Hada Y, Sakamoto T, Amano K, Yamaguchi T, Ishimitsu T, Takenaka K, Takahashi H, Takikawa R
J Cardiogr. 1982 Sep;12(3):655-65.
The high-frequency vibrations of the first heart sound (S1) have been reported to be associated with the closure of atrioventricular valves. However, the genesis of the low-frequency component (LFC) preceding S1 remains controversial. In order to investigate the genesis of the production of this LFC, we recorded phonocardiograms simultaneously with M-mode echocardiograms in 10 healthy subjects and 26 patients with various diseases including mitral valve replacement. The apical phonocardiograms were recorded using a 100 Hz/12 dB high-pass filter and a commercially available acceleration microphone. Patients with rheumatic mitral valve disease and bundle branch block were excluded from this study. The electrocardiograms demonstrated sinus rhythm in 23, atrial fibrillation in nine, complete atrioventricular block in two and atrial flutter in two. The P-R interval in sinus rhythm ranged from 130 to 200 msec. The LFC occurred an average of 24 msec after the QRS complex, but 38 msec before the first high-frequency component of S1. The final fast closing movement of the mitral valve echogram started following the onset of LFC in sinus rhythm or the arrhythmias. Coaptation of the mitral valve leaflets was coincident with the first high-frequency S1. In 23 cases with the visible tricuspid valve, the valve closure occurred 28 msec after that of the mitral valve. The onset of the LFC was almost synchronous in timing with, or very close (10 msec or less) to the initial upstroke of apex cardiograms simultaneously recorded in 10 cases. The amplitude of the LFC was constantly smaller than that of S1 in all cases, but it was variable in atrial fibrillation or complete atrioventricular block. The LFC became loudest after a short RR interval and then ventricular systole was coincided in time with the rapid filling of the left ventricle, or when atrial systole was very close in time to an expected time of ventricular systole. It is certain that antegrade mitral blood flow was decelerated at that time, though the mitral valve was in the rapidly closing process. We conclude that the LFC is produced by the vibration of cardiohemic system, or the acceleration of the left ventricular mass plus the deceleration of blood flow, and that atrial activity and atrioventricular valve tension are not prerequisite to the production of this soft apical vibration preceding S1.
第一心音（S1）的高频振动据报道与房室瓣关闭有关。然而，S1之前低频成分（LFC）的起源仍存在争议。为了研究该LFC产生的起源，我们在10名健康受试者和26例患有包括二尖瓣置换在内的各种疾病的患者中同步记录了心音图和M型超声心动图。使用100Hz/12dB高通滤波器和市售加速度麦克风记录心尖心音图。本研究排除了风湿性二尖瓣疾病和束支传导阻滞患者。心电图显示23例为窦性心律，9例为心房颤动，2例为完全性房室传导阻滞，2例为心房扑动。窦性心律时P-R间期为130至200毫秒。LFC平均在QRS波群后24毫秒出现，但在S1的第一个高频成分前38毫秒出现。二尖瓣超声心动图的最终快速关闭运动在窦性心律或心律失常时LFC开始后开始。二尖瓣叶的贴合与第一个高频S1同时发生。在23例可见三尖瓣的病例中，瓣膜关闭发生在二尖瓣关闭后28毫秒。在10例同时记录的心尖心动图中，LFC的起始时间与初始上升几乎同步，或非常接近（10毫秒或更短）。在所有病例中，LFC的幅度始终小于S1，但在心房颤动或完全性房室传导阻滞中其幅度可变。在短RR间期后LFC变得最响亮，然后心室收缩与左心室快速充盈同时发生，或者当心房收缩与预期的心室收缩时间非常接近时。尽管二尖瓣处于快速关闭过程中，但此时二尖瓣前向血流肯定减速。我们得出结论，LFC是由心脏血液系统的振动产生的，或者是左心室质量的加速加上血流的减速产生的，并且心房活动和房室瓣张力不是S1之前这种柔和的心尖振动产生的先决条件。
