Abstract
The effects of excess thyroid hormone on the performance of the [human, animal] heart, as well as the structure of myosin and its role in the contraction process are reviewed. The effects of thyroid hormone on myocardial contractile performance may be explained by the appearance of a new myosin isozyme, myosin-T, that has a greater actin-activated ATPase activity than the original myosin. There is evidence to suggest that in other forms of cardiac hypertrophy, such as pressure overload, adaptations in cardiac performance also may be mediated by a change in myosin species.