Sherrid M V, Chu C K, Delia E, Mogtader A, Dwyer E M
Division of Cardiology, St. Luke's-Roosevelt Hospital Center, College of Physicians and Surgeons, New York, New York 10019.
J Am Coll Cardiol. 1993 Sep;22(3):816-25. doi: 10.1016/0735-1097(93)90196-8.
The goal of this study was to investigate the hydrodynamic cause of mitral-septal contact and obstruction in patients with hypertrophic cardiomyopathy.
Mitral-septal apposition has been shown to be the cause of obstruction in patients with hypertrophic cardiomyopathy. With obstruction, characteristic continuous wave Doppler tracings show an increasing acceleration of flow. (Tracing is concave to the left.)
We studied 24 consecutive patients who had a Doppler echocardiographic pressure gradient > or = 36 mm Hg. We pursued two lines of inquiry. 1) Before the onset of obstruction, we systematically measured the angle between the direction of left ventricular Doppler color flow and the protruding mitral leaflet in early systole. 2) After the onset of obstruction, we qualitatively analyzed the concave contour of the continuous wave Doppler tracings in our patients and developed a hydrodynamic theory of the obstruction phase to explain the characteristic tracings. We present a mathematic model to support this concept.
We measured 129 angles. Just before mitral-septal contact, the protruding mitral leaflet projects at a mean 40 degrees and 45 degrees relative to flow in the apical long-axis and apical five-chamber views, respectively. At mitral-septal contact, the obstructing leaflet projects at a mean 52 degrees and 58 degrees relative to flow in the same respective views. Even very early in systole, at leaflet coaptation, 11 of 23 patients had angles > 15 degrees relative to flow. After mitral-septal apposition, obstruction across a cowl-shaped orifice begins. During this stage, the obstructing leaflet projects at a mean 55 degrees and 63 degrees relative to flow. In 22 patients, the continuous wave Doppler tracing of the left ventricular outflow jet showed an increasing acceleration of flow.
Just before mitral-septal contact, the protruding leaflets project at high angles relative to flow. At these high angles, flow drag, the pushing force of flow, is the dominant hydrodynamic force on the protruding leaflet and appears to be the immediate cause of obstruction. The high angle between flow direction and the protruding leaflet precludes significant Venturi effects. Even earlier in systole, at leaflet coaptation, flow drag is dominant in half of the patients, with angles relative to flow > 15 degrees. After obstruction is triggered, it appears from our data and model that the leaflet is forced against the septum by the pressure difference across the orifice. The increasing acceleration of Doppler flow is explained by a time-dependent amplifying feedback loop in which the rising pressure difference across the orifice leads to a smaller orifice and a higher pressure difference.
本研究旨在探讨肥厚型心肌病患者二尖瓣-室间隔接触及梗阻的流体动力学原因。
二尖瓣-室间隔贴合已被证明是肥厚型心肌病患者梗阻的原因。出现梗阻时,特征性的连续波多普勒描记显示血流加速度增加。(描记线向左凹陷。)
我们研究了24例连续的患者,其多普勒超声心动图压力阶差≥36mmHg。我们进行了两条研究途径。1)在梗阻发生前,我们系统地测量了左心室多普勒彩色血流方向与收缩早期突出的二尖瓣叶之间的夹角。2)在梗阻发生后,我们定性分析了患者连续波多普勒描记的凹陷轮廓,并建立了梗阻期的流体动力学理论来解释特征性描记。我们提出一个数学模型来支持这一概念。
我们测量了129个夹角。就在二尖瓣-室间隔接触前,在心尖长轴和心尖五腔心视图中,突出的二尖瓣叶相对于血流方向分别平均成40度和45度角。在二尖瓣-室间隔接触时,梗阻叶在相同视图中相对于血流方向分别平均成52度和58度角。即使在收缩期很早的时候,在瓣叶贴合处,23例患者中有11例相对于血流的夹角>15度。二尖瓣-室间隔贴合后,跨兜帽状孔口的梗阻开始。在此阶段,梗阻叶相对于血流方向分别平均成55度和63度角。在22例患者中,左心室流出道射流的连续波多普勒描记显示血流加速度增加。
就在二尖瓣-室间隔接触前,突出的瓣叶相对于血流成高角度。在这些高角度下,流动阻力,即血流的推力,是突出瓣叶上占主导地位的流体动力,似乎是梗阻的直接原因。血流方向与突出瓣叶之间的高角度排除了显著的文丘里效应。甚至在收缩期更早的时候,在瓣叶贴合处,一半患者中流动阻力占主导,相对于血流的夹角>15度。在梗阻触发后,从我们的数据和模型来看,瓣叶似乎被孔口两侧的压力差压向室间隔。多普勒血流加速度增加是由一个随时间变化的放大反馈回路解释的,其中孔口两侧不断上升的压力差导致孔口变小和压力差更高。