The aim —  to create algorithm of treatment of patients with varicose veins of the lower extremities (VVLE) with differential use of various types of fibers depending on the diameter of sapheno-femoral junction (SFJ), and evaluate its effectiveness in long-term post-operative period (in 1 year).
Materials and methods. The prospective study which was performed in period from 2014 to 2017 on the base of Oleksandrivska City Clinical Hospital (Kyiv, Ukraine) included 265 patients with VVLE. Among them, there were 185 (69.8 %) women and 80 (30.2 %) men aged from 20 to 71, on an average 39.9 ± 0.7 years old, of class II-VI according to CEAP classification. The diameter of SFJ ranged from 5 mm to 30 mm. The mean value of the general clinical score according to venous severity scoring (VSS) system was 11.29 ± 0.41 points. The term of patient’s follow up was 1 year. Endovenous laser treatment (EVLT) was performed with application of diode laser of 1470 nm wavelength. The comparison group (group C) included 209 patients who underwent EVLT with application of bare-tip fiber (in case of SFJ diameter ≤ 21 mm in period from 2014 to 2015) and radial fiber (in case of SFJ diameter ≤ 30 mm in period from 2015 to 2016). The main group (group O) included 56 patients who underwent EVLT in 2016 with application of bare-tip fiber (in case of SFJ diameter ≤ 16 mm), radial fiber (in case of SFJ diameter of 17 mm — 23 mm); cross-ectomy and EVLT with the use of bare-tip or radial fiber in case of SFJ diameter > 23 mm. Groups C and O were representative of sex, age, class of CEAP, SFJ diameter, points according to VSS scale, and length of ablated great saphenous vein (GSV) segment. In case of total vertical reflux, in order to prevent thermic neuritis of the saphenous nerve, we applied an original method of combined laser and foam ablation of the GSV.
Results and discussion. The average duration of surgical intervention in patients of group C was 63.2 ± 1.4 mins (from 34 mins to 105 mins), in patients of group O — 62.1 ± 1.8 mins (from 38 mins to 94 mins), р = 0.662. The length of GSV segment which was ablated with the help of EVLT in patients of group C was from 7 to 96 cm, median — 37 cm; in patients of group O — from 7 cm to 94 cm, median — 38 cm. Among patients with total vertical reflux, the frequency of thermic neuritis of the saphenous nerve was statistically higher in group C than in group O (35.5 % versus 0.0 %; р = 0.043). In a year after surgery, cumulative frequency of recurrence of vertical reflux in patients of group C was 11.5 %, and in patients of group O — 1.8 % (р = 0.03); the mean value according to VSS scale was 2.9 ± 0.4 points and 1.4 ± 0.3 points, respectively, (р = 0.049).
Conclusions. The created algorithm of treatment of patients with VVLE of C2-C6 class according to CEAP classification with differential use of various types of fibers, improved with combined method of elimination of severe vertical reflux and cross-ectomy allowed decreasing the frequency of post-traumatic neuritis (in patient with total reflux) in long-term (1-year) post-operative period from 35.5 % to 0 %, frequency of recurrence of the vertical reflux — from 11.5 % to 1.8 %, mean value of general clinical point — from 2.8 to 1.8 points.

Keywords: endovenous laser treatment, radial fiber, bare-tip fiber, sapheno-femoral junction diameter, varicose veins, cross-ectomy, long-term results.

