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Mitral valve motion and pressure correlates of the Austin Flint murmur (AFM) were investigated in nine patients with aortic regurgitation using high fidelity catheter tip micromanometers and the mitral valve echocardiogram (MVE). External phonocardiography demonstrated a mid-diastolic murmur (MDM) in eight subjects and a presystolic murmur (PSM) in five. Maximum intensity of both AFM components was found in the left ventricular (LV) inflow tract; the murmur was not recordable in the left atrium (LA). In two patients, an apparent AFM was recorded in the intracardiac phonocardiogram when absent externally. Only one subject had a significant late diastolic "reversed" or LV to LA gradient; in this patient, presystolic mitral regurgitation was shown angiographically but no PSM was present and MVE revealed absence of atriogenic mitral valve re-opening. In two subjects, a PSM disappeared from the external phono when a "reversed" gradient occurred during the diastolic pause following a ventricular premature systole; this LV to LA gradient was associated with diastolic mitral regurgitation recordable in the left atrial phono. In two patients, LV inflow phono showed the MDM to begin 80-120 msec after the aortic second sound and during the D to E phase of the MVE. The rate of early diastolic mitral valve closure in patients (152 +/- 24 mm/sec) was not significantly different from 13 normals (232 +/- 10 mm/sec). With regard to the genesis of the AFM, the present study concludes: 1) diastolic mitral regurgitation plays no role, and 2) antegrade mitral valve flow is required but simultaneous retrograde aortic flow may also be necessary.

Simultaneous quantitative recordings of pressure in the aorta near a prosthetic valve and at two locations externally on the chest provide data on certain aspects of sound propagation in the human thorax. On the basis of the different speeds of propagation, it is possible to distinguish between the longitudinal and transverse vibrations contributing to the external phonocardiographic signal. Digital signal processing was employed to derive transfer functions, correlations and power spectra.

Several investigators have noted external gallop sounds to be of higher amplitude than their corresponding internal sounds (S3 and S4). In this study we hoped to determine if S3 and S4 are transmitted in the same manner as S1. In 11 closed-chest dogs, external (apical) and left ventricular pressures and sounds were recorded simultaneously with transducers with identical sensitivity and frequency responses. Volume and pressure overload and positive and negative inotropic drugs were used to generate gallop sounds. Recordings were made in the control state and after the various interventions. S3 and S4 were recorded in 17 experiments each. The amplitude of the external S1 was uniformly higher than that of internal S1 and internal gallop sounds were inconspicuous. With use of Fourier transforms, the gain function was determined by comparing internal to external S1. By inverse transform, the amplitude of the internal gallop sounds was predicted from external sounds. The internal sounds of significant amplitude were predicted in many instances, but the actual recordings showed no conspicuous sounds. The absence of internal gallop sounds of expected amplitude as calculated from the external gallop sounds and the gain function derived from the comparison of internal and external S1 make it very unlikely that external gallop sounds are derived from internal sounds.

A unitary concept is proposed to explain the genesis of the third heart sound and associated "rapid filling wave" of the apexcardiogram in physiological and pathological states including constrictive pericarditis. This theory not only clarifies the hitherto unexplained phenomenon such as presence of S3 in significant mitral stenosis, but also places in proper perspective the hemodynamic significance of S3 in physiological and various pathological states.

The absolute intensity of the first (S1), third (S3), and fourth (S4) heart sounds (in mm Hg) and the relative intensity of S4 compared with S1 were measured in 146 normal persons, aged 8 to 91 years, using an infinite time-constant, calibrated pressure mechanocardiograph applied to the chest wall with a loading pressure of 400 mm Hg. The absolute intensity of S1 (r = 0.28) and S3 (r = 0.43) decreases with age, but the absolute intensity of S4 does not increase with age (r = 0.06). Therefore, the relative intensity of S4 compared with S1 increases with age (r = 0.31). This finding may explain the increased frequency of S4 in qualitative phonocardiograms in older persons.