Lin C S, Chen K S, Lin M C, Fu M C, Tang S M
Department of Internal Medicine, Chung Shan Medical and Dental College Hospital, Taichung, Taiwan, Republic of China.
Am Heart J. 1991 Dec;122(6):1671-82. doi: 10.1016/0002-8703(91)90286-q.
In an attempt to investigate the role of left ventricular blood outflow in the generation of systolic anterior motion (SAM) of the mitral valve in patients with hypertrophic cardiomyopathy, we precisely analyzed the temporal relation of SAM and the left ventricular outflow tract (LVOT) systolic Doppler events obtained at the maximal mitral-septal apposition or equivalent area in eight patients with severe SAM, in five patients with mild/moderate SAM, and in seven patients with no SAM, using M-mode and pulsed Doppler echocardiography; the results were compared with those in 10 normal subjects. In all 13 patients with SAM, the timing of SAM generation corresponded to the LVOT Doppler events either between the onset of SAM and the onset of Doppler (r = 0.834, p less than 0.0001) or between the peak of SAM and the peak of Doppler (r = 0.836, p less than 0.0001). The excursion rate of the development of SAM showed a correlation with the LVOT blood outflow acceleration (r = 0.828, p less than 0.0001). The timing of SAM resolution also correlated with the Doppler events, either between the offset of SAM and the offset of Doppler (r = 0.795, p less than 0.001) or the end of SAM and the end of Doppler (r = 0.859, p less than 0.0001). The LVOT blood outflow deceleration showed a correlation with the regression rate of SAM (r = 0.668, p less than 0.013). The LVOT blood outflow acceleration was significantly higher in patients with severe SAM than in patients with mild/moderate SAM or no SAM. This study suggests that the high LVOT blood outflow acceleration in early systole possibly plays an important part in the generation of the Bernoulli pressure drop and results in anterior motion of the mitral valve. At mid-systole, a drag force and/or suction effect of pressure drop produced by continuous outflow blood may sustain the anterior motion of the mitral valve. At late systole, as the blood flow decelerates, the regression of SAM then occurs.
为了研究肥厚型心肌病患者左心室血液流出在二尖瓣收缩期前向运动（SAM）产生中的作用，我们使用M型和脉冲多普勒超声心动图，精确分析了8例重度SAM患者、5例轻度/中度SAM患者和7例无SAM患者在二尖瓣-室间隔最大贴合处或等效区域获得的SAM与左心室流出道（LVOT）收缩期多普勒事件的时间关系；并将结果与10名正常受试者的结果进行比较。在所有13例有SAM的患者中，SAM产生的时间与LVOT多普勒事件相对应，要么在SAM开始与多普勒开始之间（r = 0.834，p小于0.0001），要么在SAM峰值与多普勒峰值之间（r = 0.836，p小于0.0001）。SAM发展的偏移率与LVOT血液流出加速度相关（r = 0.828，p小于0.0001）。SAM消退的时间也与多普勒事件相关，要么在SAM结束与多普勒结束之间（r = 0.795，p小于0.001），要么在SAM终点与多普勒终点之间（r = 0.859，p小于0.0001）。LVOT血液流出减速与SAM的消退率相关（r = 0.668，p小于0.013）。重度SAM患者的LVOT血液流出加速度显著高于轻度/中度SAM患者或无SAM患者。本研究表明，收缩早期LVOT血液流出加速度较高可能在伯努利压降的产生中起重要作用，并导致二尖瓣前向运动。在收缩中期，持续流出血液产生的压降的拖曳力和/或抽吸效应可能维持二尖瓣的前向运动。在收缩晚期，随着血流减速，SAM随后消退。
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