AIM: The aim of the study was to determine the predictive possibility of the GDF-15 marker in the stratification of the ACS complications risk within 5 years after the event.
MATERIALS AND METHODS: 70 patients with ACS were involved. The mean age was (61.8 +/- 1.3) years, the following diagnosis was established in the patients: 76 patients had acute myocardial infarction with Q (AMI with Q), 28 - acute myocardial infarction without Q (AMI without Q) and 36 patients were diagnosed unstable angina (UA). During the follow-up period the endpoint was reached by 28 patients.
RESULTS: A statistical relationship between the elevated level of GDF - 15 and the 5-year survival of these patients (χ2 = 4.75, p = 0.03) has been found. It was established that the level of the GDF-15 biomarker > 2350 pg/ml independently predicted the onset of adverse events with the sensitivity of 80% and the specificity of 60% (p = 0.006). To investigate the influence of the GDF-15 levels on mortality in the remote period, the Cox regression analysis was performed. It was revealed that the level of GDF-15 significantly predicted the onset of the primary endpoint within 5 years after ACS (p = 0.004).
CONCLUSIONS: The increased level of GDF-15, determined in the first 24 hours after development of ACS, is highly associated with the adverse outcome within 5 years after the event.
AIM: The aim of the study was to determine the influence of various risk factors on ST2 levels in patients with HFpEF and diabetes mellitus type 2 (T2DM).
MATERIALS AND METHODS: A total of one hundred and thirty-four patients (74 females and 60 males, 51 diabetic patients and 83 patients without T2DM with HFpEF were examined. Duration of HF and T2DM, common risk factors, such as smoking, overweight, clinical examination, parameters of carbohydrate and lipid metabolism, glomerular filtration rate (GFR) and M235T polymorphism of ATG have been used. Multivariate backward stepwise cox regression analysis was performed in Statistica 10,0. p<0,05 was considered statistically significant.
RESULTS: ST2 level in patients with HFpEF associated with T2DM exceeded this value in patients with HFpEF without T2DM and was 23.26 ng/ml (18.5: 29.3) vs. 20.39 ng/ml (18.3: 24.6), respectively (p<0,05). To assess the cumulative effect of the studied factors on the ST2 level, we performed the Cox's stepwise multivariate regression analysis. Smoking, HOMA-IR (Homeostatic Model Assessment for Insulin Resistance), glucose, HbA1 and insulin levels were found to be the most significant factors influencing ST2 levels in patients with HF and T2DM, indicating a significant effect of DM type 2 on ST2 concentration.
CONCLUSIONS: Smoking, HOMA-IR, glucose, HbA1, and insulin levels can significantly affect ST2 levels in patients with T2DM and HFpEF.
AIM: The aim of study was to evaluate the relationship of β-adrenergic receptors gene polymorphisms with low triiodothyronine syndrome in patients with a heart failure.
MATERIALS AND METHODS: 354 patients with HF on a background of postinfarction cardiosclerosis were included to the study. At 89 (25.1%) patients LT3S was diagnosed. The course of HF was studied for 2 years. Mean levels of thyroid stimulating hormone (TSH), free T3f and T4f were evaluated. Genotyping of 4 single nucleotide polymorphisms (Gly389Arg of β1-AR gene, Ser49Gly of β1-AR gene, Gln27Glu of β2- AR gene and Ser275 of GNβ3 gene) was performed by polymerase chain reaction. Genetic and epidemiological analysis was performed using the SNPStats program.
RESULTS: The risk of LT3S in patients with HF increases with homozygous G/G variant of Gln27Glu polymorphism of the β2-AR gene (OR=2.21, p=0.037), described as a recessive model of inheritance. There was a tendency to increase the risk of LT3S development in the presence of the genotype C/T of the Ser275 polymorphism of the GNb3 gene (OR=1.75, p=0.054), described as an over-dominant model. The genotype C/G of the Gln27Glu polymorphism of the β2-AR gene was associated with a decreased risk of LT3S development (OR=0.54, p=0.037), described as over-dominant model. Patients with HF carriers the A allele (A/GA/A) of the Ser49Gly polymorphism of the β1-AR gene have a lower risk of repeated hospitalization due to HF decompensation (OR=0.50, p=0.032), described as a dominant model. There was a tendency to increase the risk of re-hospitalization in the G-allele (C/GG/ G) variant of the Gln27Glu polymorphism of the β2-AR gene (OR=1.68, p=0.057), described as a dominant heredity model. At patients with HF in combination with LT3S the risk of re-hospitalization increases at C/G variant of the Gln27Glu polymorphism of β2-AR gene (OR=1.25, p=0.025), described as an over-dominant model.
CONCLUSIONS: The results suggest that congenital genetic alterations in β-adrenergic pathways may be associated with the development of LT3S in patients with HF and the features of the HF course.
PATIENTS AND METHODS: Materials and methods: In the present study, the lytic bacteriophage, k3w7, isolated by the host Klebsiella pneumoniae kP2 was characterised using transmission electron microscope (TEM), plaque assay, and restriction digestive enzyme to investigate mor¬phology, host spectrum, bacteriophage life cycle and stability accordingly.
RESULTS: Results and conclusions: As shown by TEM, k3w7 was observed to have the characteristic of icosahedral heads 100 nm and contractile sheaths 120 nm suggesting it belongs to the family of myoviridae.The Investigation has done on the phage growth cycle showed a short latent period of 20 min and a burst size of approximately 220 plaque forming units per infected cell. Stability test showed the phage was stable over a wide range of pH and temperatures. According to restriction analysis, k3w7 had 50 -kb double-stranded DNA genome as well as the heterogeneous nature of genetic material. These findings suggest that K3W7 has a potential use in therapy against infections caused by K. pneumonia produces carbapenemase.
PATIENTS AND METHODS: Materials and methods: The study included 165 patients admitted with STEMI within 12 hours of the onset of symptoms be¬tween January 2020 and August 2021. All patients underwent primary PCI according to the guidelines, followed by standard examination and treatment at the hospital. Blood samples for biomarker analysis (MMP-9, cTnI) and other routine tests were taken on admission. At six months after the event, all patients underwent clinical follow-up. Patients were contacted either by phone, through family members or their physicians 1 year after the event.
RESULTS: Results: The composite endpoint reached 9% of patients at one-year follow-up. ROC analysis of MMP-9 with the one-year com¬posite endpoint showed an AUC=0.711, with 91.7% sensitivity, and 47.4% specificity, 95% CI - 0.604 to 0.802, p=0.0037. ROC analysis of EQ-5D questionnaire with the one-year composite endpoint showed AUC = 0.73, the 95% CI - 0.624 to 0.820, p< 0.0195, with sensitivity 54.5% and specificity 94.7%. A logistic regression model showed a statistical association with the com¬posite endpoint at one year after STEMI in both EQ-5D (OR=0.89, 95% CI: 0.8313- 0.9725, p=0.0079) and MMP-9 (OR=1.0151, 95% CI:1.0001-1.0304, p=0.0481).
CONCLUSION: Conclusions: The level of MMP-9 more than 194 ng/ml and <55 points in EQ-5D predicts major adverse cardiovascular events, in¬cluding cardiovascular mortality and progressive heart failure, as well as other elements of composite endpoints, during a 1-year follow-up in patients with STEMI after primary PCI. Future studies are needed to clarify this result.