This study tested the hypothesis that stable cardiac disease occurs wh
en hypertrophy is sufficient to normalize wall stress imposed by a hem
odynamic load and that cardiac decompensation occurs when wall stress
becomes abnormal as the limit of the hypertrophic process is reached.
Toward this end, comprehensive stress analysis of the left ventricle w
as performed on 46 autopsy heart specimens constituting three groups:
normal control, concentric left ventricular hypertrophy, and eccentric
left ventricular hypertrophy. Our analytical method took into account
the effect of residual stress on the total stress distribution and re
presented an approach to stress analysis of the left ventricle that is
more accurate than the conventional approach. The stress gradient in
the left ventricular wall attributable to pressure alone showed very h
igh values in all three groups according to the conventional model. Us
ing our newly developed model, the resultant stress gradients attribut
able to the superimposed residual stress were much lower. There was a
significant association between clinical cardiac decompensation and bo
th maximum resultant stress (p<0.005) and resultant stress gradient (p
<0.05). We also found close association between cardiac decompensation
and heart weight (p<0.0015). Furthermore, maximum resultant stress sh
owed a close correlation with heart weight (p<0.025). Maximum resultan
t stress in the eccentric hypertrophy group was higher than that in th
e other groups (p<0.0015). The results from this study indicate that t
he left ventricular wall stress is closely correlated with left ventri
cular performance and is a good predictor of chronic cardiac failure.