The aim — to analyze 2016 year data of acute coronary syndrome (ACS) registry in Transcarpathian region.
Materials and methods. ACS Registry in Transcarpathian region (hereafter — Registry) was initiated on 01 January, 2016. It systematically collects information on each ACS case that has been registered in healthcare facilities of the region. The Registry is a retrospective observational regional single-center study. Registry comprises specially designed electronic registration forms, which were filled in with systematic, tertiary center coordinated collection of data on each ACS case that has been registered in healthcare facilities of the region.
Results and discussion. During 9 months of 2016, data on 904 cases of ACSs were entered into the Registry — mostly ACS with ST segment elevation (STE-ACS) (291 cases, 32.2 %) and Q-wave myocardial infarction (319 cases, 35.3 %). Among patients with STE-ACS median of time from onset of symptoms to diagnosis was 140 minutes (interquartile range 70.0 — 360.0), in 113 cases (45.4 %) the diagnosis was made in less than 2 hours, in 189 (75.9 %) patients it was made in less than 6 hours, and in 224 (90.0 %) patients — less than in 12 hours. Primary coronary intervention (PCI) was performed in 261 patients (28.9 % of all ACS), thrombolytic treatment was given to 56 patients (6.2 %). Total mortality among all ACS patients was 14.2 %, with large inter-district variability: 0 % in Perechyn and Mizhhirya districts, 26.7 % in Volovets district, 29.3 % in Vynohradiv district, 37.5 % in Velykyy Bereznyy district. Among PCI patients mortality was 7.3 %, in non-PCI cohort it was 17.0 %, which corresponds to 0.43 relative risk (PCI vs non-PCI) with 95 % CI 0.27 — 0.68 and NNT to avoid one death 10.3. The proportion of deaths in PCI-treated patients was 24.1 % out of all deaths. This measure was highly variable throughout districts: starting from 0 % in Berehovo, Mizhhirya, Perechyn and Rakhiv districts and up to 50 % in Velykyy Bereznyy and Volovets districts. There was a sustained trend towards fewer deaths as percentage of reperfused patients increased. Comparison of Registry data on mortality and official medical statistics report figures revealed systematic excess of mortality as reported by official medical statistics (14.2 vs 21.7 %).
Conclusions. Registry data analysis demonstrated low numbers of diagnosed ACS (especially non-STE ACS and non-Q MI), substantial differences in quality of care between different districts and notable decrease up to 57 % in ACS mortality in reperfused patients.

Keywords: acute coronary syndrome, reperfusion therapy, registry.

The aim — to evaluate possible relationship between T(–786)C polymorphism of eNOS gene and values of intracardiac hemodynamics in patients with acute myocardial infarction (MI) after thrombolytic therapy.
Materials and methods. We examined 64 patients with MI with ST segment elevation (STEMI) after intravenous thrombolytic therapy. Cardiac ultrasound and evaluation of allelic T(–786)C polymorphism of eNOS gene with polymerase chain reaction were performed in all patients.
Results and discussion. 22 (34.4 %) of the examined patients had TT genotype, 34 (53.1 %) — ТС genotype and 8 (12.5 %) — СС genotype. The patients were divided into two groups: І group consisted of TT genotype carriers, II group — of ТС and СС genotype carriers. We found that patients in II group were significantly more likely to have the history of arterial hypertension (р = 0.046), T2DM (р = 0.052), family history of early onset of cardiovascular diseases (р = 0.048). Patients of II group were better informed about dyslipidemia before they developed STEMI (р = 0.047). Mean left ventricular (LV) end-diastolic volume (EDV) on cardiac ultrasound was significantly lower in group I than in group II: (128.82 ± 20.70 vs 138.41 ± 21.40 ml; р = 0.054). Mean LV end-systolic volume (ESV) in group I was also significantly lower than in II group (63.27 ± 9.67 vs 69.78 ± 13.76 ml; р = 0.052). We performed stepwise regression analysis and obtained statistically significant regression model (p < 0.01). According to it, T(–786) C polymorfhism of eNOS gene with presence of C allele in patient’s genotype was responsible for 3.0 % of EDV increase (р = 0.001) and for 3.8 % of ESV increase (р = 0.005).
Conclusions. STEMI patients with С allele of T(–786) C polymorphism of eNOS gene are significantly more likely to have arterial hypertension, T2DM and family history of cardiovascular diseases with early onset. Presence of С allele of T(–786)C polymorphism of eNOS gene is an independent factor of increase in LV ESV and LV EDV.

Keywords: acute myocardial infarction, left ventricular remodeling, endothelial NO-synthase gene polymorphism.

