Background
Vitamin D deficiency is associated with cardiovascular diseases, including coronary artery diseases (CAD). As vitamin D manifests its biological function through its vitamin D receptor (VDR), VDR gene polymorphisms potentially affect VDR functionality and vitamin D activity. Therefore, the objective of this study was to analyze three well-studied VDR gene polymorphisms—Fok1 (rs2228570), BsmI (rs1544410) and Taq1 (rs731236)—in a cohort of CAD patients after acute myocardial infarction.
Methods
In the presented cross-sectional study, 155 participants with CAD after acute myocardial infarction and 104 participants in a control group without CAD were enrolled. The participants in both groups were Caucasians of European origin. The genotyping of VDR polymorphisms rs2228570, rs1544410 and rs731236 was assessed by RT-PCR.
Results
The results show an association between the T/T genotype of the BsmI (rs1544410) and the G/G genotype of the Taq1 (rs731236) VDR polymorphism and CAD patients after acute myocardial infarction. There was no association between the Fok1 (rs2228570) VDR polymorphism and CAD patients after acute myocardial infarction.
Conclusion
The presented results suggest a potential association of the BsmI (rs1544410) and Taq1 (rs731236) VDR polymorphisms with CAD patients after myocardial infarction.
The aim of this investigation was to examine the role of perforin (P)‐mediated cytotoxicity in the dynamics of tissue damage in patients with non‐ST‐segment elevation myocardial infarction (NSTEMI) treated with anti‐ischaemic drugs. We enrolled 48 patients with NSTEMI in this study [age, 71.5 years; 61.5/76 (median, 25th/75th percentiles)]. The percentage of total peripheral blood P+ lymphocytes was elevated owing to the increased frequency of P+ cells within natural killer (NK) subsets, T and NKT cells in patients on day 1 after NSTEMI when compared with healthy controls. Positive correlations were found between cardiac troponin I plasma concentrations and the frequency of P+ cells, P+ T cells, P+ NK cells and their CD56+dim and CD56+bright subsets during the first week after the NSTEMI. The expression of P in NK cells was accompanied by P‐mediated cytotoxicity against K‐562 targets at all days examined, except day 21, when an anti‐perforin monoclonal antibody did not completely abolish the killing. The percentage of P+ T cells, P+ NKT cells and P+ NK subsets was the highest on the day 1 after NSTEMI and decreased in the post‐infarction period. CD56+ lymphocytes were found in damaged myocardium, suggesting their tissue recruitment. In conclusion, patients with NSTEMI have a strong and prolonged P‐mediated systemic inflammatory reaction, which may sustain autoaggressive reactions towards myocardial tissue during the development of myocardial infarction.
Background: Cardiovascular diseases (CVD) are among leading causes of death worldwide and amongst CVD, coronary artery disease (CAD) accounts for almost half of all cardiovascular deaths as the most common cause of death in the developed world. Vitamin D and the vitamin D-binding protein (VDBP) have been studied as possible CAD pathogenesis factors but literature data provide opposing evidence on their role in CAD. Herein we aimed to present novel evidence on the association of two VDBP polymorphisms (rs4588) and (rs7041) with CAD in patients after acute myocardial infarction and study possible correlations of these polymorphisms with 25-hydroxyvitamin D [25(OH)D] serum levels. Methods: The cross-section genotyping study included 155 subjects with CAD upon acute myocardial infarct and 104 control subjects. All patients and control group were Caucasians of European descent. VDBP polymorphisms (rs4588) and (rs7041) were studied by use of RT-PCR. Liquid chromatography, tandem mass spectrometry (LC-MS/MS) method was used for measurement of vitamin D in the serum. Results: Association of the VDBP (rs4588) T/T genotype with CAD patients after acute MI and correlation of VDBP (rs4588) genotype G/G with higher levels of total vitamin D were found. No correlation of 25(OH)D serum levels with CAD were established but the multivariate logistic regression modelling enabled association of total vitamin D level and VDBP (rs4588) T/T genotype with CAD and anteroseptal myocardial infarction (ASMI) CAD occurrence. Conclusions: Obtained data speak in favor to the VDBP (rs4588) T/T genotype as a susceptibility factor for anteroseptal myocardial infarction where the same genotype showed to be generally more prevalent in smokers.
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