Background The third heart sound (S-3) occurs shortly after the early
(E-wave) peak of the transmitral diastolic Doppler velocity profile (D
VP). It is thought to be due to cardiohemic vibrations powered by rapi
d deceleration of transmitral blood how. Although the presence, timing
, and clinical correlates of the S-3 have been extensively characteriz
ed, derivation and validation of a causal, mathematical relation betwe
en transmitral flow velocity and the S-3 are lacking. Methods and Resu
lts To characterize the kinematics and physiological mechanisms of S-3
production, we modeled the cardiohemic system as a forced, damped, no
nlinear harmonic oscillator. The forcing term used a closed-form mathe
matical expression for the deceleration portion of the DVP. We tested
the hypothesis that our model's predictions for amplitude, timing, and
frequency of S-3 accurately predict the transthoracic phonocardiogram
, using the simultaneously recorded transmitral Doppler E wave as inpu
t, in three subject groups: those with audible pathological S-3, those
with audible physiological S-3, and those with inaudible S-3. Conclus
ions We found excellent agreement between model prediction and the obs
erved data for all three subject groups. We conclude that, in the pres
ence of a normal mitral valve, the kinematics of filling requires that
all hearts have oscillations of the cardiohemic system during E-wave
deceleration. However, the oscillations may not have high enough ampli
tude or frequency to be heard as an S-3 unless there is sufficiently r
apid fluid deceleration (of the Doppler E-wave contour) with sufficien
t cardiohemic coupling.