title: The effects of cross-fiber deformation on axial fiber stress in myocardium.
abstract: We incorporated a three-dimensional generalization of the Huxley cross-bridge theory in a finite element model of ventricular mechanics to examine the effect of nonaxial deformations on active stress in myocardium. According to this new theory, which assumes that macroscopic tissue deformations are transmitted to the myofilament lattice, lateral myofilament spacing affects the axial fiber stress. We calculated stresses and deformations at end-systole under the assumption of strictly isometric conditions. Our results suggest that at the end of ejection, nonaxial deformations may significantly reduce active axial fiber stress in the inner half of the wall of the normal left ventricle (18-35 percent at endocardium, depending on location with respect to apex and base). Moreover, this effect is greater in the case of a compliant ischemic region produced by occlusion of the left anterior descending or circumflex coronary artery (26-54 percent at endocardium). On the other hand, stiffening of the remote and ischemic regions (in the case of a two-week-old infarct) lessens the effect of nonaxial deformation on active stress at all locations (9-32 percent endocardial reductions). These calculated effects are sufficiently large to suggest that the influence of nonaxial deformation on active fiber stress may be important, and should be considered in future studies of cardiac mechanics.
authors.affiliation: Department of Biomedical Engineering, Washington University, St. Louis, MO 63130-4899, USA.
authors.forename: G I
authors.initials: GI
authors.lastname: Zahalak
authors.forename: V
authors.initials: V
authors.lastname: de Laborderie
authors.forename: J M
authors.initials: JM
authors.lastname: Guccione
mesh_terms: D003331:Coronary Vessels / Q000503:physiopathology; D004548:Elasticity; D020342:Finite Element Analysis; D006321:Heart / Q000502:physiology*; D006801:Humans; D007537:Isometric Contraction; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D012518:Sarcomeres / Q000502:physiology; D013314:Stress, Mechanical