List of references:  
1.    Parkhomenko, A. N., Lutay, Y. M., Irkin, O. I. et al.  Clinical and prognostic value of endothelial NO–synthetase gene polymorphism in patients with acute coronary syndromes (Russian). Meditsina neotlozhnyih sostoyaniy [Emergency Medicine]. 2014;3 (58):45-54.
2.    Tseluyko VI, Yakovleva LM, Bondar TM. Role of endothelial NO–syntase T-786C gene polymorphism for nitric oxide metabolism violations and development of atherosclerosis (Ukrainian). Ukrajinsjkyj kardiologhichnyj zhurnal [Ukrainian Journal of Cardiology]. 2012;4:130-134.
3.    Tseluyko VI, Yakovleva LN. Genetic aspects of hypertension in patients with coronary heart disease (Russian). Arterialjna ghipertenzija [Arterial Hypertension]. 2013;5 (31):16-20.
4.    Tseluyko V.I ., Yakovleva LN, Luchkov AB. Intracardiac hemodynamics indicators in patients with coronary artery disease depending on T-786C polymorphism of endothelial NO–synthase gene promoter (Russian). Emergency Medicine. 2013. №8 (55):99-104.5.    Flachskampf FA, Schmid M, Rost C et al. Cardiac imaging after myocardial infarction. Eur Heart J. 2010;32(3):272-283.
6.    Fraccarollo D, Galuppo P, Bauersachs J. Novel therapeutic approaches to post-infarction remodelling. Cardiovasc Res. 2012;94(2):293-303.
7.    Galli A, Lombardi F. Postinfarct Left Ventricular Remodelling: A Prevailing Cause of Heart Failure. Cardiology Research and Practice;2016. Article ID 2579832, 12 pages, 2016.
8.    Go AS, Mozaffarian D, Roger VL et al. Heart disease and stroke statistics—2014 update: a report from the American heart association. Circulation. 2014;129(3):399-410.
9.    He Y, Fan Z, Zhang J et al. Polymorphisms of eNOS gene are associated with diabetic nephropathy: a meta-analysis. Mutagenesis. 2010;26(2):339-349.
10.    Kazakov A, Müller P, Jagoda P et al. Endothelial nitric oxide synthase of the bone marrow regulates myocardial hypertrophy, fibrosis, and angiogenesis. Cardiovasc Res. 2012;93(3):397-405.
11.    Konsola T, Antonopoulos A, Siasos G et al. The Impact of Genetic Variability of eNOS on Progression of Microvascular Disease in Type 2 Diabetes Patients: Effects on Angiogenesis Mechanisms. Circulation. 2016;134(1). A19698
12.    Loyer X, Heymes C, Samuel JL. Constitutive nitric oxide synthases in the heart from hypertrophy to failure. Clin Exp Pharmacol Physiol. 2008;35(4):483-488.
13.    Morrow DA, Antman EM, Charlesworth A et al. TIMI risk score for ST-elevation myocardial infarction: a convenient, bedside, clinical score for risk assessment at presentation: an InTIME II trial substudy. Circulation. 2000;102:2031-2037.
14.    Niu W, Qi Y. An Updated Meta-Analysis of Endothelial Nitric Oxide Synthase Gene: Three Well-Characterized Polymorphisms with Hypertension. PLoS One. 2011;6(9). Р. e24266.
15.    Ponikowski P, Voors AA, Anker SD et al. Task force Members and Document Reviewers. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur J Heart Fail. 2016;18(8):891-975.
16.    Rai H, Parveen F, Kumar S et al. Association of Endothelial Nitric Oxide Synthase Gene Polymorphisms with Coronary Artery Disease: An Updated Meta-Analysis and Systematic Review. PLoS One. 2014;9 (11). Р. e113363.
17.    Roffi M, Patrono C, Collet JP et al. 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: the Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology. Eur Heart J. 2016;37(3):267-315.
18.    Tseluyko V, Yakovleva LN. Clinical and anamnestic characteristics of patients with CAD depending on gene polymorphism T786C promotor of endotelial NO syntase. Eur Heart J. 2013;34 (suppl. 1):4014.
19.    Vecoli C, Andreassi MG, Liga R et al. T (-786)→C polymorphism of the endothelial nitric oxide synthase gene is associated with insulin resistance in patients with ischemic or non ischemic cardiomyopathy. BMC medical genetics. 2012;13(1):92.

