142 
CARDIAC MODELS 
indication of heart failure since alterations in 
the passive pressure-volume relationship of the 
ventricular chambers will alter end-diastolic 
pressure at any ventricular volume. Thus, the 
importance of accurately assessing the contrac- 
tility of the myocardium in the study of the pa- 
tient with heart disease has become apparent ; it 
is imperative to evaluate the myocardial con- 
tractility in both experimental and clinical ven- 
tricular hypertrophy and congestive heart 
failure to achieve a proper basic understanding 
of these conditions. Further, the compensatory 
mechanisms which maintains circulatory func- 
tion when cardiac muscle function is depressed 
are more readily understood when congestive 
heart failure is considered in terms of cardiac 
muscle work, load and performance. 
The detailed work of A. V. Hill on skeletal 
muscle has been extended recently to the under- 
standing of the intrinsic contractile state of 
cardiac muscle, making it possible to examine 
the function of the heart in terms of myocardial 
muscle mechanics.^ Cardiac muscle is thought 
of as a three-component mechanical model with 
a freely extensible contractile element which 
when activated develops force and shortens. 
This contractile element is connected in series 
with an elastic component, the series elastic and 
in parallel with another elastic component re- 
ferred to as the parallel elastic. Myocardial con- 
tractile state is a basic property of the contractile 
element. Study of the force velocity rela- 
tionships of the isolated heart muscle with ex- 
trapolation to zero load allows determination of 
the maximum velocity of shortening and a 
quantitative description of the mechanical func- 
tion of the contractile element. Cardiac muscle 
function can be described in terms of the in- 
stantaneous force, velocity and shortening and 
the function of the intact ventricle can also be 
expressed within these concepts. 
To more clearly delineate the pathophysiologic 
process, several questions had to be answered. 
What is the degree of hypertrophy and the time 
course of hypertrophy of the ventricle after an 
excessive load was placed on the heart? What is 
the intrinsic contractile state of each unit of 
myocardium in the hypertrophied heart with 
and without overt heart failure ? Is overall com- 
pensation in the hypertrophied heart main- 
tained by an increased muscle mass, each unit 
of which has a normal or even increased con- 
tractile function or is the function of each unit 
of hypertrophied muscle depressed while overall 
compensation is maintained by an increase in 
the contractile mass? What is the contractile 
state of each unit of myocardium in the hyper- 
trophied ventricle when overt heart failure has 
occurred? Does failure of the ventricle as a 
pump occur in the presence of inadequate con- 
tractile mass although the contractile function 
of each unit is normal or even supernormal, or 
is congestive heart failure the consequence of 
the depression of the contractility of myocar- 
dium that is not compensated for by the in- 
crease in muscle mass? 
Furthermore, elucidation of the biochemical 
basis for congestive heart failure is necessary. 
Of particular interest is the efficiency of the 
conversion of chemical energy to mechanical 
work in heart failure. Adenosine triphosphate 
(ATP) and creatine phosphate are the immedi- 
ate sources of energy for muscle contraction 
and it has recently been demonstrated that the 
utilization of these high energy phosphates by 
isolated heart muscle preparations can be di- 
rectly correlated with their mechanical 
activity."'^ This has been accomplished by in- 
hibiting energy production by blockade of both 
oxidative phosphorylation and anaerobic glyco- 
lysis, and subsequently estimating the utiliza- 
tion of energy stores both at rest and during 
activity. 
Lastly, although the synthesis of myofibrillar 
protein in heart subjected to a systolic overload 
has been studied, the extent to which the 
connective tissue elements participate in this 
response has not been defined. In hypertrophy 
of skeletal and smooth muscle the content of col- 
lagen has been shown to increase along with 
muscle proteins without a change in their rela- 
tive proportions.^' ^° In the normal human 
heart, the concentration of collagen is independ- 
ent of age, except for increase in the right 
ventricle during the first ten years of life. Blum- 
gard et al.'^ measured collagen concentrations 
in the hypertrophied human heart and found it 
increased in nine of twenty-four. Of these nine, 
five had demonstrable coronary disease. How- 
ever, Montforte and Perez-Tamaya^- found 
