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[重组人生长激素治疗扩张型心肌病]

[Therapy of dilated cardiomyopathy with recombinant human growth hormone].

作者信息

Osterziel K J, Markus U, Willenbrock R, Strohm O, Dietz R

机构信息

Franz-Volhard-Klinik des Virchow-Klinikums, Humboldt-Universität zu Berlin.

出版信息

Z Kardiol. 1997 Oct;86(10):803-11.

PMID:9454447
Abstract

Dilated cardiomyopathy is a disease of the myocardium which is characterized by predominant enlargement of the left ventricle, decreased systolic function, and reduced myocardial wall thickness. The reduction in the number and function of myocardial fibers induces hypertrophy and leads to interstitial fibrosis. Ventricular dilatation and reduced wall thickness contributes to a further increase of the already elevated myocardial wall stress and triggers the continuous decrease of myocardial function. The initial myocyte injury by different and mostly unknown causes leads to progressive myocyte damage resulting in a similar uniform clinical picture independent from the initial myocellular derangement. One of the common pathways may be an inadequate response of the heart to human growth hormone (GH). Several studies support this hypothesis: GH deficiency results in a significant reduction of ventricular wall thickness and myocardial function, and GH-substitution is able to normalize the depressed left ventricular function. In addition, Sacca et al. reported in an uncontrolled study that GH-therapy reduced left ventricular wall stress by 40% in 7 patients with dilated cardiomyopathy. There was a parallel increase of the ejection fraction from 34% to 47%. This improvement was accompanied by a decrease of the functional classification of heart failure from NYHA 2.7 to 1.6. This therapeutic approach to alter the myocyte function directly by growth factors may open a new therapeutic concept in dilated cardiomyopathy. If double blind, randomized studies confirm the results of Sacca's study, a new era of therapeutic options may be available for the treatment of dilated cardiomyopathy.

摘要

扩张型心肌病是一种心肌疾病,其特征是左心室显著扩大、收缩功能减退和心肌壁厚度变薄。心肌纤维数量和功能的减少会导致心肌肥大并引发间质纤维化。心室扩张和壁厚度变薄会导致已经升高的心肌壁应力进一步增加,并引发心肌功能的持续下降。不同的且大多未知的原因导致的初始心肌细胞损伤会导致进行性心肌细胞损伤,从而产生相似的统一临床症状,而与初始的心肌细胞紊乱无关。一个常见的途径可能是心脏对人生长激素(GH)的反应不足。多项研究支持这一假设:生长激素缺乏会导致心室壁厚度和心肌功能显著降低,而生长激素替代能够使降低的左心室功能恢复正常。此外,萨卡等人在一项非对照研究中报告称,生长激素治疗使7例扩张型心肌病患者的左心室壁应力降低了40%。射血分数从34%平行增加到47%。这种改善伴随着心力衰竭功能分级从纽约心脏协会(NYHA)2.7降至1.6。这种通过生长因子直接改变心肌细胞功能的治疗方法可能会为扩张型心肌病开辟一种新的治疗理念。如果双盲、随机研究证实了萨卡研究的结果,那么治疗扩张型心肌病的新时代可能会有新的治疗选择。

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Z Kardiol. 1997 Oct;86(10):803-11.
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