Residual strain in ischemic ventricular myocardium

Structural remodeling during acute myocardial Infarction affects ventricula r wall stress and strain. To sec whether acute myocardial infarction alters residual stress and strain in the left ventricle (LV), we measured opening angles in rat hearts after 30 minutes of left coronary artery occlusion. T he mean opening angle in 18 ischemic hearts (51 +/- 20 deg) was significant ly greater than in Jive sham-operated controls (29 +/- 11 deg, P < 0.05). T o determine whether these alterations in residual strain may be associated with strain softening caused by systolic overstretch of the noncontracting ischemic tissue, we also measured opening angles in isolated hearts that ha d been passively inflated to high LV pressures (120 mmHg). The mean opening angle of the strain-softened hearts was not significantly different from t he sham-operated hearts (34 +/- 27 deg, P = 0.74). Mean collagen area fract ions in the myocardium were not significantly different between ischemic he arts (0.027 +/- 0.014) and the nonischemic group (0.022 +/- 0.011). Althoug h there were significant differences in opening angles measured with ischem ia, they do not appear to be a result of altered extracellular collagen con tent or softening associated with overstretch. Thus, there is a significant change in residual strain associated with acute ischemia that may be relat ed to changes in collagen fiber structure, myocyte structure, or metabolic state.