AN INTEGRATED MECHANISM FOR SYSTOLIC ANTERIOR MOTION OF THE MITRAL-VALVE IN HYPERTROPHIC CARDIOMYOPATHY BASED ON ECHOCARDIOGRAPHIC OBSERVATIONS
AN INTEGRATED MECHANISM FOR SYSTOLIC ANTERIOR MOTION OF THE MITRAL-VALVE IN HYPERTROPHIC CARDIOMYOPATHY BASED ON ECHOCARDIOGRAPHIC OBSERVATIONS
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DOI：
10.1016/0002-8703(87)90701-0
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发表时间：
1987-03-01
影响因子：
4.8
通讯作者：
WEYMAN, AE
中科院分区：
文献类型：
--
作者：
JIANG, L;LEVINE, RA;WEYMAN, AE
虽然已经提出了许多机制来解释肥厚性心肌病中二尖瓣的收缩前运动（SAM），但其发生和停止的确切机制仍不明确。文丘里理论基于狭窄流出道中流速增加的理论，被广泛接受，但未能解释SAM的几个重要特征。它还忽略了小叶插入射血路径所产生的阻力的潜在作用，以及会降低乳头肌约束有效性的因素。为了进一步了解SAM的发病机制，我们采用横断面超声心动图对三组大小相等的肥厚性心肌病合并SAM患者、肥厚且无前运动患者和正常对照组的左心室和二尖瓣进行了详细的几何研究。一个显著的发现是肥厚性心肌病患者SAM开始证明射血，这不能用文丘里理论来解释。此外，SAM开始并在小叶的中心部分最突出，而不是其外侧边缘；这一发现并不是文丘里机制所预测的。除了流出道狭窄外，SAM患者特有的其他结构变化包括乳头肌前向和向内移位、二尖瓣前向移位和二尖瓣伸长，平均比其他受试者长1.5 ~ 1.7 cm （p < 0.0001）。在这些观测的基础上，提出了SAM的形成和消退的综合机制，该机制将解释观测到的特征，如在抛射和中心日珥之前开始。这一机制结合了流出道狭窄和乳头肌移位的影响。特别是，可以预测乳头肌的前向内移位会改变脊索支撑的有效性，从而使中央小叶部分变得相对松弛，更容易向前移位。在收缩开始时，在主动脉瓣打开之前，将远端小叶向上导向流出道，也可以预测索张力分布的改变，因此心室射血实际上会将中间的小叶向前拖。SAM的解决可以理解为二尖瓣反流产生的反文丘里效应，以及在侧小叶边缘中央移位的乳头肌的持续牵引。根据这一机制，冠状动脉-二尖瓣装置的错位在改变作用于二尖瓣小叶的力平衡和形成二尖瓣SAM方面起着根本的作用，其形态和时间过程具有超声心动图观察到的特征。
Although many mechanisms have been proposed to explain systolic anterior motion (SAM) of the mitral valve in hypertrophic cardiomyopathy, the precise mechanism of its onset and cessation remain undefined. The Venturi theory, based on increased flow velocity in a narrowed outflow tract, is widely accepted but fails to explain several important characteristics of SAM. It also neglects the potential role of drag forces generated by interposition of the leaflets into the path of ejection and of factors that would decrease the effectiveness of papillary muscle restraint. In order to obtain further insight into the mechanism of SAM, a detailed geometric study of the left ventricle and mitral apparatus was performed with cross-sectional echocardiogrpahy in three equal-sized groups of patients with hypertrophic cardiomyopathy and SAM, patients with hypertrophy and no anterior motion, and normal control subjects. A salient finding was that SAM began pror to ejection in patients with hypertrophic cardiomyopathy, which cannot be explained by the Venturi theory. Further, SAM began and was most prominent in the central portion of the leaflet as opposed to its lateral edges; this finding is not predicted by the Venturi mechanism. In addition to outflow tract narrowing, other structural changes unique to patients with SAM included anterior and inward displacement of the papillary muscle, anterior displacement of the mitral leaflets, and elongation of the mitral leaflets, which were, on the average, 1.5 to 1.7 cm longer than the other subjects (p < 0.0001). On the basis of these observations, an integrated mechanism for the initiation and resolution of SAM is proposed that would explain observed features such as onset before ejection and central prominence. This mechanism combines the effects of outflow tract narrowing with those of papillary muscle displacement. In particular, anterior and inward displacement of the papillary muscles can be predicted to alter the effectiveness of chordal support so that the central leaflet portions become relatively slack and are more readily displaced anteriorly. The altered distribution of chordal tension can also be predicted by orient the distal leaflets upward into the outflow tract at the onset of systole, prior to aortic valve opening, so that ventricular ejection will actually drag the interposed leaflets anteriorly. The resolution of SAM can be understood in terms of a reverse Venturi effect created by mitral regurgitation, as well as continued traction of the centrally displaced papillary muscles on the lateral leaflet margins. According to this mechanism, the malposition of the papillary-mitral apparatus plays a fundamental role in altering the balance of forces acting on the mitral leaflets and creating SAM of the mitral valve which has the morphology and time course observed echocardiographically.