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). AIM: The aim of the study was the evaluation of the prevalence of low T3 syndrome in MI, in relation to selenium deficiency. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Selenium deficiency and the dynamics of changes of thyroid profile in patients with acute myocardial infarction and chronic heart failure.

BACKGROUND: Selenium (Se) is incorporated in 25 enzymes, for example, glutathione peroxidase (activatedb by oxidative stress) and deiodinases (converting thyroid hormones). Oxidative stress present in heart failure (HF) and myocardial infarction (MI) might cause Se deficiency and decreased thyroxine to triiodothyronine conversion. AIMS: We sought to evaluate Se levels in Polish patients with MI, HF, and healthy volunteers in relation to thyroid hormone levels. METHODS: The study group consisted of 143 participants: 54 patients with MI, 59 patients with decompensated HF, and 30 healthy matched volunteers. The patients underwent echocardiography and laboratory tests on admission and 5 months later. RESULTS: Se levels were lower in patients with MI and HF than in controls (median [interquartile range, IQR], 65.9 [55.2-76.1] µg/l and 59.7 [47.7-70.7] µg/l vs 93.2 [84.2-99.1] µg/l, respectively; P <0.001). The Se deficiency was very common in patients with MI and HF, while it was rare in controls (70.37% and 74.58% vs 10%, respectively; P <0.001). Patients with MI and HF presented lower free triiodothyronine (FT3) levels and lower FT3 to free thyroxine (FT4) ratio in comparison with controls (median [IQR], 3.90 [3.60-4.38] pmol/l and 4.25 [3.57-4.60] pmol/l vs 4.92 [4.50-5.27] pmol/l; P <0.001; and 0.25 [0.23-0.29] and 0.25 [0.21-0.28] vs 0.32 [0.29-0.37]; P <0.001, respectively). There was a weak to moderate correlation between Se level, FT3 level, and the FT3/FT4 ratio. At follow­up, the FT3/FT4 ratio tended to normalize in patients with MI and remained decreased in patients with HF (mean [SD], 0.31 [0.06] vs 0.27 ([0.05]; P <0.001. CONCLUSIONS: Se deficiency is very common in Polish patients with MI and HF. Thyroid hormones disturbances were more transient in patients with MI, but more chronic in those with HF.

Distribution of selected elements in calcific human aortic valves studied by microscopy combined with SR-µXRF: influence of lipids on progression of calcification.

Calcified heart valves display a significant imbalance in tissue content of trace and essential elements. The valvular calcification is an age-related process and there are data suggesting involvement of lipids. We studied elemental composition and lipid distribution in three distinct regions of calcified human aortic valves, representing successive stages of the calcific degeneration: normal, thickened (early lesion) and calcified (late lesion), using SR-µXRF (Synchrotron Radiation Micro X-Ray Fluorescence) for elemental composition and Oil Red O (ORO) staining for demonstration of lipids. Two-dimensional SR-µXRF maps and precise point spectra were compared with histological stainings on consecutive valve sections to prove topographical localization and colocalization of the examined elements and lipids. In calcified valve areas, accumulation of calcium and phosphorus was accompanied by enhanced concentrations of strontium and zinc. Calcifications preferentially developed in lipid-rich areas of the valves. Calcium concentration ratio between lipid-rich and lipid-free areas was not age-dependent in early lesions, but showed a significant increase with age in late lesions, indicating age-dependent intensification of lipid involvement in calcification process. The results suggest that mechanisms of calcification change with progression of valve degeneration and with age.