[Phonoechocardiographic study on the genesis of the initial low-frequency component of the first heart sound].

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.