Since Frank (1898)((1)) and Starling (1918)((2)) showed that the quant
ified pressure-volume relationship of the heart offers a good view of
the transfer of energy by the heart, many attempts have been made to u
se this relationship in diagnostics. The basis of the description is f
ound in the microscopic structure of the striated muscle cell in which
a simple relation can be found between force, developed after full ac
tivation of the muscle cell, and the length of the contractile unit, t
he sarcomere. The advantage was that factors affecting the geometry of
the cell could be separated from those affecting the biochemical proc
esses from excitation to contraction. The relationship gives insight i
nto the mechanisms of oxygen consumption and work performed by the hea
rt.((4)) In this study we used isolated rat hearts, perfused in a modi
fied Langendorff system. Filling of the heart is controlled by the FDP
. This filling of the left ventricle runs along the EDP-EDV relationsh
ip. The slope of this relation represents the stiffness of the diastol
ic myocardium. We show that the diastolic stiffness is the sum of two
separated elastic elements: a calcium-independent, passive, and a calc
ium-dependent, active, element. Both elements can be affected. Pharmac
ological interventions (Ca channel blocking, beta-receptor stimulation
/blocking, etc.) can change the contribution of the active element. Pa
thological changes (hypertrophy, diabetes mellitus) affect the passive
part. If in medical treatment the intracellular calcium is decreased,
the EDV is found to be increased based on the changed diastolic stiff
ness. To maintain a comparable cardiac output, EDP has to increase. Th
is mechanism shifts the cardiac reserve toward the region in which dec
ompensation occurs. It is evident that reliable, and possibly noninvas
ive recording of the diastolic pressure-volume relationship prevents u
nexpected mechanisms.