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Spontaneous coronary artery dissection (SCAD) is defined as a spontaneous dissection of the coronary artery wall that occurs independently of atherosclerosis, percutaneous coronary intervention, or mechanical trauma. Its distinctive feature is high prevalence in young women. This condition is associated with pregnancy and hormonal changes. A number of risk factors have been identified, including vascular pathology (most commonly fibromuscular dysplasia), other hereditary connective tissue disorders, systemic inflammatory diseases, migraine, and thyroid diseases. Nevertheless, the precise mechanisms of the pathophysiological relationship remain to be elucidated, and risk factors cannot be identified in all patients, indicating the complex and incompletely understood nature of the disease. The present article presents a case series on the development of SCAD in women and a review of the predisposing factors for the disease.

Aim. To identify clusters of patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS) depending on the laboratory data, including platelet function tests.Material and methods. The study included 109 patients hospitalized in the cardiology department with NSTE-ACS. All patients underwent a standard examination, including a complete blood count. In addition, the platelet function was assessed using impedance aggregometry with various inducers (adenosine diphosphate (5 and 10 μmol/L), collagen (2 μmol/L)). We assessed the P-selectin expression level using flow cytometry. Patients were followed up for 6 months. As a statistical method, we performed сluster analysis by K-means algorithm.Results. We registered 18 adverse outcomes (myocardial infarction, unstable angina) during 6-month follow-up. Cluster analysis revealed 3 clusters. The first cluster included 39 (36%) patients with higher monocyte values and lower hemoglobin values, probably indicating chronic inflammation and a tendency towards anemia. The second cluster included 13 older patients (12%) with high comorbidity and high platelet function. Both the first and second clusters recorded 23% adverse outcomes. Third cluster, on the contrary, included mostly younger patients with fewer comorbidities, which had more favorable course of ACS (no signs of platelet hyperaggregation, chronic inflammation and anemia). This cluster included more than half (n=57, 52%) of all patients; adverse outcomes at 6 months in these patients developed 2-fold less frequently than in the other clusters (11% vs 23%).Conclusion. Among patients with NSTE-ACS, groups differing in laboratory parameters were identified, based on which clusters were formed using the k-means method. Clusters with high levels of platelet functional activity, monocyte count and low hemoglobin values included older patients with severe comorbidity and showed a tendency towards more frequent adverse outcomes of the disease.

Aim. To evaluate the functional state of mitochondria isolated from peripheral blood mononuclear leukocytes using flow cytometry in patients with chronic heart failure receiving ubidecarenone (coenzyme Q).Materials and methods. The study included 53 patients with chronic heart failure who had experienced myocardial infarction. The patients were divided into two groups: group 1 received optimally chosen standard therapy, while group 2 received optimally chosen standard therapy and ubidecarenone (“Kudevite”). The mitochondrial membrane potential was evaluated by flow cytometry using propidium iodide and 3,3′-dihexyloxacarbocyanine iodide (DiOC6(3)). The levels of coenzyme Q were determined using high-performance liquid chromatography with ultraviolet (UV) detection.Results. A direct correlation was established between the coenzyme Q levels in the blood plasma and the percentage of DiOC6(3)-positive cells (R = 0.39; р < 0.05) in the patients with chronic heart failure. In group 1, no significant differences in the coenzyme Q levels and the percentage of DiOC6(3)-positive and DiOC6(3)-negative cells before and after the therapy were observed. In group 2, a significant increase in the proportion of DiOC6(3)-positive cells and a significant decrease in the percentage of DiOC6(3)-negative cells were revealed.Conclusion. The increase in the functional activity of mitochondria in the patients with chronic heart failure receiving ubidecarenone was identified. Flow cytometry can be used to evaluate the functional state of mitochondria and observe the efficiency of the selected therapy.

