Structure and torsion in the normal and situs inversus totalis cardiac left ventricle. II. Modeling cardiac adaptation to mechanical load.
Mathematical models provide a suitable platform to test hypotheses on the relation between local mechanical stimuli and responses to cardiac structure and geometry. In the present model study, we tested hypothesized mechanical stimuli and responses in cardiac adaptation to mechanical load on their ability to estimate a realistic myocardial structure of the normal and situs inversus totalis (SIT) left ventricle (LV). In a cylindrical model of the LV, 1) mass was adapted in response to myofiber strain at the beginning of ejection and to global contractility (average systolic pressure), 2) cavity volume was adapted in response to fiber strain during ejection, and 3) myofiber orientations were adapted in response to myofiber strain during ejection and local misalignment between neighboring tissue parts. The model was able to generate a realistic normal LV geometry and structure. In addition, the model was also able to simulate the instigating situation in the rare SIT LV with opposite torsion and transmural courses in myofiber direction between the apex and base [Delhaas et al. (6)]. These results substantiate the importance of mechanical load in the formation and maintenance of cardiac structure and geometry. Furthermore, in the model, adapted myocardial architecture was found to be insensitive to fiber misalignment in the transmural direction, i.e., myofiber strain during ejection was sufficient to generate a realistic transmural variation in myofiber orientation. In addition, the model estimates that, despite differences in structure, global pump work and the mass of the normal and SIT LV are similar.
Kroon
Wilco
W
Dept. of Physiology, Cardiovascular Research Institute Maastricht, Maastricht Univ., PO Box 616, Maastricht NL-6200 MD, The Netherlands. jw.kroon@fys.unimaas.nl
Delhaas
Tammo
T
Bovendeerd
Peter
P
Arts
Theo
T
D000222:Adaptation, Physiological; D003198:Computer Simulation; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D008953:Models, Anatomic; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology*; D015203:Reproducibility of Results; D012399:Rotation; D012857:Situs Inversus / Q000473:pathology* / Q000503:physiopathology; D013314:Stress, Mechanical; D013997:Time Factors; D014102:Torsion Abnormality; D018487:Ventricular Dysfunction, Left / Q000473:pathology* / Q000503:physiopathology