STRUCTURAL BASIS OF END-STAGE FAILURE IN ISCHEMIC CARDIOMYOPATHY IN HUMANS
STRUCTURAL BASIS OF END-STAGE FAILURE IN ISCHEMIC CARDIOMYOPATHY IN HUMANS
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DOI：
10.1161/01.cir.89.1.151
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发表时间：
1994-01-01
期刊：
影响因子：
37.8
通讯作者：
ANVERSA, P
中科院分区：
文献类型：
--
作者：
BELTRAMI, CA;FINATO, N;ANVERSA, P
背景 缺血性心肌病的特征是心肌细胞丢失、反应性细胞肥大和心室疤痕。然而，这些组织和细胞过程对晚期衰竭的相对贡献仍有待确定。 方法和结果 从因慢性冠状动脉疾病末期而接受心脏移植的个体中获得十颗心脏。在尸检时从死于心血管疾病以外的原因的患者中收集了相同数量的对照心脏，并将形态测量方法应用于左心室和右心室心肌的分析。左心室肥大表现为器官重量、总肌细胞质量和每核肌细胞体积的变化，分别增加了 85%、47% 和 103%。右心室相应增加分别为75%、74%和112%。左心室和右心室的肌细胞丢失分别占 28% 和 30%，这是心室、组织和细胞水平上肌细胞肥大评估差异的原因。左心室肌细胞肥大是通过肌细胞直径和长度增加16%和51%来实现的，而右心室肌细胞肥大是这些线性尺寸分别增加13%和67%的结果。此外，发现左心室壁厚度中包含的肌细胞数量减少了 36%。节段性、替代性和间质性纤维化形式的胶原蛋白积聚分别占左心室心肌和右心室心肌的平均 28% 和 13%。细胞损失和心肌纤维化、肌细胞延长和细胞壁滑移共同导致左心室空腔体积扩大4.6倍，心室质量与心室体积比减少56%。结论这些结果与心肌细胞和胶原室均参与失代偿性偏心心室肥厚发展的论点是一致的。 缺血性心肌病性心脏。
Background Ischemic cardiomyopathy is characterized by myocyte loss, reactive cellular hypertrophy, and ventricular scarring. However, the relative contribution of these tissue and cellular processes to late failure remains to be determined.Methods and Results Ten hearts were obtained from individuals undergoing cardiac transplantation as a result of chronic coronary artery disease in its terminal stage. An identical number of control hearts were collected at autopsy from patients who died from causes other than cardiovascular disease, and morphometric methodologies were applied to the analysis of the left and right ventricular myocardium. Left ventricular hypertrophy evaluated as a change in organ weight, aggregate myocyte mass, and myocyte cell volume per nucleus showed increases of 85%, 47%, and 103%, respectively. Corresponding increases in the right ventricle were 75%, 74%, and 112%. Myocyte loss, which accounted for 28% and 30% in the left and right ventricles, was responsible for the difference in the assessment of myocyte hypertrophy at the ventricular, tissue, and cellular levels. Left ventricular muscle cell hypertrophy was accomplished through a 16% and 51% increase in myocyte diameter and length, whereas right ventricular myocyte hypertrophy was the consequence of a 13% and 67% increase in these linear dimensions, respectively. Moreover, a 36% reduction in the number of myocytes included in the thickness of the left ventricular wall was found. Collagen accumulation in the form of segmental, replacement, and interstitial fibrosis comprised an average 28% and 13% of the left and right ventricular myocardia, respectively. The combination of cell loss and myocardial fibrosis, myocyte lengthening, and mural slippage of cells resulted in 4.6-fold expansion of left ventricular cavitary volume and a 56% reduction in the ventricular mass-to-chamber volume ratio.Conclusions These results are consistent with the contention that both myocyte and collagen compartments participate in the development of decompensated eccentric ventricular hypertrophy in the cardiomyopathic heart of ischemic origin.