146 
CARDIAC MODELS 
N RVH CHF 
(8) (9) (10) 
'-p<.05-''-p<05-' 
N RVH CHF 
(8) (9) (10) 
Figure 5. — Left, maximum rate of isometric force de- 
velopment shown for the three groups of muscles in 
g/mm-/sec. All muscles were studied at the apex of 
their length-tension curves. Right, time from stimula- 
tion to the peak of developed isometric tension in 
milliseconds. All muscles were studied at the apex of 
their length-tension curves. Numbers in parentheses 
= number of animals. Vertical lines with cross bars 
= ±1SEM. (Reproduced with permission from the 
American Heart Association, Inc. from Circulation 
Res. 21:341, 1967.) 
tive heart failure is markedly reduced, averag- 
ing 2.4 ±: 0.4 gms./mm. sq. On the other hand, 
as shown by the dotted lines on the lower por- 
tion of Figure 4, there are no significant differ- 
ences among the average resting length-tension 
curves in any of the three groups of muscles. 
These observations allowed elimination of the 
possibility that the decrease in force in failing 
muscle is due to the disengagement of the actin 
and myosin filaments known to occur on the de- 
scending limb of the Frank-Starling curve. Spe- 
cifically, it was noted that the tension at all 
points on the ascending limb of the active 
length-tension curve is depressed in the failing 
muscle. The decreased tension developed by the 
failing and hypertrophied heart muscle can be 
related to an intrinsic weakness of the muscle 
rather than an abnormal position on a basically 
normal length-tension curve, thus allowing 
rejection of the hypothesis that the decreased 
contractility of the failing heart muscle is due 
to its operation along the descending limb of the 
Frank-Starling curve. Also, the depression of 
the active length-tension curves could not be at- 
tributed to a change in compliance since the 
resting length-tension curves of the hypertro- 
phied and failing heart muscle were normal. 
The time relations of the isometrically con- 
tracting muscle can also be determined in the 
right ventricular papillary muscle preparations. 
The rate of tension development (dF/dt) and 
the time required for development of peak ten- 
sion were determined (Figure 5). The dF/dt is 
markedly depressed in the hypertrophied and 
failing heart muscle. However, the time to peak 
tension is normal in both of these groups of 
muscles. Since series elasticity is unchanged in 
cardiac muscle from the hypertrophied and fail- 
ing heart,^^ the depression of dF/dt reflects a 
decrease in the intrinsic speed of contraction 
and is a manifestation of a reduction of the in- 
tensity of the active state in the failing heart 
muscle. However, the time to peak tension is not 
altered. This later finding suggests that, al- 
though the maximal intensity of the active state 
1.0 
VELOCITY 0.6 
Ln/SEC 
0.4 
i 
u 
/i/orma/ (15) 
• 
RVH III) 
A 
CHF III! 
0.2 
LOAD g/mm' 
Figure 6. — The force-velocity relations of the three 
groups of cat papillary muscles. Average values with 
± SEM are given for each point. Velocity has been 
corrected to muscle lengths per second (Lo/sec). 
Numbers in parentheses = number of animals. (Re- 
produced with permission from the American Heart 
Association, Inc. from Circulation Res. (21:341, 
1967.) 
