Cell thickening accounts for less then one third of normal left ventricular wall thickening. Systolic deformation along the cleavage planes separating the laminae would produce transverse shear strains. Significant radial longitudinal and radial circumferential systolic shearing deformation has recently been found using a finite deformation approach developed in the investigator s laboratory. In recent studies the investigator explored the hypothesis that shearing deformation between these laminae produces wall thickening. He took advantage of the fact that the cleavage planes course in different directions on the septum and the left ventricular free wall. The investigator found that shearing deformation was of the opposite sign at the two sites and wall thickening was proportional to the initial cleavage plane angle. These results strongly support his hypothesis that motion of radially orientated laminae of myocytes produces wall thickening. In this proposal, modeling and experimental studies will be used to explore this unique mechanism of wall thickening. The investigator will test the hypothesis that it is the unique nonaxisymmetric ventricular architecture and endocardial-to- epicardial activation sequence that produce the shears. Further studies will explore the regulation of transverse shears by hemodynamic factors and the effects of changes in cleavage plane anatomy observed in ventricular remodeling and hypertrophy on this mechanism of wall thickening.
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