title: Basal metabolic state of hearts of patients with congenital heart disease: the effects of cyanosis, age, and pathology.
abstract: BACKGROUND
  Experimental models have established numerous myocardial metabolic changes with chronic hypoxia and maturation. We conducted this study to specifically look at the effects of cyanosis, age, and pathology upon the basal metabolic state of the immature human heart.
  
  
  METHODS
  One hundred and eighty-one pediatric patients (37 cyanotic, 144 acyanotic) undergoing open heart surgery were recruited. A myocardial biopsy was collected before ischemia and analyzed for adenine nucleotides, purines, and lactate. The effect of cyanosis was estimated by an analysis of age-matched pairs of children with either ventricular septal defects or tetralogy of Fallot, and by multiple regression modeling. The effects of age and pathology were estimated in acyanotic children also by multiple regression modeling (adjustments were made for baseline differences).
  
  
  RESULTS
  The only effect of cyanosis was for lactate where the paired t test, and unadjusted and adjusted regression analyses were all consistent (ranging from 1.33 to 1.48 times higher in cyanotic than acyanotic children). The concentrations of adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP) declined with age, whereas the ATP/ADP ratio increased; these associations remained significant even in the adjusted regression analysis. None of the effects of acyanotic pathology were highly significant (p < 0.01), implying that few important metabolic differences were attributable to pathology.
  
  
  CONCLUSIONS
  Cyanosis and age are important factors that determine the basal metabolic state of the pediatric heart. Cyanotic patients have higher myocardial lactate concentrations, whereas young age is associated with lower ATP/ADP ratios and higher adenine nucleotide levels.
authors.affiliation: Bristol Heart Institute, University of Bristol, Bristol Royal Infirmary, Bristol, United Kingdom. paulmodi@doctors.org.uk
authors.forename: Paul
authors.initials: P
authors.lastname: Modi
authors.forename: M-Saadeh
authors.initials: MS
authors.lastname: Suleiman
authors.forename: Barnaby C
authors.initials: BC
authors.lastname: Reeves
authors.forename: Ash
authors.initials: A
authors.lastname: Pawade
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Parry
authors.forename: Gianni D
authors.initials: GD
authors.lastname: Angelini
authors.forename: Massimo
authors.initials: M
authors.lastname: Caputo
mesh_terms: D000227:Adenine Nucleotides / Q000032:analysis; D000367:Age Factors; D001706:Biopsy; D002648:Child; D002675:Child, Preschool; D003490:Cyanosis; D017558:Elective Surgical Procedures; D004734:Energy Metabolism; D005260:Female; D006330:Heart Defects, Congenital / Q000150:complications / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D006344:Heart Septal Defects, Atrial / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D006345:Heart Septal Defects, Ventricular / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007773:Lactates / Q000032:analysis; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D010100:Oxygen / Q000009:adverse effects / Q000627:therapeutic use; D011183:Postoperative Complications / Q000209:etiology / Q000378:metabolism; D011687:Purines / Q000032:analysis; D012044:Regression Analysis
chemical_list: D000227:Adenine Nucleotides; D007773:Lactates; D011687:Purines; D010100:Oxygen