title: Influence of endocardial-epicardial crossover of muscle fibers on left ventricular wall mechanics.
abstract: The influence of variations of fiber direction on the distribution of stress and strain in the left ventricular wall was investigated using a finite element model to simulate the mechanics of the left ventricle. The commonly modelled helix fiber angle was defined as the angle between the local circumferential direction and the projection of the fiber path on the plane perpendicular to the local radial direction. In the present study, an additional angle, the transverse fiber angle, was used to model the continuous course of the muscle fibers between the inner and the outer layers of the ventricular wall. This angle was defined as the angle between the circumferential direction and the projection of the fiber path on the plane perpendicular to the local longitudinal direction. First, a reference simulation of left ventricular mechanics during a cardiac cycle was performed, in which the transverse angle was set to zero. Next, we performed two simulations in which the spatial distribution of either the transverse or the helix angle was varied with respect to the reference situation, the spatially averaged variations being about 3 and 14 degrees, respectively. The changes in fiber orientation hardly affected the pressure-volume relation of the ventricle, but significantly affected the spatial distribution of active muscle fiber stress (up to 50% change) and sarcomere length (up to 0.1 micron change). In the basal and apical region of the wall, shear deformation in the circumferential-radial plane was significantly reduced by introduction of a nonzero transverse angle. Thus, the loading of the passive tissue may be reduced by the endocardial-epicardial crossover of the muscle fibers.
authors.affiliation: Department of Mechanical Engineering, Eindhoven University of Technology, The Netherlands.
authors.forename: P H
authors.initials: PH
authors.lastname: Bovendeerd
authors.forename: J M
authors.initials: JM
authors.lastname: Huyghe
authors.forename: T
authors.initials: T
authors.lastname: Arts
authors.forename: D H
authors.initials: DH
authors.lastname: van Campen
authors.forename: R S
authors.initials: RS
authors.lastname: Reneman
mesh_terms: D001011:Aorta / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002306:Cardiac Volume / Q000502:physiology; D003198:Computer Simulation; D003238:Connective Tissue / Q000033:anatomy & histology / Q000502:physiology; D004548:Elasticity; D004699:Endocardium / Q000033:anatomy & histology* / Q000502:physiology; D006321:Heart / Q000502:physiology; D006801:Humans; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000502:physiology; D009210:Myofibrils / Q000502:physiology / Q000648:ultrastructure; D010210:Papillary Muscles / Q000033:anatomy & histology / Q000502:physiology; D010496:Pericardium / Q000033:anatomy & histology* / Q000502:physiology; D012399:Rotation; D012518:Sarcomeres / Q000502:physiology / Q000648:ultrastructure; D013314:Stress, Mechanical; D013318:Stroke Volume / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*; D017725:Ventricular Pressure / Q000502:physiology