THE ROLE OF BIOMARKER MACROPHAGE MIGRATION INHIBITORY FACTOR IN CARDIAC REMODELING PREDICTION IN PATIENTS WITH ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION.

OBJECTIVE: The aim: To estimate the role of macrophage migration inhibitory factor and soluble ST2 in predicting the left ventricle remodeling six months after ST-segment elevation myocardial infarction. 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.

THE ROLE OF BIOCHEMICAL MARKERS AND PATIENT-REPORTED OUTCOMES IN PREDICTING COMPOSITE ONE-YEAR ENDPOINT IN ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION.

OBJECTIVE: Aim of our study was to determine the role of the clinical and biochemical markers in predicting the outcomes at one year in patients with STEMI who have undergone primary PCI. 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.

Myocardial Mechanical Dispersion Predicts Adverse Cardiac Remodeling in Patients with ST Segment Elevation Myocardial Infarction Who Underwent Primary Percutaneous Coronary Intervention.

OBJECTIVE: The aim of the study was to investigate whether increased left ventricular mechanical dispersion is an early predictor for adverse cardiac remodeling in ST-segment elevation myocardial infarction patients who had post-percutaneous coronary intervention thrombolysis in myocardial infarction (TIMI) flow grade > 2. METHODS: A total of 119 post-percutaneous coronary intervention ST elevation myocardial infarction patients with TIMI flow grade >2 were prospectively included in the study. Left ventricular global longitudinal strain was quantified by 2-dimensional speckletracking echocardiography, and left ventricular mechanical dispersion was determined at baseline and after 1 year to assess adverse cardiac remodeling. The levels of circulating biomarkers were measured at the baseline. TIMI score and the Global Registry of Acute Coronary Events score systems were used to evaluate the prognosis of patients. RESULTS: Patients with high quartile versus low quartile of left ventricular mechanical dispersion exerted higher Global Registry of Acute Coronary Events and TIMI score grades, left ventricular endsystolic volume, global longitudinal strain, and levels of the N-terminal fragment of brain natriuretic peptide and lower left ventricular ejection fraction. Multivariate log regression showed that N-terminal fragment of brain natriuretic peptide > 953 pg/mL, global longitudinal strain > -8%, and high quartile of left ventricular mechanical dispersion remained independent predictors for adverse cardiac remodeling. Addition of left ventricular mechanical dispersion to the N-terminal fragment of brain natriuretic peptide improved the discriminative potency of the whole model. CONCLUSION: Measurement of left ventricular mechanical dispersion might be useful in determining the risk of adverse cardiac remodeling in post-percutaneous coronary intervention ST elevation myocardial infarction patients.

The role of growth differentiation factor 15 as a predictor of 5-year survival of patients after acute coronary syndrome.

One of the problems of modern cardiology in Ukraine and the world is acute coronary syndrome (ACS), which results in high mortality and invalidation of patients. Recently, much attention is drawn to the growth differentiation factor 15 (GDF-15). A lot of studies provided, in which the role of GDF-15 in cardiovascular pathology proved. 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.

The effect of beta-blockers on a course of chronic heart failure in patients with a low triiodothyronine syndrome.

OBJECTIVE: The aim: The aim is to study the effect of ß-ABs in patients with LT3 S on the course of HF. 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 ß-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 ß-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 ß-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.

Subclinical emotional distress predicts 6-month clinical outcomes after ST-segment elevation myocardial infarction.

Aim: To investigate associations between subclinical distress and 6-month clinical outcomes after ST-segment elevation myocardial infarction (STEMI). Materials & methods: The case-control study involved 144 STEMI patients (72 STEMI having subclinical emotional disturbances were included to the case group and 72 STEMI individuals matched with age, sex and cardiovascular risk factors were enrolled to the control group). The primary end point was the combination of 6-month events including CV death, recurrent angina, newly diagnosed heart failure and re-hospitalization. Results: The emotional distress predicted out-hospital combined end point (odds ratio [OR] = 2.48; 95% CI: 1.12-5.33; p = 0.034). Other independent predictors of out-hospital end point were Type 2 diabetes mellitus (OR = 1.10; 95% CI: 1.02-1.23; p = 0.048), thrombolysis in myocardial infarction score <6 units (OR = 0.86; 95% CI: 0.67-0.92; p = 0.001) and the number of culprit vessels (OR = 1.19; 95% CI: 1.02-1.34; p = 0.002). Conclusion: Premorbid emotional distress independently predicted 6 month combined clinical end point in STEMI patients.

The association of polymorphisms of ß-adrenergic receptors genes with the low triiodothyronine syndrome in patients with a heart failure.

The course of heart failure (HF) and its progression is associated with comorbidities, genetic factors and a dynamics of a number of biomarkers. The low triiodothyronine syndrome (LT3S) is observed in some patients with HF. Extremely little data are available in the literature regarding the effect of ß-adrenoreceptors (ß-AR) genes polymorphisms on the development of LT3S and many contradictory results about their association with HF course. This encourages new research in this area. AIM: The aim of study was to evaluate the relationship of ß-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 ß1-AR gene, Ser49Gly of ß1-AR gene, Gln27Glu of ß2- AR gene and Ser275 of GNß3 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 ß2-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 ß2-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 ß1-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 ß2-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 ß2-AR gene (OR=1.25, p=0.025), described as an over-dominant model. CONCLUSIONS: The results suggest that congenital genetic alterations in ß-adrenergic pathways may be associated with the development of LT3S in patients with HF and the features of the HF course.