The aim — to determine the relationship of renal dysfunction with the severity of clinical and hemodynamic signs of congestion by means of markers of acute renal damage (ARD) and the effectiveness of decongestion in patients with acute decompensated heart failure (ADHF).
Materials and methods. The prospective study involved 107 «warm and wet» patients with ADHF aged 38 to 85 years (mean age (65.7 ± 2.2) years), including 78 (70.1 %) men who were consecutively hospitalized in the cardiological department of Oleksandrivska Clinical Hospital in Kyiv in 2013 — 2014. Patients were divided into two groups depending on glomerular filtration rate (GFR) at admission: less than 60 ml/(hr · 1.73 m2), that is, significantly reduced GFR, and 60 ml/(hr · 1.73 m2) and more, that is, relatively preserved GFR.
Results and discussion. In the group with decreased GFR, the patients were significantly older (64.8 ± 2.72) vs. (55.3 ± 2.32) years, respectively, p < 0.01) and had a greater incidence of arterial hypertension (86.9 % vs. 54.3 % p < 0.01), diabetes (32.8 % vs. 15.2 %, p < 0.05), decrease in EF < 45 % (88.5 % vs. 63.0 %, respectively, p < 0.01). The mean time of inpatient treatment was (14.9 ± 0.9) days in the group with GFR < 60 ml/(hr · 1.73 m2), and (11.7 ± 0.7) days in the group with GFR ≥ 60 ml/(hr · 1.73 m2), (p < 0.01). High severity of heart failure by NYHA and predominance of IV functional class in patients of this group were associated with a greater severity of clinical manifestations of congestion — dyspnea on the Borg scale, Lala ortho-edema index and modified Gheorghiade congestion index (all p < 0.05), and an increase in E/E′ by 23.5 % and NT-proBNP — by 22.5 % (p < 0.01).
Conclusions. In «warm and wet» patients with ADHF, chronic kidney disease (CKD) was observed in 57 % of cases and was associated with a greater expression of clinical signs of congestion. Conventional decongestive therapy with diuretics and nitrates for ADHF with CKD was accompanied by a more pronounced decrease in GFR on day 3 of hospitalization and an increase in NGAL only in patients with CKD, probably, resulting from their acute damage.

Keywords: acute renal damage, acute decompensated heart failure, lipocalin, gelatinase-associated neutrophils (NGAL), decongestion and glomerular filtration rate.

