title: Randomized comparison between normothermic and hypothermic cardiopulmonary bypass in pediatric open-heart surgery.
abstract: BACKGROUND
  The purpose of this study is to investigate the effect of cardiopulmonary bypass (CPB) temperature on myocardial reperfusion injury, oxidative stress, and inflammatory response in pediatric open heart surgery.
  
  
  METHODS
  Fifty-nine children (median age 78 months; interquartile range, 39-130) undergoing correction of simple congenital heart defects were randomized to receive either hypothermic (28 degrees C) or normothermic (35-37 degrees C) CPB. Troponin I and 8-isoprostane, complement activation C3a, interleukin (IL) -6, -8, and -10, were measured preoperatively, on removal of the aortic cross clamp, 30 minutes, 6, and 24 hours postoperatively.
  
  
  RESULTS
  Troponin I and 8-isoprostane were significantly raised, compared to baseline, in both groups, and remained high at 24 hours. Overall, troponin I and 8-isoprostane levels were 37% and 84% higher in the hypothermic than in the normothermic group, respectively (ratio 1.37, 95% CI 1.00 to 1.88, p = 0.053 and 1.84, 95% CI 1.22 to 2.78, p = 0.0045, respectively), and there was no evidence to suggest the treatment effect changed significantly over the time points measured (p = 0.63). Adjusting for aortic cross-clamp time reduced the effect of hypothermia on troponin (p = 0.18) but not on 8-isoprostane levels (p = 0.0028). The C3a, IL-6, and IL-8 release was similar in the two groups. The IL-10 release between the groups changed over time (p = 0.059) and examining differences at individual time points highlighted a statistically significant difference at the end of the cross-clamp time (p = 0.0079).
  
  
  CONCLUSIONS
  Normothermic CPB is associated with reduced oxidative stress compared with hypothermic CPB, and similar myocardial reperfusion injury and whole body inflammatory response, in children undergoing open heart surgery. A larger study with clinical outcomes as primary end points is now warranted.
authors.affiliation: Bristol Heart Institute, University of Bristol, Bristol Royal Infirmary, Bristol, United Kingdom.
authors.forename: Massimo
authors.initials: M
authors.lastname: Caputo
authors.forename: Simon
authors.initials: S
authors.lastname: Bays
authors.forename: Chris A
authors.initials: CA
authors.lastname: Rogers
authors.forename: Ash
authors.initials: A
authors.lastname: Pawade
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Parry
authors.forename: Saadeh
authors.initials: S
authors.lastname: Suleiman
authors.forename: Gianni D
authors.initials: GD
authors.lastname: Angelini
mesh_terms: D015415:Biomarkers / Q000378:metabolism; D001831:Body Temperature; D002315:Cardiopulmonary Bypass / Q000009:adverse effects / Q000379:methods*; D002648:Child; D002675:Child, Preschool; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D005260:Female; D006330:Heart Defects, Congenital / Q000378:metabolism / Q000601:surgery*; D006801:Humans; D007036:Hypothermia, Induced / Q000009:adverse effects / Q000379:methods*; D007249:Inflammation / Q000209:etiology / Q000378:metabolism; D007378:Interleukins / Q000378:metabolism; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000378:metabolism; D018384:Oxidative Stress; D010372:Pediatrics / Q000379:methods*; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood
chemical_list: D015415:Biomarkers; D007378:Interleukins; D019210:Troponin I; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost