Hasegawa I, Sakamoto T, Hada Y, Amano K, Yamaguchi T, Takenaka K, Takahashi H, Takikawa R, Takahashi T, Sugimoto T
J Cardiogr. 1985 Sep;15(3):655-67.
Two-dimensional echocardiographic studies were performed for 22 patients with asymmetric septal hypertrophy and systolic anterior motion (SAM) of the mitral valve to clarify the mechanism of SAM and left ventricular outflow obstruction. The long-axis view of the left ventricle showed that a distal portion of the anterior mitral leaflet became surplus when the mitral valve was closed in 15 of 16 patients with SAM-septal contact and in four of six patients without it. In these patients, the mitral leaflet coaptation was displaced anteriorly, and/or the anterior leaflet was elongated, showing an anterior motion. In an unusual patient with SAM-septal contact, a distal portion of the long posterior mitral leaflet was surplus. The remaining two patients without SAM-septal contact had a rather widely coapted portion of the mitral leaflets. The distal surplus portion and the coapted portion of the mitral valve were displaced anteriorly prior to the onset of ejection, and moved forward and protruded into the outflow tract more rapidly and more excessively than the papillary muscles during early to mid systole in all patients. Then, the distal mitral valve and the chordae tendineae adopted the configuration of an inverted V in mid systole. The tip of the surplus leaflet contacted the interventricular septum in patients with SAM-septal contacts. In the short-axis view of the left ventricle, the central portion of the distal mitral valve moved forward excessively and bent like an inverted U during early to mid systole. Therefore, SAM of the distal mitral valve is thought to be caused by the hydrodynamic force generated by the ejection flow. This force is supposed to be not only due to the Venturi effect, but is more properly understood as a "pushing force". Left ventricular outflow obstruction is considered to be formed by the protruding distal mitral valve and the hypertrophied septum.
对22例患有不对称性室间隔肥厚和二尖瓣收缩期前向运动（SAM）的患者进行了二维超声心动图研究，以阐明SAM和左心室流出道梗阻的机制。左心室长轴视图显示，在16例存在SAM-室间隔接触的患者中的15例以及6例不存在SAM-室间隔接触的患者中的4例中，二尖瓣关闭时二尖瓣前叶远端部分多余。在这些患者中，二尖瓣叶对合向前移位，和/或前叶拉长，呈现前向运动。在1例存在SAM-室间隔接触的特殊患者中，二尖瓣后叶远端部分多余。其余2例不存在SAM-室间隔接触的患者二尖瓣叶对合部分相当宽。在所有患者中，二尖瓣远端多余部分和对合部分在射血开始前向前移位，并在收缩早期至中期比乳头肌更快、更过度地向前移动并突入流出道。然后，二尖瓣远端和腱索在收缩中期呈倒V形。存在SAM-室间隔接触的患者中多余叶尖与室间隔接触。在左心室短轴视图中，二尖瓣远端中央部分在收缩早期至中期过度向前移动并弯曲成倒U形。因此，二尖瓣远端的SAM被认为是由射血血流产生的流体动力引起的。这种力不仅被认为是由于文丘里效应，更确切地应理解为一种“推力”。左心室流出道梗阻被认为是由突出的二尖瓣远端和肥厚的室间隔形成的。