List of references:  
1.    Adams K. F., Jr, Fonarow G. C., Emerman C. L. et al. Characteristics and outcomes of patients hospitalized for heart failure in the United States: rationale, design, and preliminary observations from the first 100,000 cases in the Acute Decompensated Heart Failure National Registry (ADHERE) // Am. Heart J. — 2005. — Vol. 149. — P. 209 — 216.
2.    American Heart Association. Heart Disease and Stroke Statistics 2007 Update // Dallas, TX. — American Heart Association. — 2007.
3.    Borg G. Psychophysical bases of perceived exertion // Med. Sci. Sports Exercise. — 1982. — Vol. 14. — P. 377 — 381.
4.    Brisco M. A., Testani M. Novel Renal Biomarkers to Assess Cardiorenal Syndrome // Curr. Heart Fail. Rep. —2014. — Vol. 11 (4). — P. 485 — 499.
5.    Cleland J. G., Swedberg K., Cohen-Solal A. et al. The Euro Heart Failure Survey of the EUROHEART survey programme: a survey on the quality of care among patients with heart failure in Europe: the Study Group on Diagnosis of the Working Group on Heart Failure of the European Society of Cardiology: the Medicines Evaluation Group Centre for Health Economics University of York // Eur. J. Heart Fail. —2000. — Vol. 2. — P. 123 — 132.
6.    Cleland J. G., Swedberg K., Follath F. et al. Study Group on Diagnosis of the Working Group on Heart Failure of the European Society of Cardiology: The Euro- Heart Failure survey program—A survey on the quality of care among patients with heart failure in Europe // Eur. Heart J. — 2003. — Vol. 24. — P. 442 — 463.
7.    Dries D. L., Exner D. V., Domanski M. J. et al. The prognostic implications of renal insufficiency in asymptomatic and symptomatic patients with left ventricular systolic dysfunction // J. Am. Coll. Cardiol. — 2000. — Vol. 35 (3). — P. 681 — 689.
8.    Farmakis D., Parissis J., Lekakis J., Filippatos G. Acute heart failure: Epidemiology, risk factors, and prevention // Rev. Esp. Cardiol. — 2015. — Vol. 68. — P. 245 — 248.
9.    Felker M., O’Connor C. M., Braunwald E. Loop diuretics in acute decompensated heart failure: necessary? Evil? A necessary evil? // Circ. Heart Fail. — 2009. — Vol. 2 (1). — P. 56 — 62.
10.    Fonarow G. C. The Acute Decompensated Heart Failure National Registry (ADHERE): opportunities to improve care of patients hospitalized with acute decompensated heart failure // Rev. Cardiovasc. Med. — 2003. — Vol. 4 (suppl. 7). — P. 21 — 30.
11.    Fonarow G. C., Abraham W. T., Albert N. M. et al. OPTIMIZE-HF Investigators and Hospitals: Influence of a performance-improvement initiative on quality of care for patients hospitalized with heart failure: Results of the organized program to initiate lifesaving treatment in hospitalized patients with heart failure (OPTIMIZE-HF) // Arch. Intern. Med. — 2007. — Vol. 167. — P. 1493 — 1502.
12.    Gandhi S. K., Powers J. C., Nomier A. M. et al. The pathogenesis of acute pulmonary edema associated with hypertension // N. Engl. J. Med. — 2001. — Vol. 344. — P. 17 — 22.
13.    Gheorghiade M., Follath F., Ponikowski P. et al. Assessing and grading congestion in acute heartfailure: a scientific statement from the Acute Heart Failure Committee of the Heart Failure Association of the European Society of Cardiology and endorsed by the European Society of Intensive Care Medicine // Eur. J. Heart Fail. — 2010. — Vol. 12. — P. 423 — 433.
14.    Gheorghiade M., Zannad F., Sopko G. et al. Acute heart failure syndromes // Circulation. —2005. — Vol. 112. — P. 3958 — 3968.
15.    Haase M., Devarajan P., Haase-Fielitz A. et al. The Outcome of Neutrophil Gelatinase-Associated Lipocalin-Positive Subclinical Acute Kidney Injury: A Multicenter Pooled Analysis of Prospective Studies // J. Am. Coll. Cardiol. —2011. — Vol. 57. — P. 1752 — 1761.
16.    Haase-Fielitz A., Haase M., Devarajan P. Neutrophil gelatinase-associated lipocalin as a biomarker of acute kidney injury: a critical evaluation of current status // Ann. Clin. Biochem. — 2014. — Vol. 51. — P. 335 — 351.
17.    Heywood J. T., Fonarow G. C., Costanzo M. R. et al. ADHERE Scientific Advisory Committee and Investigators: High prevalence of renal dysfunction and its impact on outcome in 118,465 patients hospitalized with acute decompensated heart failure: A report from the ADHERE database // J. Card. Fail. — 2007. — Vol. 13. — P. 422 — 430.
18.    Lala A., McNulty S. E., Mentz R. J. et al. Relief and Recurrence of Congestion During and After Hospitalization for Acute Heart Failure: Insights From Diuretic Optimization Strategy Evaluation in Acute Decompensated Heart Failure (DOSE-AHF) and Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARESS-HF) // Circ. Heart Fail. —2015. — Vol. 8 (4). — P. 741 — 748.
19.    Leithe M. E., Margorien R. D., Hermiller J. B. et al. Relationship between central hemodynamics and regional blood flow in normal subjects and in patients with congestive heart failure // Circulation. — 1984. — Vol. 69. — P. 57 — 64.
20.    Levey A. S., Stevens L. A. et al. A new equation to estimate glomerular filtration rate // Ann. Intern. Med. — 2009. — Vol. 150. — P. 604 — 612.
21.    Liu P. P. Cardiorenal syndrome in heart failure: A cardiologist’s perspective // Can. J. Cardiol. — 2008. — Vol. 24 (suppl. B). — P. 25 — 29.
22.    Ljungman S., Laragh J. H., Cody R. J. Role of the kidney in congestive heart failure: relationship of cardiac index to kidney function // Drugs. — 1990. — Vol. 39 (4). — P. 10 — 21.
23.    Marti C. N., Georgiopoulou V. V., Kalogeropoulos A. P. Acute heart failure: patient characteristics and pathophysiology // Curr. Heart Fail. Rep. — 2013. — Vol. 10 (4). — P. 427 — 33.
24.    McCullough P. A., Ahmad A. Cardiorenal syndromes // World J. Cardiol. —2011. — Vol. 26. — P. 1 — 9.
25.    Mehta R. L., Kellum J. A., Shah S. V. et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury // Crit. Care. — 2007. — Vol. 11. — P. 31.
26.    Mentz R. J., Kjeldsen K., Rossi G. P. et al. Decongestion in acute heart failure // Eur. J. Heart Fail. — 2014. — Vol. 16 (5). — P. 471 — 482.
27.    Milo-Cotter O., Adams K. F., O’Connor C. M. et al. Acute heart failure associated with high admission blood pressure — a distinct vascular disorder? // Eur. J. Heart Fail. — 2007. — Vol. 9. — P. 178 — 183.
28.    Molitch M. E., Adler A. I., Flyvbjerg A. et al. Diabetic kidney disease — A clinical update from Kidney Disease: Improving Global Outcomes (KDIGO) // Kidney Int. — 2015. — Vol. 87 (1). — P. 20 — 30.
29.    Nieminen M. S., Harjola V. P. Definition and epidemiology of acute heart failure syndromes // Am. J. Cardiol. — 2005. — Vol. 96 (6A). — P. 5 — 10.
30.    Palazzuoli A., Ruocco G., Ronco C., McCullough P. A. Loop diuretics in acute heart failure: beyond the decongestive relief for the kidney // Critical Care. — 2015. — Vol. 19. — P. 296.
31.    Qiugen Zhou, Chunmei Zhao, Di Xie. et al. Acute and acute-on-chronic kidney injury of patients with decompensated heart failure: impact on outcomes // BMC Nephrology. — 2012. — Vol. 13. — P. 51.
32.    Reid R., Ezekowitz J. A., Brown P. M. et al. The prognostic importance of changes in renal function during treatment for acute heart failure depends on admission renal function // PLoS One. — 2015. — Vol. 10 (9).
33.    Sarnak M. J. A Patient with heart failure and worsening kidney function // Clin. J. Am. Soc. Nephrol. — 2014. — Vol. 9 (10). — P. 1790 — 1798.
34.    Stewart S., MacIntyre K., Hole D. J. More ‘malignant’ than cancer? 5-year survival following a first admission with heart failure // Eur. J. Heart Fail. — 2001. — Vol. 3. — P. 315 — 322.
35.    The Criteria Committee of the New York Heart Association. Nomenclature and сriteria for diagnosis of diseases of the heart and great vessels. — 9th ed. — Boston, Mass: Little, Brown & Co; 1994. — Р. 253 — 256.
36.    Zannad F., Mebazaa A., Juillière Y. et al. EFICA Investigators. Clinical profile, contemporary management and one-year mortality in patients with severe acute heart failure syndromes: The EFICA study // Eur. J. Heart Fail. — 2006. — Vol. 8 (7). — P. 697 — 705.