Aim. To reveal the features of monocyte response in myocardial infarction (MI) in pa­­tients with type 2 diabetes (T2D).Material and methods. The study included 121 patients with MI and T2D as follows: 76 — with target glycated hemoglobin (HbA1c), 45 — with elevated HbA1c values. In addition to the standard examination, all patients underwent a blood test for HbA1c on day 1 of MI, while on days 1, 3, 5, and 12±1, monocyte subpopulations were assessed by flow cytometry.Results. Patients with target HbA1c were older than patients with elevated HbA1c levels. In the group with target HbA1c, the number of CD16(+) monocytes on the 1st day of MI was significantly higher: 61,38 (39,2; 100,08) cells/µl vs 35,7 (28,98; 40,33) cells/µl, p=0,03; on the 3rd day of MI, the number of "intermediate" CD14(+)CD16(+) monocytes was higher: 74,82 (71,78; 83,2) cells/µl vs 25,90 (14,04; 57,12) cells/µl, p=0,03, while the CD16(-) to CD16(+) monocyte ratio on the 3rd day of MI was lower: 8,32 (6 ,87; 10,03) vs 10,81 (8,90; 21,10), p=0,04. At the same time, in the group of patients with target HbA1c values, the level of CD16(+) monocytes on the 3rd day of MI was significantly higher in patients aged

We identified insufficient awareness of patients about risk factor and symptoms of myocardial infarction in both groups. Respondents without acute coronary syndrome were better informed and had fewer modifiable risk factors. Low awareness of risk factors for myocardial infarction leads to their inadequate correction. In most cases, insufficient knowledge of symptoms causes delays in the patient 's decision to see a doctor, and, therefore, delays in qualified care.

At the end of the last century and, especially, in the first two decades of the 21st century, a significant technological breakthrough took place in clinical laboratory diagnostics in Russia. The transition from manual techniques to high-tech and high-performance automated systems has changed the potential of laboratory medicine. The laboratory has become a high-tech, rapidly developing branch of medical organizations. Following the changes in technology, the range of diagnostic tests began to alter, while the list of laboratory tests available grew. These dynamics are growing every year. Simple routine techniques, practiced for all patients, are complemented by more specific tests. The place of conventional routine tests has been determined by many years of practical experience, while modern analyzers allow the use of tests with a high evidence value of recommendations, which, in the context of evidence-based medicine, enable the clinician to conduct a personalized diagnostic search. At the same time, in order to use all the possibilities of laboratory medicine, the discipline Clinical Laboratory Diagnostics should be included in educational programs at different stages of a doctor's training.

Aim. To study the association between the levels of inflammation and myocardial remodelling biomarkers and the progression of post-infarction left ventricular (LV) remodelling, based on the cardiac magnetic resonance tomography data. Material and methods. The study included 60 patients with ST segment elevation myocardial infarction, who underwent the standard examination, measurement of serum biomarker levels, and cardiac magnetic resonance tomography, in order to assess the progression of myocardial remodelling. Results. Progressing post-infarction myocardial remodelling was observed in 28,3% of the patients. There was an association between the levels of matrix metalloproteinase (MMP) 1 precursor, MMP-9, tissue inhibitor of MMP-1, N-terminal pro-brain natriuretic peptide (N-proBNP), interleukin-6 (IL-6), end-systolic and enddiastolic volume indices,LV ejection fraction, and damaged myocardial mass index. Conclusion. The study emphasised the important role of the increased levels of MMP and their tissue inhibitor, N-proBNP, and IL-6 in the process of structural and functional post-infarctionLV remodelling.

The study aimed to assess the risk of life-threatening ventricular arrhythmias (LTVA) in patients with non-ST elevation acute coronary syndrome (ACS) and ventricular extrasystolia (VE) developing in the first 24 hours of ACS. In 46 dogs, VE with early, postponed post-depolarisation, re-entry and ischemic mechanisms was modelled. In total, 168 patients with non-ST elevation ACS and Class II-V Lawn VE were examined. All patients underwent general clinical examination as well as the assessment of late ventricular potentials (LVP), QT interval dispersion (QTd), and heart rate turbulence (HRT). In the experimental study, persistent ventricular tachycardia and/or ventricular fibrillation developed in 100%, 75%, and 85,71% of the animals with early post-depolarisation, re-entry and ischemic VE mechanisms, respectively. In the clinical study, LTVA was observed in 13,76 % of ACS patients, including 69,32 % with arrhythmia development in the first 3 days. Positive predictive value for LVP, QTd>80 ms and pathologic HRT was no more than 42%. LTVA risk could be assessed by the formula: LTVAR = А ÷ В, where LTVAR is LTVA risk in units, A – linear deviation of corrected pre-ectopic interval (ms) for at least 20 ventricular extrasystoles, calculated separately for left and right VE, and B – analysed ventricular extrasystole number (per hour). LTVAR

A rare case is described, of myocardial infarction developed in a young male with rare pathology of coronary arteries — multiple ectasies.