title: B-type natriuretic peptide and cardiovascular function in young children with obstructive sleep apnea.
abstract: OBJECTIVE
  N-terminal pro-B-type natriuretic peptide (NT-proBNP), a marker of ventricular strain, and C-reactive protein (CRP), a marker of inflammation, are reportedly elevated in school-aged children with obstructive sleep apnea (OSA). We hypothesized that cardiovascular morbidity affects circulating markers and their echocardiographic and polysomnographic (PSG) correlates in young children with OSA.
  
  
  METHODS
  We assessed young children undergoing adenotonsillectomy (TA) for OSA by polysomnography, echocardiography, and serum CRP and NT-proBNP levels.
  
  
  RESULTS
  A total of 90 children with OSA (mean age 19 +/- 7 months; 71.2% male; BMI, z = 0.62 +/- 1.04) and 45 age- and sex-matched controls were included. Three months following TA, 72 children were reassessed for NT-proBNP and CRP. NT-proBNP level (pg/mL) was higher in subjects with OSA (189.1 +/- 112.7) vs control subjects (104.8 +/- 49.5; P = .006). Both NT-proBNP (187.8 +/- 114 vs 86 +/- 32.6; P = .002) and CRP levels (mg %) (0.49 +/- 0.41 vs 0.1 +/- 0.17; P < .05) decreased following TA. Doppler pulse wave measuring tricuspid regurgitation (TR), a reflection of pulmonary hypertension, correlated with CRP (r = 0.61, P < .01) but not NT-proBNP (r = -0.14, P = .53) levels. Left ventricle end-diastolic diameter (LVEDD) was at the maximal normal range (0.91 +/- 0.11), but did not correlate with CRP or NT-proBNP levels. Both CRP level and TR correlated with PSG variables reflecting nocturnal hypoxemia, whereas NT-proBNP level and LVEDD did not. Echocardiography in 40 children (out of 90) showed a decline in TR that was abnormal before TA and correlated with the decrease in CRP following TA.
  
  
  CONCLUSIONS
  NT-proBNP levels are increased in children with OSA and decrease following TA. Echocardiographic parameters suggesting increased pulmonary pressure in young children with OSA are related to nocturnal hypoxemia and systemic inflammation, which also decrease following therapy.
authors.affiliation: Department of Pediatrics, Sleep Wake Disorder Unit, Soroka University Medical Center, Beer-Sheva, Israel. avivgold@bgu.ac.il
authors.forename: Aviv D
authors.initials: AD
authors.lastname: Goldbart
authors.forename: Aviva
authors.initials: A
authors.lastname: Levitas
authors.forename: Sari
authors.initials: S
authors.lastname: Greenberg-Dotan
authors.forename: Shalom
authors.initials: S
authors.lastname: Ben Shimol
authors.forename: Arnon
authors.initials: A
authors.lastname: Broides
authors.forename: Marc
authors.initials: M
authors.lastname: Puterman
authors.forename: Asher
authors.initials: A
authors.lastname: Tal
mesh_terms: D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism; D002302:Cardiac Output / Q000502:physiology*; D016022:Case-Control Studies; D002675:Child, Preschool; D015331:Cohort Studies; D015150:Echocardiography, Doppler; D005260:Female; D006801:Humans; D007223:Infant; D008297:Male; D020097:Natriuretic Peptide, Brain / Q000097:blood*; D010446:Peptide Fragments / Q000097:blood*; D017286:Polysomnography; D020181:Sleep Apnea, Obstructive / Q000097:blood* / Q000175:diagnosis / Q000503:physiopathology*; D014262:Tricuspid Valve Insufficiency / Q000175:diagnosis / Q000453:epidemiology / Q000503:physiopathology
chemical_list: D010446:Peptide Fragments; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain; D002097:C-Reactive Protein