The aim — of study: to evaluate the results of usage of different methods of cardioplegic solution delivery into the miocardium in combined surgeries of diseases of coronary arteries and heart valves.
Materials and methods. For the period of 2014 — 2016, prosthetics or plastic surgery of the heart valves was performed in 3,067 patients. Of these, 766 (25.0 %) needed combination with coronary artery bypass grafting (CABG). They were the subject of the study. Several ways of cardioplegic solution delivery to the myocardium were used to protect the myocardium: the solution was injected after CABG and was performed at different stages after aortic clamping.
Results and discussion. Analysis of the results of surgical treatment of combined valvular and coronary pathology with the use of various methods of cardioplegia, minimizing the on-pump effect on the patient’s body showed the advantage of the preventive CABG method on the working heart to achieve subsequent full cardioplegia, which reduced the time of heart-lung machine usage by 21.4 %, and cardiac ischemia — by 42.3 %.
Conclusions. In the surgical treatment of acquired valvular heart disease, combined coronary artery bypass surgery was necessary in 25.0 % of patients, i.e., in every fourth patient. Using the methods of preventive restoration of coronary blood flow by coronary artery bypass on a working heart before clamping the aorta showed the advantages of this option for the subsequent uniform delivery of the cardioplegic solution to the myocardium.

Keywords: cardioplegia, coronary pathology, valvular heart disease, myocardial protection options.

