Thyroid Hormones and Cardiac Function

Thyroid hormones have profound effects on growth, development, and metabolism of virtually all tissues of higher organisms. Both thyroxine (T4) and triiodothyronine (T3) have been shown to induce major effects on cell replication and differentiation, calorigenesis and O2 consumption, stimulation of enzyme activity, beta-adrenergic responsiveness, and production and secretion of various hormones. As our main interest is in the heart, we will restrict ourselves to issues related to cardiac effects of thyroid hormones. The major changes in cardiac function produced by hyperthyroidism in humans and in experimental animals include marked increases in cardiac output, resting heart rate, and left ventricular ejection fraction, whereas hypothyroid patients have reduced cardiac output, resting heart rate, stroke volume and contractility [1]. These alterations have been attributed both to changes in the peripheral circulation and to direct inotropic and chronotropic effects on the heart. More specifically, the hyperthyroid myocardium is characterized by a decrease in the isometric time to peak tension, an increased shortening velocity and relaxation time, an increased sarcoplasmic reticulum (SR) Ca2+ pumping rate, an elevated actin and Ca2+-myosin ATPase activity, and a high percentage of myosin isoenzyme V1, the fast form of the enzyme.