‘Low — T3 syndrome’ among patients with acute myocardial infarction

Background Recent clinical studies have found that cardiovascular incidents are sufficient triggers to affect HPA hypothalamic-pituitarythyroid axis and cause a decrease in the serum levels of triiodothyronine (T3). This phenomenon is so called ‘Low — triiodothyronine (T3) syndrome’ and is related to changes in heart remodeling. However, the pathophysiology of Low—T3 syndrome remains unclear. The present systemic literature review was designed to organize the latest scientific papers and is seeking to draw evidence-based conclusions regarding clinical aspects of the topic. Methods Accessible scientific databases were analyzed using key words to obtain scientific papers regarding the field of interest. Research findings were assessed and compared between studies in order to find out clinical impact of thyroid hormone and heart function following acute myocardial injury. Results Different studies indicate that the presence of Low-T3 syndrome after myocardial infarction is a strong predicting factor of patient morbidity and mortality. Some researchers believe that the decrease in T3 concentrations might be a compensatory reaction of the body in order to suppress cellular metabolism during tissue damage. On the other hand, a limited number of recent experimental and clinical investigations have shown positive response to treatment with thyroid hormone. Conclusion Deeper analysis is needed to understand the pathophysiology of Low-T3 syndrome and possibilities of its use for treatment.