Objectives: The aim of the present study was to test two hypotheses: (
1) the momentum of the blood flowing out of the left ventricle toward
the aorta (inertia force) plays an important role in the initiation of
decay and the maximum rate of decay (peak (- dP/dt)) of left ventricu
lar pressure (P); (2) a normal heart itself generates the inertia forc
e which enhances its function. Methods: The contribution of the inerti
a force to (-dP/dt) was theoretically given as rho c alpha, where rho
is the blood density, c the pulse wave velocity, and alpha the deceler
ation rate of aortic blood flow. The correlations of peak (-dP/dt) wit
h rho c alpha and with the time constant (tau) of the pressure decay d
uring isovolumic relaxation, which was considered to represent myocard
ial relaxation characteristics, were compared in seven does. We develo
ped a method of grading the strength of the inertia force, using the p
hase loop of left ventricular pressure (dP/dt vs, P relation). The met
hod was applied to the records of 25 patients with ischemic heart dise
ase, from which high fidelity left ventricular pressure recordings wer
e available. Results: The correlation of peak (-dP/dt) with rho c alph
a was much higher than with tau (0.75 vs. - 0.46). 16 of the 25 patien
ts showed evidence of the inertia force. However, other patients showe
d no inertia force. The strength of the inertia force showed a signifi
cant (P < 0.05) correlation with left ventricular end-diastolic pressu
re (r = -0.46), cardiac index (r = 0.62), stroke volume index (r = 0.6
9), ejection fraction (r = 0.46), and peak (-dP/dt) (r = 0.56). Conclu
sion: The inertia force of late systolic aortic flow contributed to ve
ntricular relaxation in the normal heart.