Hisako Takahashi

Follow-Up in mitral valve prolapse by phonocardiography, M-mode and two-dimensional echocardiography and Doppler echocardiography

To assess the serial phonocardiographic and echocardiographic change in patients with mitral valve prolapse (MVP), phonocardiograms and echocardiograms were reviewed retrospectively in 116 patients (48 men and 68 women, mean age 27 years) who had been determined to have MVP and were reexamined 4.3 years (range 1 to 14) later by phonocardiography and echocardiography between 1971 and 1988. Follow-up phonocardiograms showed periods when 5 of 18 patients with silent MVP developed mid- or late systolic clicks. Of 57 patients with mid- or late systolic clicks, 15 had silent MVP, 6 developed a late systolic murmur with or without systolic clicks and 1 developed a pansystolic murmur. Two of 9 patients with an isolated late systolic murmur developed a pansystolic murmur. M-mode echocardiograms showed that left atrial and left ventricular dimensions at end-diastole and end-systole increased in patients with systolic murmur (33 +/- 10 vs 35 +/- 11, 46 +/- 6 vs 50 +/- 7 and 29 +/- 4 vs 31 +/- 5 mm, respectively, all p less than 0.001) and no statistically significant changes in any of these dimensions were found in patients without a systolic murmur. The degree of MVP evaluated by the anteroposterior mitral leaflet angle on the 2-dimensional echocardiogram was more severe in patients with a systolic murmur than in patients without systolic murmur (157 +/- 12 vs 131 +/- 16 degrees, p less than 0.001). The degree of prolapse did not change during the follow-up periods. The number of patients with mitral regurgitation detected by pulsed Doppler echocardiography increased from 21 of 72 (29%) to 31 of 72 (43%).(ABSTRACT TRUNCATED AT 250 WORDS)

Noninvasive study of the presystolic component of the first heart sound in mitral stenosis.

Echophonocardiography and pulsed Doppler echocardiography were performed in 30 patients with mitral stenosis (19 with atrial fibrillation and 11 with sinus rhythm) to investigate the genesis of the presystolic component or small apical vibrations preceding the first heart sound in mitral stenosis. In 27 patients, mitral valve closure preceded or coincided with tricuspid valve closure regardless of the preceding RR interval. Of three patients whose tricuspid valve closed prematurely, two had a prolonged PR interval. The soft apical vibrations, which were recorded during the final rapid closing motion of the mitral valve echogram (B-C slope), began with the upstroke of the apexcardiogram. During this event the pulsed Doppler echocardiogram revealed a deceleration in the velocity of mitral inflow. In two exceptional patients with a prolonged PR interval, this apical sound was separated from a presystolic rumble that occurred during an accelerated phase of mitral inflow or at the A wave of mitral valve echograms. In conclusion, the tricuspid valve is not a factor contributing to the genesis of the small apical vibrations preceding the first heart sound in mitral stenosis. These vibrations are caused by acceleration of left ventricular contraction and deceleration of mitral inflow in the presence of a stenotic valve.

Echophonocardiographic study of the initial low frequency component of the first heart sound.

To investigate the genesis of the initial low frequency component of the first heart sound that precedes the high frequency vibrations associated with closure of the atrioventricular valves, echophonocardiograms of 36 persons were recorded. These included 10 normal subjects and 26 patients with various types of heart disease including mitral valve replacement. Electrocardiograms demonstrated normal sinus rhythm in 23 subjects, atrial fibrillation in 9, complete atrioventricular block in 2 and atrial flutter in 2. In the phonocardiogram, the low frequency component of the first heart sound followed the onset of the QRS complex and preceded the first high frequency component of this sound. The low frequency component occurred simultaneously with the beginning of the final fast closing movement of the mitral valve on the echocardiogram and was found both in normal rhythm and in arrhythmias. However, in arrhythmias its intensity varied on a beat to beat basis, being loudest after a short RR interval or when atrial systole occurred very close to the expected time of ventricular systole. In patients in whom apexcardiograms were recorded, the low frequency component was coincident with or very close to the onset of ventricular systole. It is concluded that the low frequency component of the first heart sound represents vibrations caused by contraction of the left ventricle and deceleration of antegrade blood flow across the mitral valve. Neither atrial contraction nor mitral valve tension is necessary for the production of this soft initial component.