T H Reif1, M D Silver. 1. Republic Medical, Inc, Vero Beach, Florida, USA.
Abstract
OBJECTIVE: To study the cause of myocardial rupture and its related complications using a computer-assisted model of left ventricular (LV) function following acute myocardial infarction. DESIGN: A model previously described by other authors was modified. The LV was portrayed as a three-layered ellipsoid at end-diastolic volume (135 mL). The aspect ratio of the ellipsoid's semi-minor: semi-major axis was 0.6. The apical middle layer was infarcted with an angle of damage of 40%, the infarcted layer being 81.8% of total LV wall thickness. A one-half symmetry condition generated an axisymmetrical, linear, elastic finite element model with 1056 first-order elements and 1127 nodes. The endocardial surface was subjected to static internal pressure, modelling the instant of end-isovolumetric contraction. Noninfarcted myocardium was assumed to be variably stiffer than infarcted muscle. A simple orthotropic model was used to approximate the directional characteristics of muscle layers. RESULTS: Maximum von Mises stresses were found on the endocardial surface near the centre and edge of the angle of damage, the latter generally observed as the site of myocardial rupture. Static stress concentration factors were computed for the isotropic and orthotropic cases. The directional characteristics of the myocardium appeared to be protective. CONCLUSIONS: A more complete pathogenic model for myocardial rupture following acute infarction is stress concentration --> endocardial tear --> dissecting hemorrhage. Marked deformation is predicted in the endocardial surface within the angle of damage, consistent with the correlation between acute myocardial infarction and LV aneurysm formation.
OBJECTIVE: To study the cause of myocardial rupture and its related complications using a computer-assisted model of left ventricular (LV) function following acute myocardial infarction. DESIGN: A model previously described by other authors was modified. The LV was portrayed as a three-layered ellipsoid at end-diastolic volume (135 mL). The aspect ratio of the ellipsoid's semi-minor: semi-major axis was 0.6. The apical middle layer was infarcted with an angle of damage of 40%, the infarcted layer being 81.8% of total LV wall thickness. A one-half symmetry condition generated an axisymmetrical, linear, elastic finite element model with 1056 first-order elements and 1127 nodes. The endocardial surface was subjected to static internal pressure, modelling the instant of end-isovolumetric contraction. Noninfarcted myocardium was assumed to be variably stiffer than infarcted muscle. A simple orthotropic model was used to approximate the directional characteristics of muscle layers. RESULTS: Maximum von Mises stresses were found on the endocardial surface near the centre and edge of the angle of damage, the latter generally observed as the site of myocardial rupture. Static stress concentration factors were computed for the isotropic and orthotropic cases. The directional characteristics of the myocardium appeared to be protective. CONCLUSIONS: A more complete pathogenic model for myocardial rupture following acute infarction is stress concentration --> endocardial tear --> dissecting hemorrhage. Marked deformation is predicted in the endocardial surface within the angle of damage, consistent with the correlation between acute myocardial infarction and LV aneurysm formation.