The aim — to evaluate the effect of the selective mineralocorticoid receptor antagonist eplerenone in the long-term prognosis of patients with myocardial infarction (MI) of the right ventricle (RV) against the background of Q-MI of the left ventricular posterior wall (PWLV).
Materials and methods. The study involved 155 patients with MI of the RV against Q-MI of the PWLV aged (64.11 ± 0.78) years. Patients were divided into two groups. Group 1 consisted of 88 (56.8 %) patients including 13 (14.8 %) which had left ventricular ejection fraction ≤ 40 %. On the 3rd — 4th day of MI they received eplerenone. Group 2 consisted of 67 (43.2 %) patients treated with standard therapy. The follow-up was 30.6 ± 4.5 months. The endpoints were: cardiovascular (CV) death, unstable angina (UA), recurrent MI (Re-MI), hospitalizations for heart failure (HF) and acute cerebrovascular accidents (ACVA).
Results and discussion. The endpoints occurred in 65 (41.9 %) patients: UA — in 50 (32.2 %), Re-MI — in 15 (9.6 %), ACVA — in 9 (5.8 %), HF-hospitalization — in 22 (14.2 %), CV-death — in 16 (10.3 %) persons. CV-events occurred in 27 (30.7 %) patients of the eplerenone group, which was significantly lower than in patients of the 2nd group — 38 (56.7 %), (Cox F-test: p = 0.00389). The frequency of Re-MI (p = 0.168) and ACVA (p = 0.144) were not significantly different between the groups at the end of observation. However the frequency of UA (p = 0.0267), HF-hospitalization (p = 0.0107) and CV-deaths (p = 0.0295) were significantly less frequent in patients who received eplerenone.
Conclusions. The use of eplerenone in addition to standard therapy in patients with right ventricular infarction is associated with a statistically significant reduction in the number of cardiovascular events, including death, UA, and HF-hospitalizations during 30.6-month follow-up.

Keywords: myocardial infarction, right ventricle, eplerenone, prognosis, cardiovascular events.

