Low triiodothyronine syndrome and serum selenium status in the course of acute myocardial infarction

Both glutathione peroxidase and deiodinases are selenoproteins requiring selenium. Oxidative stress accompanying acute myocardial infarction (MI) may lead to activation of peroxidase and relative selenium deficiency. That may impair conversion of tetraiodothyronine (T4) to triiodothyronine (T3).

The aim of the study was the evaluation of the prevalence of low T3 syndrome in MI, in relation to selenium deficiency.

The study group consisted of 59 consecutive patients hospitalized due to STEMI or NSTEMI, treated with primary percutaneous coronary intervention. Exclusion criteria: thyroid dysfunction, severe systemic disease, treatment with amiodarone, steroids or propranolol. Group A consisted of 7 patients with low fT3 concentration, Group B consisted of remaining 52 patients with normal fT3 levels.

The prevalence of low T3 syndrome was 11.9%. The prevalence of selenium deficiency was 71.2%. Patients with low T3 syndrome had higher heart rate at admission and more often needed intravenous diuretics or inotropic agents. Low fT3 group presented higher levels of NT-proBNP, hsCRP, WBC, admission CKMB levels. There was a nonsignificant trend towards lower selenium levels in A group. We demonstrated correlations between fT3 and hsTnT, CKMB, NT-proBNP, hsCRP, MAPSE but we did not find correlation between fT3 and selenium or LVEF.

Selenium deficiency was found in majority of MI patients, while low T3 was identified in 11.9% of patients. fT3 levels correlate with markers of infarction severity and inflammatory markers. Se deficiency alone does not explain the reason of low fT3 concentration.