THE CELLULAR BASIS OF DILATED CARDIOMYOPATHY IN HUMANS
THE CELLULAR BASIS OF DILATED CARDIOMYOPATHY IN HUMANS
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DOI：
10.1016/s0022-2828(08)80028-4
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发表时间：
1995-01-01
影响因子：
5
通讯作者：
ANVERSA, P
中科院分区：
文献类型：
--
作者：
BELTRAMI, CA;FINATO, N;ANVERSA, P
本研究旨在评估扩张型心肌病（DC）患者的终末期心力衰竭是否依赖于广泛的肌细胞死亡和肌肉质量的减少，或者是心肌中胶原蛋白积聚的结果，而不依赖于肌细胞损失。此外，分析了心室扩张的机制，以确定心脏解剖结构的变化是否是顽固性心绞痛发生的重要变量。充血性心力衰竭DC的特征是在没有显著冠状动脉粥样硬化的情况下腔室扩张、心肌瘢痕形成和心肌细胞肥大，然而，这些因素中的每一个对心室重构的相对贡献目前尚不清楚。此外，没有关于心肌胶原沉积的潜在病因学以及这种疾病的心室肌细胞数量和大小变化的信息。应用形态计量学方法对10例心脏移植患者的DC心脏进行分析。从死于心血管疾病以外的原因的个体中收集了相同数量的对照心脏。DC使左心室重量和心室容积增加2.2倍和4.2倍，导致质量体积比降低48%。在右心室中，组织重量和腔室大小几乎都增加了一倍。左心室扩张是心肌细胞延长59%和由于壁内心肌细胞滑动导致横周长增加20%的结果。以节段性、替代性和间质性纤维化为代表的心肌瘢痕约占每个心室的20%，表明广泛的肌细胞损失。然而，在两个心室中，肌细胞数量没有减少，平均细胞体积增加了2倍。总之，反应性生长过程中的心肌细胞和结构重排的肌肉室的心肌似乎是心室重构和心力衰竭的发生在DC的主要决定因素。
The present investigation was designed to evaluate whether end-stage cardiac failure in patients affected by dilated cardiomyopathy (DC) was dependent upon extensive myocyte cell death with reduction in muscle mass or was the consequence of collagen accumulation in the myocardium independently from myocyte cell loss, In addition, the mechanisms of ventricular dilation were analysed in order to determine whether the changes in cardiac anatomy were important variables in the development of intractable congestive heart failure. DC is characterized by chamber dilation, myocardial scarring and myocyte hypertrophy in the absence of significant coronary atherosclerosis, However, the relative contribution of each of these factors to the remodeling of the ventricle is currently unknown. Moreover, no information is available concerning the potential etiology of collagen deposition in the myocardium and the changes in number and size of ventricular myocytes with this disease. Morphometric methodologies were applied to the analysis of 10 DC hearts obtained from patients undergoing cardiac transplantation. An identical number of control hearts was collected from individuals who died from causes other than cardiovascular diseases. DC produced a 2.2-fold and 4.2-fold increase in left ventricular weight and chamber volume resulting in a 48% reduction in mass-to-volume ratio. In the right ventricle, tissue weight and chamber size were both nearly doubled. Left ventricular dilation was the result of a 59% lengthening of myocytes and a 20% increase in the transverse circumference due to slippage of myocytes within the wall. Myocardial scarring represented by segmental, replacement and interstitial fibrosis occupied approximately 20% of each ventricle, and was indicative of extensive myocyte cell loss. However, myocyte number was not reduced and average cell volume increased 2-fold in both ventricles. In conclusion, reactive growth processes in myocytes and architectural rearrangement of the muscle compartment of the myocardium appear to be the major determinants of ventricular remodeling and the occurrence of cardiac failure in DC.