The variable morphological coexistence of apoptosis and necrosis in human myocardial infarction: significance for understanding its pathogenesis, clinical course, diagnosis and prognosis
The variable morphological coexistence of apoptosis and necrosis in human myocardial infarction: significance for understanding its pathogenesis, clinical course, diagnosis and prognosis
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DOI：
10.1097/00019501-199809050-00007
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发表时间：
1998-01-01
影响因子：
1.8
通讯作者：
James, TN
中科院分区：
文献类型：
--
作者：
James, TN
背景心肌梗死包括细胞凋亡和坏死，但很少有人知道这两种不同形式的细胞死亡在人类心脏的形态学关系，尽管这可能具有临床importance.Methods心脏从77例致命性心肌梗死进行了检查。选取12个有代表性的心脏进行免疫组化染色，观察凋亡区的组织学和细胞学特征。坏死的肌细胞迅速崩解并引起急性炎症。凋亡的心肌细胞保持其膜完整性，不会引起急性炎症。凋亡细胞和凋亡小体的吞噬作用与相邻的肌细胞或巨噬细胞的吞噬一起发生，但主要是后者。在许多凋亡的地区，吞噬能力被淹没，导致大量的凋亡小体躺在细胞外的空间。结论由于凋亡细胞保留其膜的完整性，心肌梗死的酶诊断只能反映心肌梗死的部分是由于坏死。因此，任何细胞内酶的测量总是低估心肌梗死的程度，通常是很大的幅度。心肌梗死中细胞死亡的形态学进展，从凋亡到坏死，可能取决于超过凋亡细胞的局部吞噬能力。然而，细胞凋亡或坏死死亡的细胞同样是死亡的。有必要更好地定义细胞凋亡在心肌冬眠（或顿抑），缺血预处理和无症状心绞痛的发病机制，心肌梗死后重塑中的作用。冠状动脉疾病9：291-307（C）1998 Lippincott-Raven Publishers。
Background Myocardial infarction includes both apoptosis and necrosis, but little is known of the morphological relationship of these two different forms of cell death in the human heart, despite the possibility that this may have clinical importance.Methods Hearts from 77 cases of fatal myocardial infarction were examined. Twelve morphologically representative hearts were selected for immunohistochemical staining to define in detail the histology and cytology of apoptotic areas.Results Both apoptosis and necrosis were present in every heart. Necrotic myocytes quickly disintegrate and evoke acute inflammation. Apoptotic myocytes retain their membrane integrity and do not evoke acute inflammation. Phagocytosis of apoptotic cells and apoptotic bodies occurred with engulfment by either neighboring myocytes or macrophages, but predominantly the latter. In many apoptotic areas, the phagocytic capacity was overwhelmed, resulting in large pools of apoptotic bodies lying free in the extracellular space.Conclusions Because apoptotic cells retain their membrane integrity, enzymatic diagnosis of myocardial infarction can only reflect that portion of myocardial infarction that is due to necrosis. Measurement of any intracellular enzyme consequently always underestimates the extent of myocardial infarction, often by a large margin. Morphological progression of cell death in myocardial infarction, from apoptosis to necrosis, may depend upon exceeding the local capacity for phagocytosis of apoptotic cells. However, cells dying by either apoptosis or necrosis are equally dead. There is a need for better definition of the role of apoptosis in myocardial hibernation (or stunning), in ischemic preconditioning and in the pathogenesis of silent angina, and post-myocardial infarction remodeling. Coronary Artery Dis 9:291-307 (C) 1998 Lippincott-Raven Publishers.