Cohen M V, Teichholz L E, Gorlin R
Br Heart J. 1976 Jun;38(6):595-604. doi: 10.1136/hrt.38.6.595.
Studies were made with standard time motion and B-scan echocardiography on 48 patients including 5 with idiopathic hypertrophic subaortic stenosis (hypertrophic obstructive cardiomyopathy), undergoing diagnostic cardiac catheterization. The dimensions of the left ventricular outflow (O) and inflow (I) tracts were measured on the B-scan images. The outflow tract was significantly narrowed in idiopathic hypertrophic subaortic stenosis at both end-systole (1-1+/-0-1 cm) and end-diastole (1-3+/-0-1 cm) when compared with the average width in other patients (2-6+/-0-1 and 3-0+/-0-1 cm, at end-systole and end-diastole, respectively) (P less than 0-001) or normal subjects (2-4+/-0-3 and 2-9+/-0-2 cm) (P less than 0-01). Furthermore, the O/I ratio differed significantly in idiopathic hypertrophic subaortic stenosis (0-5+/-0-1 at end-systole and 0-6+/-0-1 at end-diastole) from that in all other groups (1-4+/-0-1 at both end-systole and end-diastole) (P less than 0-005). There was no appreciable change in the width of the outflow tract from mid- to end-systole in the two patients in whom this was examined. The data support the contention that the anterior leaflet of the mitral valve assumes an abnormally anterior position in idiopathic hypertrophic subaortic stenosis. Though the systolic anterior movement of the tip of the anterior leaflet of the mitral valve shown by M-mode echocardiography could not readily be confirmed with B-scans, we believe that the narrowed outflow tract found in the present investigation contributes to the obstruction that occurs in this disease. We suggest that this outflow tract narrowing is probably caused by hypertrophy of the ventricular septum which in itself contributes to the narrowing, but which also displaces the papillary muscles and thus produces abnormal traction on the mitral valve and striking anterior displacement of the valve apparatus.
对48例患者进行了标准时间运动和B型超声心动图研究,其中包括5例特发性肥厚性主动脉瓣下狭窄(肥厚性梗阻性心肌病)患者,这些患者正在接受诊断性心导管检查。在B型超声图像上测量左心室流出道(O)和流入道(I)的尺寸。与其他患者(收缩末期和舒张末期平均宽度分别为2.6±0.1和3.0±0.1cm)(P<0.001)或正常受试者(收缩末期和舒张末期平均宽度分别为2.4±0.3和2.9±0.2cm)(P<0.01)相比,特发性肥厚性主动脉瓣下狭窄患者在收缩末期(1.1±0.1cm)和舒张末期(1.3±0.1cm)时流出道明显变窄。此外,特发性肥厚性主动脉瓣下狭窄患者的O/I比值(收缩末期为0.5±0.1,舒张末期为0.6±0.1)与所有其他组(收缩末期和舒张末期均为1.4±0.1)有显著差异(P<0.005)。在检查的2例患者中,从收缩中期到收缩末期流出道宽度没有明显变化。这些数据支持二尖瓣前叶在特发性肥厚性主动脉瓣下狭窄中处于异常前位的观点。虽然M型超声心动图显示的二尖瓣前叶尖端收缩期前向运动在B型超声检查中不易得到证实,但我们认为本研究中发现的流出道狭窄是该疾病发生梗阻的原因之一。我们认为这种流出道狭窄可能是由于室间隔肥厚引起的,室间隔肥厚本身导致流出道狭窄,但同时也使乳头肌移位,从而对二尖瓣产生异常牵拉,使瓣膜装置显著向前移位。