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Triiodothyronine: spectrum of use in heart transplantation
1Temple University Health Sciences Center, Philadelphia, Pennsylvania 19140, USA.
Insights
Triiodothyronine (T3) effectively resuscitates poorly functioning donor hearts and improves recipient metabolism after heart transplantation (HT). T3 also reduces the need for and duration of inotropic support in heart transplant patients.
Area of Science:
- Cardiology
- Endocrinology
- Transplantation Medicine
Background:
- Triiodothyronine (T3) deficiency is common in heart transplant (HT) donors and recipients.
- This deficiency may impair donor heart function post-transplantation.
- Investigating T3's role in HT is crucial for improving outcomes.
Purpose of the Study:
- To evaluate the efficacy of T3 in resuscitating compromised donor hearts.
- To assess T3's impact on normal donor hearts.
- To determine T3's effect on recipients undergoing heart transplantation.
Main Methods:
- Three studies were conducted: T3 resuscitation of poor-function donors, T3 vs. placebo in normal donors, and T3 administration before reperfusion in recipients.
- Dosing varied, including bolus and infusion regimens.
- Echocardiography, hemodynamic monitoring, and lactate measurements were used.
Main Results:
- T3 effectively resuscitated donor hearts with poor function, showing improved lactate levels and reduced inotropic support needs.
- No significant differences were observed in normal donors or long-term outcomes in the first study.
- T3 administration before reperfusion decreased lactate and inotropic support in recipients.
Conclusions:
- Triiodothyronine (T3) is effective for resuscitating selected donor hearts with impaired function.
- T3 improves myocardial aerobic metabolism in heart transplant recipients.
- T3 therapy can decrease the amount and duration of inotropic support required post-HT.
Abstract:
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.