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[甲状腺毒症性心力衰竭的发病机制]

[Pathogenesis of cardiac insufficiency in thyrotoxicosis].

作者信息

Levine L I, Volgin E G

出版信息

Kardiologiia. 1975 Oct;15(10):136-42.

PMID:138009
Abstract

The purpose of the work was to study some problems relating to the pathogenesis of cardiac insufficiency in patients with thyrotoxicosis. To do this a total of 108 patients suffering from thyrotoxicosis with varying degree of severity and aged from 17 to 59 were examined. In addition to the general clinical examination vectoro-, poly- and mechanocardiography was employed. The resulting findings ascertained two possible ways for the development of cardiac insufficiency in patients under consideration. One of them is cardiac hyperfunction that comes to the forefront. In this case the myocardial changes are of a stage-wise nature. The myocardial contractility at the onset of the affection is up, a slight hypertrophy is developing, chiefly, of the outflow passages. As the disease progresses further hypertrophy gains in intensity and dilation of the heart comes in as an intercurrent factor. At this time the contractile function of the myocardium is still unaffected and the patients are at a stage of compensation. With progressing dystrophy and wearing away of the myocardium its contractility is declining and signs of cardiac incompetence appear. Such a development is characteristic of patients with severe course of thyrotoxicosis, long-standing disease and frequent relapses. Of the other way is typical cardiac hyperfunction of low intensity. To the forefront come dystrophic alterations in the myocardium unaccompanied by hypertrophy, and in this case cardiac insufficiency is of latent nature. Such alterations are seen to occur with a milder course of thyrotoxicosis, with the disease of short duration. Dynamic observations bear proof to a reversible nature of hypertrophy and dystrophy of the myocardium.

摘要

这项工作的目的是研究与甲状腺毒症患者心脏功能不全发病机制相关的一些问题。为此,对108例年龄在17至59岁之间、患有不同严重程度甲状腺毒症的患者进行了检查。除了常规临床检查外,还采用了向量心电图、多导心电图和机械心电图检查。研究结果确定了所研究患者心脏功能不全发展的两种可能方式。其中之一是心脏功能亢进处于首要地位。在这种情况下,心肌变化呈阶段性。发病初期心肌收缩力增强,主要是流出道出现轻度肥厚。随着疾病进一步发展,肥厚加剧,心脏扩张作为一个并发因素出现。此时心肌的收缩功能仍未受影响,患者处于代偿阶段。随着心肌营养不良和损耗的进展,其收缩力下降,心脏功能不全的迹象出现。这种发展是重度甲状腺毒症、病程长且频繁复发患者的特征。另一种方式是低强度的典型心脏功能亢进。心肌营养不良性改变处于首要地位,无肥厚现象,在这种情况下心脏功能不全具有潜在性质。这种改变见于甲状腺毒症病情较轻、病程较短的情况。动态观察证明心肌肥厚和营养不良具有可逆性。

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