This study aimed to examine the influence of thyroid hormone (TH) levels and genetic polymorphisms of deiodinases on long-term outcomes after acute myocardial infarction (AMI). In total, 290 patients who have experienced AMi were evaluated for demographic, clinical characteristics, risk factors, tH and NT-pro-BNP. Polymorphisms of TH related genes were included deiodinase 1 (DIO1) (rs11206244-C/T, rs12095080-A/G, rs2235544-A/C), deiodinase 2 (DIO2) (rs225015-G/A, rs225014-T/C) and deiodinase 3 (DIO3) (rs945006-T/G). Both all-cause and cardiac mortality was considered key outcomes. Cox regression model showed that NT-pro-BNP (HR = 2.11; 95% CI = 1.18-3.78; p = 0.012), the first quartile of fT3, and DIO1 gene rs12095080 were independent predictors of cardiac-related mortality (HR = 1.74; 95% CI = 1.04-2.91; p = 0.034). The DIO1 gene rs12095080 AG genotype (OR = 3.97; 95% ci = 1.45-10.89; p = 0.005) increased the risk for cardiac mortality. Lower fT3 levels and the DIO1 gene rs12095080 are both associated with cardiac-related mortality after AMI. Recent clinical research in cardiovascular disease as well as in coronary artery disease (CAD) has provided evidence that altered thyroid hormone (TH) metabolism, including low total triiodothyronine (T3) syndrome or pre-existing subclinical primary hypothyroidism, is an important indicator of adverse short-term and long-term outcomes, including mortality 1-5. These changes in thyroid homeostasis are known as "euthyroid sick syndrome" 6,7 or "non-thyroidal illness syndrome" (NTIS) 8,9 and are defined by low serum levels of free T3 (fT3), T3 and high levels of reverse T3 (rT3) followed by normal or low levels of thyroxine (T4) and thyroid-stimulating hormone (TSH). Low T3 syndrome is observed in about one third of patients following acute cardiovascular events and has been linked to the severity of the disease and its adverse prognosis 10. This syndrome has been established in patients with heart failure (HF) 11-14 , myocardial infarction (MI) 2,15-18 , and has been linked to the cardiac remodelling process 19-21 and poor prognosis 1,3,4,13,22,23. Studies suggest that variations of TH within clinically normal ranges, such as isolated reduction in fT3 level or higher level of free T4 (fT4), could constitute a model of abnormal TH metabolism. These variations could act as a risk factor for CAD, in a similar fashion to overt or subclinical hypothyroidism, thereby influencing the occurrence as well as severity of coronary atherosclerosis and its related outcomes 2,24-32 .