascular Morbidity of Pediatric OSAS
To facilitate the discussion of several aspects of cardiovascular involvement in children with OSAS, we have arbitrarily divided our review into specific sections. We would like to emphasize that this partition is artificial because a great degree of overlap exists between the various aspects of cardiac and vascular morbidity in the context of OSAS.
Conclusions
In summary, we have recently witnessed the emergence of a rather extensive, yet somewhat preliminary body of evidence, to support a causative link between OSAS and cardiovascular disease in children. Although the putative mechanisms underlying cardiovascular disease and OSAS are far from being completely elucidated, the heretofore-published studies support the notion that these processes do occur even in “supposedly protected” individuals, such as children. Although the deleterious effects of
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RB is supported by a post-doctoral fellowship in Sleep Medicine from Jazz Pharmaceuticals. LKG is supported by an investigator-initiated grant from Merck Company and by a grant from the National Space Agency (NNJ05HF 06G). DG is supported by grants from the National Institutes of Health (HL65270 and HL83075), The Children's Foundation Endowment for Sleep Research, and The Commonwealth of Kentucky Research Challenge Trust Fund.