Obstructive sleep apnea in infants.

Am J Respir Crit Care Med. 2012 Apr 15;185(8):805-16

Authors: Katz ES, Mitchell RB, D'Ambrosio CM

Abstract
Obstructive sleep apnea in infants has a distinctive pathophysiology, natural history, and treatment compared with that of older children and adults. Infants have both anatomical and physiological predispositions toward airway obstruction and gas exchange abnormalities; including a superiorly placed larynx, increased chest wall compliance, ventilation-perfusion mismatching, and ventilatory control instability. Congenital abnormalities of the airway, such as laryngomalacia, hemangiomas, pyriform aperture stenosis, choanal atresia, and laryngeal webs, may also have adverse effects on airway patency. Additional exacerbating factors predisposing infants toward airway collapse include neck flexion, airway secretions, gastroesophageal reflux, and sleep deprivation. Obstructive sleep apnea in infants has been associated with failure to thrive, behavioral deficits, and sudden infant death. The proper interpretation of infant polysomnography requires an understanding of normative data related to gestation and postconceptual age for apnea, arousal, and oxygenation. Direct visualization of the upper airway is an important diagnostic modality in infants with obstructive apnea. Treatment options for infant obstructive sleep apnea are predicated on the underlying etiology, including supraglottoplasty for severe laryngomalacia, mandibular distraction for micrognathia, tonsillectomy and/or adenoidectomy, choanal atresia repair, and/or treatment of gastroesophageal reflux.

PMID: 22135346 [PubMed - indexed for MEDLINE]

Left ventricular systolic and diastolic function in obstructive sleep apnea: impact of continuous positive airway pressure therapy.

Circ Heart Fail. 2012 Mar 1;5(2):226-33

Authors: Butt M, Dwivedi G, Shantsila A, Khair OA, Lip GY

Abstract
BACKGROUND: Previous studies in obstructive sleep apnea (OSA) were limited by study cohorts with comorbidities that confound assessment of left ventricular (LV) systolic and diastolic function. We comprehensively evaluated LV function using 2-dimensional echocardiography (2DE), tissue Doppler imaging (TDI), and 3-dimensional echocardiography (3DE) in subjects moderate-severe OSA, who were compared with disease (patients with hypertension, no OSA) and healthy control subjects.
METHODS AND RESULTS: A total of 120 subjects (n=40 each of matched OSA, hypertension and healthy cohorts) underwent echocardiographic examination for the assessment of septal and posterior wall thickness, LV mass index, LV volumes and ejection fraction, mitral valve inflow indices (E, A), mitral annular velocity (S, E'), and left atrial volume index (LAVI). OSA subjects were treated with continuous positive airway pressure (mean duration of 26 weeks), after which the echocardiographic parameters were reassessed. Posterior wall thickness and LV mass index were significantly higher in OSA and hypertensive groups compared with healthy. Systolic S velocity was reduced in OSA and hypertensive compared with healthy control subjects (P<0.05). Diastolic function (E/A, IVRT, and E/E') was impaired in both OSA and hypertensive groups. On 3DE, mean LAVI was significantly greater in OSA and hypertensive compared with healthy. In OSA patients, continuous positive airway pressure therapy resulted in reduction of the posterior wall thickness (P=0.02) and improvement in LV ejection fraction (P<0.05), systolic S velocity (P<0.05), and diastolic LV impairment parameters.
CONCLUSIONS: Moderate to severe OSA causes structural and functional changes in V function and are comparable to that seen in hypertension. These abnormalities significantly improve after CPAP therapy.

PMID: 22414938 [PubMed - indexed for MEDLINE]