title: Ischemic myocardial injuries after cardiac malformation repair in infants may be associated with oxidative stress mechanisms.
abstract: BACKGROUND
  Despite advances in pediatric cardiac surgery, perioperative myocardial injury can be the major determinant of postoperative dysfunction after cardiac surgery. This study investigated the pathology-related differences in 29 infants with congenital heart disease that led to death. The infants were treated at the University Hospital of Ribeirão Preto, Brazil.
  
  
  METHODS
  The patients were divided into four groups: Group 1, 16 infants who underwent operations for congenital heart disease on cardiopulmonary bypass; Group 2, four infants who underwent off-cardiopulmonary bypass operations for congenital heart disease; Group 3, nine infants who died from congenital heart disease prior to surgical treatment; and Group 4 (control group), five infants with no congenital heart disease and who died from other causes. The myocardial injuries and oxidative stress mechanisms were assessed by histopathology and immunohistochemistry and were quantified by morphometrical analyses.
  
  
  RESULTS
  Contraction band necrosis and dystrophic calcification were found primarily in infants of Group 1. Coagulation necrosis and healing were prominent in Group 2, while infants without repair (Group 3) showed mainly colliquative myocytolysis. Apoptotic cells were more prominent in the operative groups. The control group showed no significant myocardial lesions. Lipid peroxidation was the principal mechanism of oxidative stress accounting for the myocardial lesions.
  
  
  CONCLUSIONS
  The diversity of the lesions observed in these hearts seemed to indicate a large spectrum of cell damage due to inadequate myocardial perfusion, especially when these infants underwent surgery. Oxidative mechanisms could be a common mediator in the pathogenesis of myocardial injuries, mediated by peroxidation of the membrane phospholipids and resulting in changes in the permeability of the cell membrane, cell death, and intracellular calcium overload. Furthermore, an immature and often hypertrophied myocardium may promote unfavorable conditions, leading to heart failure and a lethal outcome.
authors.affiliation: Department of Pathology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, SP, Brazil.
authors.forename: Marcela S
authors.initials: MS
authors.lastname: Oliveira
authors.forename: Elaine M
authors.initials: EM
authors.lastname: Floriano
authors.forename: Suleimy C
authors.initials: SC
authors.lastname: Mazin
authors.forename: Edson Z
authors.initials: EZ
authors.lastname: Martinez
authors.forename: Walter V A
authors.initials: WV
authors.lastname: Vicente
authors.forename: Luiz C
authors.initials: LC
authors.lastname: Peres
authors.forename: Marcos A
authors.initials: MA
authors.lastname: Rossi
authors.forename: Simone G
authors.initials: SG
authors.lastname: Ramos
mesh_terms: D017209:Apoptosis; D002118:Calcium / Q000378:metabolism; D006348:Cardiac Surgical Procedures / Q000009:adverse effects*; D002315:Cardiopulmonary Bypass / Q000009:adverse effects; D017809:Fatal Outcome; D005260:Female; D006330:Heart Defects, Congenital / Q000473:pathology / Q000601:surgery*; D006335:Heart Injuries / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D015227:Lipid Peroxidation; D008297:Male; D017202:Myocardial Ischemia / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D011183:Postoperative Complications / Q000209:etiology* / Q000378:metabolism / Q000473:pathology
chemical_list: D002118:Calcium