Thyroid Hormone Abnormalities in Myocardial Infarction

The low T3 syndrome is characterized by low serum T3 and fT3 and normal T4, fT4, and TSH levels, in the absence of intrinsic thyroid disease and can be seen after an acute myocardial infarction in about 15–20% of cases. It is also seen in acute and chronic illness, sepsis, and after surgery, including cardiac, under cardiopulmonary bypass. It is caused by inflammation and cytokine action and increased ROS production, as well as altered deiodinase (DIO) activity (upregulation of DIO3 and downregulation of DIO1), which affect thyroid hormone action on the peripheral tissues. Thus, the actions of these hormones on the myocardium (contractility) and on peripheral vessels (vasodilation) are blunted. Low T3 levels after myocardial infarction are associated with a worse prognosis; however, the effectiveness of thyroid hormone supplementation is still under discussion, since only results from small trials after cardiac surgery and myocardial infarction are available.