病因明确的肥厚心肌的组织病理学研究,特别参考心电图变化的相关性。

R Okada, K Kitamura
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引用次数: 0

摘要

对62例由二尖瓣反流(MR)、主动脉衰竭(AR)、合并瓣膜病(CVD)、高血压(HHD)或缺血(IHD)引起的左心室肥厚(LVH)的尸检心脏和23例左心室正常的对照心脏进行形态学研究,分析肥厚模式和心电图病理相关性。基础障碍改变肥厚模式;即细长的ar型LV使外层肌纤维取向更垂直,而球状的mr型LV使其比正常情况下更水平。高电压QRS与外层肥大相关,而外层肥大通常与内层肥大相关。ST下降和T变化分别对应于内层和中层的相对恶化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Histopathological study of hypertrophied myocardium of known etiologies with special reference to correlation of ECG changes.

Sixty-two autopsied hearts, with left ventricular hypertrophy (LVH) caused by mitral regurgitation (MR), aortic failure (AR), combined valvular disease (CVD), hypertension (HHD), or ischemia (IHD), and 23 control hearts with normal left ventricles were studied morphologically for analysis of modes of hypertrophy and for ECG-pathology correlation. Basic disorders modify the mode of hypertrophy; that is, elongated AR-type LV makes muscle fiber orientation in the outer layer more vertical, and globular MR-type LV makes it more horizontal than normal. High-voltage QRS correlates with hypertrophy of the outer layer which is often associated with that of the inner layer. ST depression and T changes correspond to relative deterioration of the inner and median layers, respectively.

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