Hasegawa I, Hada Y, Sakamoto T, Amano K, Takahashi H, Takahashi T, Suzuki J, Sugimoto T
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo.
J Cardiol. 1988 Jun;18(2):339-51.
Our previous study of mitral regurgitation in obstructive hypertrophic cardiomyopathy suggested that left ventricular outflow obstruction due to systolic anterior motion of the distal residual anterior mitral leaflet may hydrodynamically induce mid-systolic mitral regurgitation. To test this hypothesis, we examined whether drug-induced left ventricular outflow obstruction in dogs might cause mitral regurgitation. Dobutamine, 20-60 micrograms/kg/min, induced the obstruction due to mitral systolic anterior motion with mitral-septal contact in 11 of 18 dogs. Pulsed Doppler and contrast echocardiography demonstrated that mitral regurgitation was concomitantly induced in the 11 dogs. The regurgitation was prominent during mid-systole from the onset to the end of mitral-septal contact. Two-dimensional echocardiography showed reduction of the mitral annular dimension and anterior shifts of the mitral valve coaptation during drug infusion in the 11 dogs. Accordingly, the distal portion of the mitral valve, especially of its anterior leaflet, became residual, and moved anteriorly in early systole and protruded into the outflow tract during mid-systole. Catheter-tip pressure recordings simultaneous with two-dimensional echocardiographic observation revealed that the outflow pressure gradient occurred across the protruding distal residual mitral valve. The onset and the end of the pressure gradient were nearly simultaneous with those of the mitral-septal contact. After cessation of the infusion, the mid-systolic mitral regurgitation disappeared together with the obstruction. These results indicate a close relationship between left ventricular outflow obstruction and mid-systolic mitral regurgitation, and strongly support the hypothesis that the obstruction due to systolic anterior motion of the distal residual anterior mitral leaflet is responsible for mitral regurgitation.
我们之前对梗阻性肥厚型心肌病二尖瓣反流的研究表明,远端残留二尖瓣前叶收缩期前向运动导致的左心室流出道梗阻可能在流体动力学上诱发收缩中期二尖瓣反流。为了验证这一假设,我们研究了犬类药物诱导的左心室流出道梗阻是否会导致二尖瓣反流。以20 - 60微克/千克/分钟的剂量静脉滴注多巴酚丁胺,在18只犬中有11只诱发了因二尖瓣收缩期前向运动及二尖瓣 - 室间隔接触所致的梗阻。脉冲多普勒和对比超声心动图显示,这11只犬同时出现了二尖瓣反流。在二尖瓣与室间隔接触的整个收缩中期,反流都很明显。二维超声心动图显示,在这11只犬静脉滴注药物期间,二尖瓣环尺寸减小,二尖瓣瓣叶闭合点向前移位。因此,二尖瓣的远端部分,尤其是前叶,变得残留,并在收缩早期向前移动,在收缩中期突入流出道。与二维超声心动图观察同步进行的导管尖端压力记录显示,流出道压力梯度出现在突出的远端残留二尖瓣上。压力梯度的起始和结束与二尖瓣 - 室间隔接触的起始和结束几乎同步。停止滴注后,收缩中期二尖瓣反流与梗阻一同消失。这些结果表明左心室流出道梗阻与收缩中期二尖瓣反流之间存在密切关系,并有力地支持了以下假设:远端残留二尖瓣前叶收缩期前向运动所致的梗阻是二尖瓣反流的原因。