The uniformity of the mechanical load of the cardiac fibers in the wall is maintained by continuous remodeling. In this proposed model the myocyte changes direction in optimizing systolic sarcomere shortening. Early systolic stretch and contractility increases the mass of contractile proteins. Cyclic strain of the myocardial tissue diminishes passive stiffness, resulting in the control of ventricular end-diastolic volume. Utilizing these rules of remodeling in our mathematical model yields that the natural helical pathways of the myocardial fibers in the wall are formed automatically.
|Original language||English (US)|
|Number of pages||12|
|Journal||Advances in Experimental Medicine and Biology|
|State||Published - 1995|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)