ABSTRACT
The arrangement of myocytes within the ventricular wall, as well as the entire orientation of the muscle mass ‘of the heart, provides the structural basis for ventricular contractile function. Beyond the normal excitation–contraction process, both intracellular signal transduction pathways and mechanical tethering via the cytoskeletal–integrin–extracellular matrix are among supportive mechanisms by which cardiac functional state can be adjusted and maintained. The spatial arrangement of myocytes within the ventricular wall is such that cell length contributes to chamber circumference while cell diameter primarily contributes to wall thickness. A large body of data on cardiac myocyte shape alterations in heart disease has appeared in the literature over many decades. Changes in cardiac myocyte shape play a major role in progressive remodeling leading to congestive heart failure (CHF). Specifically, an increase in myocyte length from series sarcomere formation in the absence of myocyte transverse growth is likely the most important cellular change leading to cardiac dilatation in CHF.
