The ultrastructure of myocardial hypertrophy: why does the compensated heart fail?

Several qualitative features of the ultrastructure of pressure overload and thyrotoxic myocardium are unique markers of the type and quantity of increased work the heart has been required to perform. Furthermore, they are reminiscent of features of normally growing myocytes, implying that the changes in the hypertrophied cell are the consequence of normally present capacities for adaptation to a demand for increased myocardial work. Thyrotoxic myocardium has two features which distinguish it from normal and pressure overloaded hearts: the mitochondria are large and have a peculiar fragile or lacey appearance. Many myocytes show considerable disorganization of sarcomeric myofilaments. Pressure overloaded hearts have smaller and more numerous mitochondria than the normal myocyte. Their sarcomeres have thicker Z bands than controls. Double intercalated discs are also a feature of these myocytes. Several features of hypertrophied myocytes are seen in both types of hypertrophy: RER and ribosomes on the external nuclear membrane. There are polyribosomes aligned along the long axes of thick filaments, presumably involved in myosin synthesis or transformation within the cell. There are areas of sarcomerogenesis both under the sarcolemma and within the cell at the intercalated disc. These are characterized by fragments of myofilaments, polyribosomes and rough endoplasmic reticulum. Quantitatively, myocyte composition is transiently disturbed but, like that of normally growing hearts, returns to control values as the adaptation to stress is negotiated.