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.
PATIENTS AND METHODS: Materials and methods: 354 patients with HF on a background of post-infarction cardiosclerosis were included in the 2-yeared follow-up study. LT3 S was diagnosed at 89 (25.1%) patients. The levels of thyroid-stimulating hormone, free T3f and T4f, and reversible T3 were determined. The echocardioscopy was performed.
RESULTS: Results: Patients with HF in combination with LT3 S have a heavier functional class by NYHA, greater dilatation of the left heart cavities, less myocardial contractility, a higher frequency of atrial fibrillation and re-hospitalization. The use of β-ABs in patients with HF without LT3 S leads to a likely decrease in hospitalization frequency, while in patients with LT3 S it has an opposite effect. The frequency of rehospitalization increases with an excess of β-ABs dose > 5 mg (equivalent to bisoprolol). At these patients a decrease in serum T3 level and negative dynamics of parameters of intracardiac hemodynamics are observed.
CONCLUSION: Conclusions: The use of β-ABs in patients with LT3 S leads to an increase in re-hospitalization at a dose over 5.0 mg (equivalent to bisoprolol). In these patients there is a decrease in serum T3, an increase in T4 level; and the ejection fraction decrease; and heart cavities size increase.
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: 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.
PATIENTS AND METHODS: Materials and methods: The study involved 134 ST-segment elevation myocardial infarction patients. Occurrence of post-percutaneous coronary (PCI) intervention epicardial blood flow of TIMI <3 or myocardial blush grade 0-1 along with ST resolution <70% within 2 hours after PCI was qualified as the no-reflow condition. Left ventricle remodeling was defined after 6-months as an increase in left ventricle end-diastolic volume and/or end-systolic volume by more than 10%.
RESULTS: Results: A logistic regression formula was evaluated. Included biomarkers were macrophage migration inhibitory factor and sST2, left ventricle ejection fraction: Y=exp(-39.06+0.82EF+0.096ST2+0.0028MIF) / (1+exp(-39.06+0.82EF+0.096ST2+0.0028MIF)). The estimated range is from 0 to 1 point. Less than 0.5 determines an adverse outcome, and more than 0.5 is a good prognosis. This equation, with sensitivity of 77 % and specificity of 85%, could predict the development of adverse left ventricle remodeling six months after a coronary event (AUC=0.864, CI 0.673 to 0.966, p<0.05).
CONCLUSION: Conclusions: A combination of biomarkers gives a significant predicting result in the formation of adverse left ventricular remodeling after ST-segment elevation myocardial infarction.
Materials and Methods: Five patients with atrial tumor thrombi who underwent piggy-back mobilization of the liver, surgical access to the right atrium from the abdominal cavity, and external manual repositioning of the thrombus apex below the diaphragm (milking maneuver) were included into the study. Extracorporeal circulation was used in none of the cases. The average length of the atrial component of the tumor was 20.0 ± 11.7 mm (10 to 35 mm), and the width was 14.8 ± 8.5 mm (10 to 30 mm). In this work, the features of patients and surgical interventions as well as perioperative complications and mortality were analyzed.
Results: External manual repositioning of the tumor thrombus apex below the diaphragm was successfully performed in all patients. Tumor thrombi with the length of the atrial part up to 1.5 cm were removed through the extrapericardial approach. For evacuation of the thrombi with the large atrial part (3.0 cm or more), a transpericardial surgical approach was required. Specific complications associated with the access to the right atrium from the abdominal cavity (paresis of the right phrenic nerve, pneumothorax, and mediastinitis) were not detected in any case. The average clamping time of the supradiaphragmatic inferior vena cava (IVC) was 6.3 ± 4.6 min. The volume of intraoperative blood loss varied from 2500 to 5600 ml (an average of 3675 ± 1398.5 ml).
Conclusion: Our work represents the initial experience in the liver transplantation technique for thrombectomy in distinct and well-selected patients with atrial tumor thrombi. The effectiveness of this approach needs further study. The video presentation of our research took place in March 2019 at the 34th Annual EAU Congress in Barcelona.