Three-wall segment (TriSeg) model describing mechanics and hemodynamics of ventricular interaction.
A mathematical model (TriSeg model) of ventricular mechanics incorporating mechanical interaction of the left and right ventricular free walls and the interventricular septum is presented. Global left and right ventricular pump mechanics were related to representative myofiber mechanics in the three ventricular walls, satisfying the principle of conservation of energy. The walls were mechanically coupled satisfying tensile force equilibrium in the junction. Wall sizes and masses were rendered by adaptation to normalize mechanical myofiber load to physiological standard levels. The TriSeg model was implemented in the previously published lumped closed-loop CircAdapt model of heart and circulation. Simulation results of cardiac mechanics and hemodynamics during normal ventricular loading, acute pulmonary hypertension, and chronic pulmonary hypertension (including load adaptation) agreed with clinical data as obtained in healthy volunteers and pulmonary hypertension patients. In chronic pulmonary hypertension, the model predicted right ventricular free wall hypertrophy, increased systolic pulmonary flow acceleration, and increased right ventricular isovolumic contraction and relaxation times. Furthermore, septal curvature decreased linearly with its transmural pressure difference. In conclusion, the TriSeg model enables realistic simulation of ventricular mechanics including interaction between left and right ventricular pump mechanics, dynamics of septal geometry, and myofiber mechanics in the three ventricular walls.
Lumens
Joost
J
Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, PO Box 616, 6200 MD, Maastricht, The Netherlands. j.lumens@fys.unimaas.nl
Delhaas
Tammo
T
Kirn
Borut
B
Arts
Theo
T
D006346:Heart Septum / Q000502:physiology*; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D008955:Models, Cardiovascular; D008962:Models, Theoretical; D014463:Ultrasonography; D016277:Ventricular Function, Left / Q000502:physiology*; D016278:Ventricular Function, Right / Q000502:physiology*