The role of ventricular wall stress in cardiac hypertrophy

This study tested the hypothesis that stable cardiac disease occurs when hypertrophy is sufficient to normalize wall stress imposed by a hemodynamic 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 was 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 represented 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 high values in all three groups according to the conventional model. Using our newly developed model, the resultant stress gradients attributable to the superimposed residual stress were much lower. There was a significant association between clinical cardiac decompensation and both 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 showed a close correlation with heart weight (p < 0.025). Maximum resultant stress in the eccentric hypertrophy group was higher than that in the other groups (p < 0.0015). The results from this study indicate that the left ventricular wall stress is closely correlated with left ventricular performance and is a good predictor of chronic cardiac failure.