A LAMINATED SHELL-MODEL FOR THE INFARCTED LEFT-VENTRICLE

Experimental studies have shown that a region of partial dysfunction o ccurs in noninfarcted heart muscle near the edge of a myocardial infar ction, where both blood flow and contractile function are compromised. Most data also indicate that the ''border zone'' for flow is much nar rower than that for function. The factors responsible for these effect s, which may lead to further infarction or other complications, are no t completely understood. Thus, to study the mechanics of this problem, we present an ellipsoidal shell model for the infarcted left ventricl e. The analysis of the model is based on a nonlinear shell theory that includes the effects of large axisymmetric deformation (with torsion) , thick-shell effects, anisotropy, muscle activation, and residual str ess. The governing equations are solved with a modified integrating ma trix technique. We study both acute and chronic apical infarcts, which are represented by relatively soft and hard passive regions, respecti vely. Comparing theoretical and experimental pressure-volume relations and wall strains indicates that the model describes the mechanical be havior of the normal and ischemic left ventricle reasonably well. The model predicts significantly elevated end-systolic stresses inside an acute infarct, which may contribute to the complication of infarct exp ansion. Near the edge of the infarct, the results show that a relative ly narrow bending boundary layer occurs within a much wider membrane b oundary layer, suggesting that these layers correspond to the perfusio n and functional border zones, respectively. The stiffer chronic infar ct alleviates the stress concentrations in the herder zone. Thus, trea tment strategies should consider the relative differences in propertie s between the infarcted and noninfarcted regions. Copyright (C) 1996 E lsevier Science Ltd.