Ischemic myocardial injuries after cardiac malformation repair in infants may be associated with oxidative stress mechanisms
Received 3 June 2009; received in revised form 12 January 2010; accepted 26 January 2010. published online 26 February 2010. Corrected Proof
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.
Conclusion
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.
aDepartment of Pathology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, SP, Brazil
bDepartment of Statistics, Faculty of Medicine of Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, SP, Brazil
cDepartment of Surgery and Anatomy, Faculty of Medicine of Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, SP, Brazil
dDepartment of Histopathology, Sheffield Children's NHS Foundation Trust, Sheffield, England
Corresponding author. Department of Pathology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Av. Bandeirantes 3900 14049-900 Ribeirão Preto, SP, Brazil. Tel.: +55 16 36023341; fax: +55 16 36023341.
Conflict of interest: None of the authors of this article have a conflict of interest, and this article has not been published previously.
Funding: Simone G. Ramos and Marcos A. Rossi are investigators of CNPq. Dr. Oliveira was a recipient of a Master of Science Degree from CNPq. This work was partially supported by Fundação de Apoio ao Ensino, Pesquisa e Assistência (FAEPA) (1299/2006).
ABSTRACT