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.

Association of serum levels of lipoprotein A-I and lipoprotein A-I/A-II with high on-treatment platelet reactivity in patients with ST-segment elevation myocardial infarction.

OBJECTIVE: High-density lipoproteins (HDLs) are a very heterogeneous group of particles. Little is known about the impact of their subfractions including lipoprotein A-I (LpA-I) and lipoprotein A-I/A-II (LpA-I/A-II) on platelet function and high on-treatment platelet reactivity (HPR), particularly in the acute phase of ST-segment elevation myocardial infarction (STEMI). The aim of the study was to evaluate the relationship between serum levels of LpA-I and LpA-I/A-II and HPR in STEMI patients. METHODS: Fifty-two consecutive STEMI patients (26.9% women, mean age 60.6±9.1 years) were enrolled into this study. Clinical and demographic data were collected and HDL subfractions were measured by rocket immunoelectrophoresis. Platelet reactivity was assessed using light transmission aggregometry and quantitative flow cytometry. RESULTS: We found a positive correlation between platelet aggregation after both ADP-5 and ADP-20 stimulation and serum level of LpA-I. Compared with subjects with satisfactory platelet response to clopidogrel, patients with HPR had 32.44% higher serum level of LpA-I (p=0.021). On the other hand, patients with HPR assessed by ADP-5 stimulation had 22.13% lower serum level of LpA-I/A-II (p=0.040). Regression analysis showed that LpA-I [odds ratio (OR) 1.03; 95% confidence interval (CI) 1-1.07; p=0.049] and current smoking (OR 0.18; 95% CI 0.04-0.81; p=0.025) were independent predictors of HPR. With receiver operating characteristic (ROC) curve analysis, we designated the cut-off point at serum level of 57.52 mg/dL for LpA-I for predicting HPR (AUC=0.71, p=0.010). CONCLUSION: This study showed that higher serum level of LpA-I measured in the acute phase of STEMI is an independent risk factor for HPR. Our study is the first to demonstrate an important and distinct activity of LpA-I and LpA-I/A-II that can prove pleiotropic and different functions of HDL subfractions in acute STEMI.

Influence of osteoclasts and osteoprotegerin on the mode of calcific degeneration of aortic valves.

INTRODUCTION: Calcific aortic valve disease is associated with inflammation and calcification, thus the osteoprotegerin (OPG), receptor activator of nuclear factor κB (RANK) and its ligand (RANKL) system involved in osteoclastogenesis and inflammation may play a significant role in valve degeneration. OBJECTIVES: The aim of this study was to assess whether circulating OPG, sRANKL, and other bone metabolism markers can predict the presence of osteoclasts in stenotic valves and to evaluate their impact on the mode of degeneration. PATIENTS AND METHODS: The study involved 60 patients with aortic stenosis who underwent valve replacement surgery and subsequently were divided into 2 groups: osteoclastic (n = 12) and nonosteoclastic (n = 48), according to the presence or absence of intravalvular osteoclasts. Before the surgery, we measured serum levels of OPG, sRANKL, osteocalcin, osteopontin, tumor necrosis factor α (TNF-α), interleukin (IL) 1ß, and IL-6. Immunohistochemistry and morphometry were used to determine the extent of valve calcification, lipid accumulation, neovascularization, and the number and phenotype of macrophages. RESULTS: Compared with the nonosteoclastic group, patients with intravalvular osteoclasts had lower levels of OPG (P = 0.0006) and TNF-α (P = 0.02) and less frequently had diabetes (P = 0.04). Their valves showed higher incidence of ossification (P = 0.002), higher total (P = 0.008) and M2 macrophage counts (P = 0.0002), increased neovascularization (P = 0.003), and lower accumulation of lipids (P = 0.04). They also showed a negative correlation between valve calcification and age (r = -0.79, P = 0.002), which was not observed in patients without osteoclasts. In a multivariate analysis, low circulating OPG levels and the absence of diabetes were predictors of intravalvular osteoclastic differentiation. CONCLUSIONS: The presence of osteoclasts in stenotic valves associated with low circulating OPG levels and an enhanced proportion of M2 macrophages can represent a variant of calcific aortic valve disease with a specifically regulated calcification process.

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.

Life-threatening cardiac manifestations of primary antiphospholipid syndrome.

We report a rare case of primary antiphospholipid syndrome (APS) in a 43-year-old man presenting as recurrent acute coronary stent thrombosis and complicated by three myocardial infarctions. As illustrated in this report, in APS patients recurrent life-threatening arterial thrombotic events may occur in spite of recommended anticoagulant therapy. We conclude that the APS should be considered as a potential cause of acute coronary syndrome, particularly in young individuals with a history of recurrent thrombotic events and/or with abnormal coagulation test results. Further studies are needed to determine the best therapeutic strategy for APS patients with acute coronary syndrome.

[Recurrence of tricuspid regurgitation in a patient with a rheumatic fever after mitral valve implantation with concomitant tricuspid valve annuloplasty]. / Ponowna niedomykalnosc zastawki trójdzielnej u chorej po operacji wszczepienia zastawki mitralnej i jednoczesnej plastyce zastawki trójdzielnej w przebiegu goraczki reumatycznej.

A case of a 62-year-old female with a recurrence of tricuspid regurgitation is presented. This complication occurred after mitral valve implantation and tricuspid valve annuloplasty. Diagnosis and treatment of this condition following rheumatic fever are discussed.

[Abscess of the mitral annulus mimicking left atrial tumour - case report]. / Ropien pierscienia zastawki mitralnej imitujacy guz lewego przedsionka. Problem diagnostyczny.

A case of a 70-year-old female with hypertension, atrial fibrillation and angina pectoris, admitted to the hospital due to echocardiographically detected left atrial tumour, is presented. Differential diagnosis included thrombus, myxoma, infectious or neoplastic tumour. The patients underwent surgery. Histopathological examination revealed the presence of an abscess in the left atrium. This report underlines the difficulties in the diagnosis of cardiac tumours.