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The article is devoted to analysis of relationship of left ventricular remodeling, plasma renin level, glomerular filtration rate in patients with arterial hypertension and renal additional arteries. It is shown that hormonal and hemodynamic factors in young patients with arterial hypertension of 1–2 degrees with renal additional arteries create a load on left ventricle, contributing to pathological myocardial remodeling in the form of eccentric hypertrophy and concentric remodeling.

Syndrome of abnormal originating of the left coronary artery from pulmonary artery (ALCAPA), or Bland-White-Garland syndrome, is an inborn heart defect of atypical coronary arteries branching. In most cases this anomaly is revealed in infancy or adolescence. Opinions exist, that the anomaly is much more prevalent than it is diagnosed. Even more, it might be a cause of myocardial infarction and sudden death of 1st year newborns. In the article, a clinical case presented of first time revealed ALCAPA in 64 year old woman.

Aim. To evaluate diagnostic significance of the type A vascular endothelial growth factor (VEGF-A) and its receptors type 1 and 2 (VEGF-R1 and VEGF-R2) in primary mitral valve prolapse (MVP) patients.Material and methods. Totally, 83 MVP patients studied: 61 males, 22 females; mean age 21,93±4,22 y. o. The signs of systemic inflammation were assessed, as the grade of connective tissue involvement. Immune enzyme analysis was done for serum levels of VEGF-А, VEGF-R1 and VEGF-R2 (“Bender MedSystems GmbH”,Austria). Controls included 20 healthy volunteers — 14 males, 6 females, mean age 21,10±0,55 y. o. with no MVP and any other dysplastic features.Results. In the MVP group, the decreased levels of circulating VEGF-R1 were found, as the increase of cases number of high (42,17%) and low (32,53%) concentration of VEGF-А. In low levels of VEGF-A and VEGF-A/ VEGF-R1 prevalence of grade II mitral regurgitation increases 5,1 times comparing to the group of retained balance of VEGF-A and VEGF-R1 — 95% confidence interval (CI) 1,25-20,88, and the prevalence of clinically significant cardiac rhythm and conduction disorders increases 5,25 times in comparison to the cases with elevated VEGF-A and VEGF-R1 — 95% CI 1,33-20,76 and 4,09 times — comparing MVP patients with retained balance of VEGF-A and VEGF-R1 — 95% CI 1,18-14,17.Conclusion. In primary MVP patients, regardless clinical phenotype of monogenic hereditary syndromes, the heterogeneity of deviation and regulation of VEGF has been established. Highest number of II grade mitral regurgitation, significant rhythm disorders was found in the group with low VEGF-A and VEGF-A/VEGF-R1, that might be implemented as optimized risk stratification in heterogenic MVP patients population.

Aim. To assess the condition of adhesion function of endothelium in various clinical variants of primary mitral valve prolapse (MVP). Material and methods. Totally, 91 patient studied with primary MVP at the age 21 (19-24) y. First grade mitral regurgitation was found in 45,1% and II — in 54,9% patients. MVP was solitary variant (6,6%) and comorbid with 1-3 minor anomalies of the heart (93,4%). Doppler-echocardiography was done on Vivid07 equipment (Israel). The grade of systemic involvement of connective tissue was 2 (1,5-4,0) points. Controls were 10 healthy persons, matched by age, sex, smoking, body mass index. By the immune enzyme method we checked plasmatic concentrations of L-, E-, Р-selectins, ICAM-1, VCAM-1, PECAM-1 (Bender MedSystems GmbH, Austria). Findings are presented as mediana (25-75 percentiles). Results. In MVP patients the levels of Е-selectin — 43,0 (33,7-54,8) ng/ mL, ICAM-1 — 669,9 (546,4-883,3) ng/mL and VCAM-1 — 925,0 (707,5- 1215,0) ng/mL, were significantly higher, and the level of РЕСАМ-1 — 49,8 (40,4-63,2) ng/mL, in opposite, lower than in control group. L- and P-selectins levels in MVP group were measured as relevant to controls values (p>0,05). In regurgitation cases of II degree, the level of E-selectin and ICAM-1 were maximal (p

Aim. To evaluate the global longitudinal strain of the left ventricle (LV) after coronary stenting (CS) in patients with stable ischemic heart disease (IHD).Material and methods. Totally, 50 IHD patients included (35 men, 15 women, age 59,3±6,89 y.). All had indications for CS. Syntax Score was not higher than 22 units (11,78±6,77 units). Before and during the first week after CS all patients underwent standard echocardiography (EchoCG), where the Global Longitudinal Strain-GLSLV was assessed with “AFI” option. All patients also got quantitative measurement of troponin I and MB-creatinkinase (CK-MB) before intervention, in 6 hours and in 24 hours after stenting.Results. Before CS, in 21 patient there was normal GLSLV (-18,0% and less), in 29 GLSLV decreased (more than -18%). After stenting the patients with improvement of GLSLV were marked (n=28) and with worsening of GLSLV (n=22). During early postoperation period there were no any clinically significant complications, electrocardiographic changes, worsenings of local contractility. In worsening of GLSLV group there was increase of troponin I and CK MB in 6 hours and in 24 hours after stenting, not more than threshold value of acute coronary syndrome (ACS).Conclusion. Worsening of global longitudinal strain of the LV after CA stenting was found in 44% of stable IHD patients. Negative dynamics of GLSLV was associated with an increase of troponin I, CK-MB levels in 6 and 24 hours after CS not higher significant for ACS level. Worsening of global strain of the LV and increase of troponin, probably, can be explained by embolism of microcirculatory pool during CA stenting. Damage of myocardium during stenting further determines the decrease of the strain in patients with such increase at the baseline.

