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肥厚性梗阻性心肌病二尖瓣收缩期前向运动机制及心室内压力梯度部位(作者译)

[Mechanism of the systolic anterior motion of the mitral valve and site of the intraventricular pressure gradient in hypertrophic obstructive cardiomyopathy (author's transl)].

作者信息

Nagata S, Sakakibara H, Beppu S, Park Y D, Masuda Y, Nimura Y

出版信息

J Cardiogr. 1981 Dec;11(4):1077-87.

PMID:7201490
Abstract

The mechanism of the systolic anterior motion (SAM) of the mitral valve and the relationship between SAM and the intraventricular pressure gradient in hypertrophic cardiomyopathy were analyzed. The subjects were 15 cases, in which SAM was observed on the M-mode echocardiograms. Real-time two-dimensional echocardiography was performed at the time of cardiac catheterization and the measurement of left ventricular pressure was made with observing the spatial relationship between the tip of of the catheter and the surrounding intracardiac structures. There were two modes of the systolic anterior motion of the mitral valve in cases with SAM as follows: (1) The hypertrophied papillary muscle protruded into the left ventricular cavity in systole and it caused the displacement of the chordae tendineae, but also the tips of both anterior and posterior mitral leaflets were anterosuperiorly pulled up by the enlarged papillary muscles and the leaflets seemed apparently to intersect the left ventricular outflow tract (type II). These two types seem to make a continuous spectrum. Seven of the 15 cases examined exhibited type I and 8 cases exhibited type II or the intermediate condition. In the cases of type I, the pressure gradient was noted at the level of the tip of the papillary muscles. The inflow tract and the suprapapillary of the outflow tract exhibited a low pressure, while the apical cavity exhibited a high pressure. It is suggested that the enlarged papillary muscles make the ventricular cavity much more narrowly, resulting in the development of pressure gradient at their level. In the cases of type II, the pressure gradient was noted across the anterior and posterior mitral leaflets perpendicular to the outflow tract (subaortic area). The inflow tract exhibited a high pressure in contrast to that in the cases of type I. It is suggested that the anterosuperiorly pulled anterior and posterior leaflets dam up the ventricular cavity, resulting in the development of pressure gradient across them. Here, it should be emphasized that not only the anterior mitral leaflet, but also the posterior leaflet participates to yield the SAM and the intraventricular pressure gradient.

摘要

分析了肥厚型心肌病中二尖瓣收缩期前向运动(SAM)的机制以及SAM与心室内压力梯度之间的关系。研究对象为15例在M型超声心动图上观察到SAM的患者。在心脏导管插入术时进行实时二维超声心动图检查,并在观察导管尖端与周围心内结构的空间关系的同时测量左心室压力。有SAM的病例中二尖瓣收缩期前向运动有两种模式,如下:(1)肥厚的乳头肌在收缩期突入左心室腔,导致腱索移位,同时二尖瓣前后叶尖端被增大的乳头肌向上前牵拉,瓣膜似乎明显与左心室流出道相交(II型)。这两种类型似乎构成一个连续谱。15例受检病例中7例表现为I型,8例表现为II型或中间状态。在I型病例中,在乳头肌尖端水平出现压力梯度。流入道和流出道乳头肌上方区域压力低,而心尖腔压力高。提示增大的乳头肌使心室腔变窄得多,导致在其水平出现压力梯度。在II型病例中,在垂直于流出道(主动脉下区域)的二尖瓣前后叶之间出现压力梯度。与I型病例相反,流入道压力高。提示向上前牵拉的二尖瓣前后叶阻塞心室腔,导致在它们之间出现压力梯度。在此应强调,不仅二尖瓣前叶,而且后叶也参与产生SAM和心室内压力梯度。

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