Abstract

Acute critically ill patients experience a rapid decline in plasma free thyroid hormone levels (free triiodothyronine (FT₃) and free levothyroxine (FT₄)), with a marked elevation of reverse T₃, recognized as the euthyroid sick syndrome (ESS) or low-T₃ syndrome. The ESS is also often associated with depressed myocardial function, sometimes referred to as the ‘stunned myocardium’. Its clinical effects may vary from minimal hemodynamic impairment to cardiogenic shock. Medical management may range from aspirin alone to placement of a left ventricular assist device. With adequate supportive therapy, recovery usually occurs within days or weeks. The effect of T₃/T₄ therapy has been studied in three conditions in which the ESS and myocardial functional depression have been documented – i) transient regional myocardial ischemia and reperfusion, ii) transient global myocardial ischemia in patients undergoing cardiac surgery on cardiopulmonary bypass, and iii) transient inadequate global myocardial perfusion in brain-dead potential organ donors. Under all three conditions, myocardial ischemia leads to rapid loss of high-energy phosphates, accumulation of myocardial tissue lactate, and probably loss of homeostasis of cytosolic calcium, which may further increase cell injury. There is an inability to generate ATP through the Krebs cycle, which reduces the high-energy phosphate pool essential for all cell ATPases. Under all three conditions, following administration of T₃/T₄, the myocardial dysfunction was rapidly reversed. We, therefore, cautiously advocate the use of thyroid hormonal therapy to any patient with the ESS and/or a stunned myocardium.