In the 'euthyroid sick syndrome' high endogenous catecholamine levels may stimulate preferential tissue conversion of thyroxine (T4) to the non- active reverse triiodothyronine (rT3) rather than to the active free triiodothyronine (T3). Plasma T3 levels, therefore, drop precipitously. There is evidence that low T3 states occur during cardiopulmonary bypass and in the brain-dead organ donor, and that both lead to depletion of myocardial energy stores with deterioration of cardiac function. Therapy with T3 reactivates the mitochondria and stimulates aerobic metabolism, leading to replacement of myocardial energy stores and improved cardiac function. Although this therapeutic concept remains controversial, T3 therapy may prove beneficial in patients with impaired cardiac function following open heart surgery, particularly those undergoing heart transplantation.
