The Effects of Triiodothyronine on Hemodynamic Status and Cardiac Function in Potential Heart Donors

Abstract

Brain death is associated with altered cardiac function and low concentrations of circulating triiodothryronine (T3). However, the effects of T3 administration on hemodynamic status and cardiac function in potential heart donors remain controversial. Thirty-seven brain-dead patients were randomly and blindly allocated to receive an intravenous bolus of either 0.2 microgram/kg T3 (n = 19) or saline placebo (n = 18). Measurements included conventional hemodynamic and echocardiographic variables of cardiac volume conditions and systolic function of the left ventricle (fractional area change [FAC], velocity of myocardial fiber shortening) using a transesophageal probe, arterial and mixed venous blood gas parameters, and serum thyroid hormone concentrations. The mean concentration of T3 was 1.86 +/- 1.55 pmol/L, and only six patients (16%) had normal values of T3 in control conditions. There was no significant correlation between T3 concentration and FAC (R = 0.17, not significant). All patients receiving T3 had normalized serum T3 concentration (7.55 +/- 2.56 pmol/L) in contrast to patients receiving saline (1.48 +/- 1.26 pmol/L). No significant differences in hemodynamic and echocardiographic parameters were observed between the placebo and T3 groups. Indeed, FAC remained unchanged after T3 (44% +/- 17% vs 46% +/- 22%) or placebo (47% +/- 18% vs 50% +/- 14%) administration. In 20 patients with impaired left ventricular function (FAC < 50%), FAC remained unchanged after T3 (n = 10; 34% +/- 12% vs 30% +/- 10%) or placebo (n = 10; 38% +/- 12% vs 35% +/- 13%) administration. In 17 patients in whom organ harvesting was delayed, transesophageal echocardiography was performed 6 h later and no significant changes in FAC were noted in the T3 group (n = 8; 49% +/- 17% vs 44% +/- 17%) and the placebo group (n = 9; 51% +/- 18% vs 47% +/- 18%). In conclusion, T3 administration did not improve hemodynamic status and myocardial function in brain-dead patients, suggesting that the euthyroid sick syndrome is not the main determinant of myocardial dysfunction in these patients.

Euthyroid Sick Syndrome

“…Initial human studies were promising, showing improvement in hemodynamic stability, decrease in requirement for inotropic support, and preservation of cardiac function prior to transplantation (58,80). However, other studies found no significant clinical benefits of T3 over placebo when there was no preceding cardiac dysfunction in the donor (25,31,45).…”

The nonthyroidal illness syndrome in the non-critically ill patient

“…As concerns T3 administration in potential organ donors, its beneficial role in improving the quality of organs of brain-dead donors and reducing the post-transplantation complications could not be established [64,65].…”

The difficult patient: drug interaction and the influence of concomitant diseases on the treatment of hypothyroidism

“…However, experimental data suggest that thyroid hormones improve myocardial functions, increase capillary flow and induce angiogenesis after myocardial infarction (42)(43)(44)(45)(46)(47)(48). In fact, thyroid hormone administration shows inotropic and antiarrhythmic properties and reduces the risk of death after and some clinical conditions such as chronic congestive heart failure (42), organ transplantation (43,44), coronary artery (45) and cardiopulmonary bypass (46), myocardial ischemia (47) and in prolonged critical illness (48). Consequently, it is important to always aim at a target TSH in the normal range for the patient's age, especially if the patient has a cardiovascular disease.…”