Department of Pathology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, SP, Brazil.
Cardiovasc Pathol. 2011 Jan-Feb;20(1):e43-52. doi: 10.1016/j.carpath.2010.01.012. Epub 2010 Feb 25.
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.
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.
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.
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.
尽管儿科心脏外科学取得了进步，但围术期心肌损伤仍然是心脏手术后心功能障碍的主要决定因素。本研究调查了导致 29 名先天性心脏病婴儿死亡的与病理学相关的差异。这些婴儿在巴西里贝朗普雷图大学医院接受治疗。
患者被分为四组：第 1 组，16 名婴儿在体外循环下接受先天性心脏病手术；第 2 组，4 名婴儿在体外循环下接受先天性心脏病手术；第 3 组，9 名婴儿在接受手术治疗前因先天性心脏病死亡；第 4 组（对照组），5 名无先天性心脏病且因其他原因死亡的婴儿。通过组织病理学和免疫组织化学评估心肌损伤和氧化应激机制，并通过形态计量学分析进行量化。
第 1 组婴儿主要表现为收缩带坏死和营养不良性钙化。第 2 组婴儿主要表现为凝固性坏死和愈合，而未修复的婴儿（第 3 组）主要表现为液化性肌溶解。凋亡细胞在手术组中更为突出。对照组未显示出明显的心肌病变。脂质过氧化是氧化应激导致心肌病变的主要机制。
这些心脏中观察到的病变多样性似乎表明由于心肌灌注不足导致了广泛的细胞损伤，尤其是当这些婴儿接受手术时。氧化机制可能是心肌损伤发病机制中的一个共同介质，通过膜磷脂的过氧化导致细胞膜通透性改变、细胞死亡和细胞内钙超载。此外，不成熟且常常肥大的心肌可能会导致不利条件，导致心力衰竭和致命后果。
