Triiodothyronine (T3) deficiency, present in 85% of donors, in recipients with end-stage cardiomyopathy, and in patients after cardiopulmonary bypass (CPB), may contribute to donor heart dysfunction after heart transplantation (HT). Three separate studies were performed to investigate the various potential applications of T3 in HT. In the first study, donor hearts with statistically higher filling pressures, lower EF on echocardiograms, and higher inotrope requirements were resuscitated with T3 (0.6 microgram/kg bolus) and compared to normal donors not receiving T3. All patients survived the immediate postoperative period, and at 1 week and 6 months there were no significant differences in SBP, DBP, HR, cardiac index, CVP, PCWP, or LVEF on echocardiography. The next study involved giving T3 (0.6 microgram/kg bolus) versus placebo to normal donors in a blinded randomized fashion. Although there was a trend toward less inotrope use in the T3 group, there were no other differences. In the third study, placebo (group A) or T3 (group B; 0.2 microgram/kg bolus, 0.4 microgram/kg infusion over 6 hours) was given immediately before donor heart reperfusion. The recipient groups were similar with regard to age, donor/recipient weight ratio, ischemic time, thyroid hormone levels, and pretransplant hemodynamics. Lactate from coronary sinus effluent after 10 minutes of reperfusion was higher in group A, and more group A patients required higher than baseline inotropic support. In conclusion, T3 can be used effectively to resuscitate selective donor hearts with poor function and in recipients to improve myocardial aerobic metabolism; and T3 decreases both the amount and duration of inotropic support.