Abstract. The levels of autoantibodies to collagen type I, II, III, IV and V were studied in blood plasma of 130 patients (18-32 years old) with undifferentiated connective tissue dysplasia, using immunoenzyme analysis. A correlation was revealed between the levels of autoantibodies to various collagen types, and external and/or heart manifestations of connective tissue dysplasia. Increased levels of autoantibodies to collagen type I and II were shown in patients with chest deformation, scoliosis, pronounced joint hypermobility syndrome, multiple minor intracardial anomalies. Increased antibodies to type I collagen were associated with flat-footedness, whereas levels of antibodies to collagen type I, II, and V correlated with myxomatous degeneration of mitral valve prolapse. Increase in anticollagen antibody levels in cases of pronounced external and cardiac markers of connective tissue dysplasia suggests an impairment of autoimmune regulatory mechanisms of collagen metabolism.

Aim. To study the selected mediators of intracellular interactions and endothelial function in patients with myxomatous mitral valve prolapse (MVP). Material and methods. In total, 25 patients with myxomatous MVP, aged 18–29 years, were examined. The comparison groups included patients with MVP but no echocardiographic signs of myxomatosis and healthy individuals. The blood levels of the following mediators were measured: interleukin 1

Aim. To investigate regulatory vasoactive mediators – endothelin-1 (ET-1), 6-ketoprostaglandin F1α (6-keto-PGF1α), thromboxane В2 (TXВ2) – in young patients with minor heart anomalies (MHA) and non-differentiated connective tissue dysplasia (CTD). Material and methods. Fifty-three patients, 37 men and 16 women (mean age 22,0±0,8 years) were examined. Plasma concentrations of ТХВ2, 6-keto-PGF1α and ET-1 were measured by immune-enzyme methods. Results. Some specific features of vasoactive mediators in MHA were observed. In patients with three MHA, ET-1 level was increased. In Stage II mitral valve prolapse (MVP), combined with atopic chord (AC) and/or Stage II mitral regurgitation, TXB2 level was increased, without any significant thromboxane-prostacyclin dysbalance. In patients with mixomatous MV degeneration, plasma ET-1 concentration was increased, and TXB2 level was higher than that of 6-keto-PGF1α. Conclusion. In MHA patients, functional endothelial status is disturbed. Disturbance severity is maximal in three MHA and mixomatous MV degeneration.

In total, 15 patients with nоn-differentiated connective tissue dysplasia (CTD) and white coat hypertension (WCH), 10 WCH-free individuals, and 10 healthy volunteers aged 18-30 years were examined. CTD and WCH patients had greater body weight and body mass index than DCT individuals without WCH. CTD and WCH combination was associated with increased levels of adrenalin and ADP-induced platelet aggregation, endothelin-1, as well as with reduced 6-keto-prostaglandin F1α (6-keto-PGF1α) concentration. In CTD without WCH, collagen-induced platelet aggregation and Willebrand factor activity were decreased.

Aim. To reveal changes in the thromboxane-prostacyclin balance and platelet aggregability in patients with various variants of minor cardiac abnormalities. Subjects and methods: Six-five patients (mean age 23.0±0.7 years) with minor cardiac abnormalities and 10 apparently healthy individuals were examined. Platelet aggregation induced by adrenaline, adenosine diphosphate, collagen) and the plasma levels of thromboxane B2 (TxB2) and 6-keto-prostaglandin F1α (6-keto-PGF1α) were determined. Results. Patients with abnormally located chordae (ALC) were found to have no deviations in the thromboxane-prostacyclin balance and platelet aggregability. Only decreased collagen aggregation was recorded in the groups of first-degree mitral prolapse (MP) and first-degree MP + ALC; in second-degree MP and second-degree MP + ALC, there was a reduction in platelet aggregation on all inductors and an increase in TxB2. Patients with myxomatous degeneration of the mitral valve exhibited reduced collagen-induced platelet aggregation and lower plasma 6-keto-PGF1α levels. Conclusion. The most pronounced changes in the thromboxane-prostacyclin balance and platelet aggregability were found in patients with MP and second-degree regurgitation, three intracardiac microabnomalities, and myxomatous degeneration of the mitral valve.