Development and regression of increased ventricular mass.

This report deals with increased cardiac mass in the light of the following variables: normal ventricular growth (embryo, fetus, neonate and child), the response to work loads (hemodynamic stress) and hypoxia, the cell responses of hyperplasia (increase in cell number), hypertrophy (increase in cell size) and the type of cell (muscle or connective tissue), the age or maturity of the myocardium at the time the hemodynamic or hypoxic stress is imposed, and the biochemistry, ultrastructure and functional morphology (modeling) of the ventricles in response to volume or pressure overload. The desirable physiologic adaptations to work loads are characterized, and the transition from physiologic to pathologic states is examined, comparing and contrasting increased ventricular mass in patients and in trained athletes. Regression of increased ventricular mass is then discussed, first at the cell level (hypertrophy/hyperplasia; muscle cell/connective tissue cell), then at the organ level. The requirements for maintaining or establishing normal ventricular function after removal of overload are reviewed, together with such variables as the type and duration of preoperative hemodynamic stress, the right versus the left ventricle and the relative rates of contractile protein synthesis and degradation.