List of references:  
1.    Voronkov L.H., Amosova K.M., Bahriy A.E. ta in. Rekomendatsiyi z diahnostyky ta likuvannya khronichnoyi sertsevoyi nedostatnosti (2012) (Ukrainian). Sertseva nedostatnist’ [Heart Failure] (Ukrainian). 2012;3:60-96.
2.    Koval’ E.A., Bahryy A.Э. Mesto anatahonystov al’dosterona v lechenyy serdechno-sosudystыkh zabolevanyy: sehodnya y zavtra (Russian). Zdorov»ya Ukrayiny [Ukraine Health] (Ukrainian). 2009;15-16:56-57.
3.    Abtahi F, Farmanesh M, Moaref A et al. Right ventricular involvement in either anterior or inferior myocardial infarction. Int Cardiovasc Res J. 2016;10(2):67-71.
4.    Ahmed A, Zannad F, Love TE et al. A propensity-matched study of the association of low serum potassium levels and mortality in chronic heart failure. Eur Heart J. 2007;28:1334-1343.
5.    Beygui F, Labbe JP, Cayla G et al. Early mineralocorticoid receptor blockade in primary percutaneous coronary intervention for ST-elevation myocardial infarction is associated with a reduction of life-threatening ventricular arrhythmia. Int J Cardiol. 2013;167:73-79.
6.    Cohn JN, Colucci W. Cardiovascular Effects of Aldosterone and Post-Acute Myocardial Infarction Pathophysiology. Am J Cardiol. 2006;97. N 10 (suppl. 1):4-12.
7.    Edelmann F, Wachter R, Schmidt AG et al. Effect of spironolactone on diastolic function and exercise capacity in patients with heart failure with preserved ejection fraction: the Aldo-DHF randomized controlled trial. J Am Heart Assoc. 2013;309. N 8:781-791.
8.    Filippatos G, McMurray J, Aboyans V et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Eur Heart J. 2016;37:2129-2200.
9.    Iraqi W, Rossignol P, Angioi M et al. Extracellular cardiac matrix biomarkers in patients with acute myocardial infarction complicated by left ventricular dysfunction and heart failure: insights from the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) study. Circulation. 2009;119:2471-2479.
10.    Li J, Becher P, Blankenberg S, Westermann D. Current treatment of heart failure with preserved ejection fraction: should we add life to the remaining years or add years to the remaining life?. Hindawi Publishing Corporation Cardiology Research and Practice;2013. Article ID 130724, 9 pages.
11.    Montalescot G, Pitt B, Lopez de Sa B et al. Early eplerenone treatment in patients with acute ST-elevation myocardial infarction without heart failure: The Randomized Double-Blind Reminder Study. Eur Heart J. 2014;33 (34). P. 2295-2302.
12.    Montalescot G, Sechtem U, Achenbach S et al. Task Force Members. 2013 ESC guidelines on the management of stable coronary artery disease: The Task Force on the management of stable coronary artery disease of the European Society of Cardiology. Eur Heart J. 2013;34:2949-3004.
13.    Pandey P, Garg S, Matulevicius SA et al. Effect of mineralocorticoid receptor antagonists on cardiac structure and function in patients with diastolic dysfunction and heart failure with preserved ejection fraction: A meta-analysis and systematic review. J Am Heart Assoc. 2015;4:18-28.
14.    Pitt B, Pfeffer M, Assmann S et al. Spironolactone for Heart Failure with Preserved Ejection Fraction. N Engl J Med. 2014;370:1383-1392.
15.    Pitt B, Remme W, Zannad F et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. The New England Journal of Medicine. 2003;348. N. 14:1309-1321.
16.    Pitt B, Zannad F, Remme WJ et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. N Eng J Med. 1999;341. N. 10:709-717.
17.    Prappa E. Eplerenone survival benefits in heart failure patients post-myocardial infarction. Hospital Chronicles. 2012;7. Suppl. 1:63-64.
18.    Rassi AN, Cavender MA, Fonarow GC et al. Temporal trends and predictors in the use of aldosterone antagonists post-acute myocardial infarction. J Am Coll Cardiol. 2013;61:35-40.
19.    Steg G, James S, Atar D et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. The Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology (ESC). Eur Heart J. 2012;33:2569-2619.
20.    Steg PG, Dabbous OH, Feldman LJ et al. Determinants and prognostic impact of heart failure complicating acute coronary syndromes: observations from the Global Registry of Acute Coronary Events (GRACE). Circulation. 2004;109:494-499.
21.    Tsutamoto T, Wada A, Maeda K et al. Effect of spironolactone on plasma brain natriuretic peptide and left ventricular remodeling in patients with congestive heart failure. J Am Coll Cardiol. 2001;37:1228-1233.
22.    Velazquez EJ, Francis CG, Armstrong PW et al. for the VALIANT registry. An international prospective on heart failure and left ventricular dysfunction complicating myocardial infarction: the VALIANT registry. Eur Heart J. 2004;25:1911-1919.
23.    Verma A, Bulwer B, Dhawan I et al. Aldosterone Receptor Antagonist and Heart Failure Following Acute Myocardial Infarction. Acta Cardiol Sin. 2010;26:203-215.
24.    Weber KT, Brilla CG, Campbell SE et al. Myocardial fibrosis: role of angiotensin II and aldosterone. Basic Res Cardiol. 1993;88:107-124.
25.    Zannad F, McMurray JJ.V., Krum H et al. Eplerenone in patients with systolic heart failure and mild symptoms. N Eng J Med. 2011;364. N. 1:11-21.

The aim — to evaluate the effectiveness and safety of methods for treating vascular anomalies in children in accordance with the approved protocol in a multidisciplinary hospital, taking into account the complications of medical manipulations.
Materials and methods. A prospective study was conducted of the results of treatment of 197 children with vascular anomalies on the basis of one multidisciplinary clinic for the period from January 2011 to December 2016. The patients’ ages ranged from 1 month to 18 years. The treatment strategy was based on the approved protocol and included conservative therapy, sclerotherapy, endovascular embolization, surgical removal, and a combination of these methods. The result of treatment and complications of medical manipulations were evaluated.
Results and discussion. To determine the tactics of treatment, all patients underwent ultrasound examination, as well as computed tomography with contrast enhancement or magnetic resonance imaging. Vascular tumors were diagnosed in 61 (30.9 %) patients, vascular malformations (VM) — in 136 (60.9 %) patients. 58 (95 %) of 61 patients with vascular tumors received only conservative therapy, 3 (5 %) — a combination of conservative treatment with subsequent surgical intervention. 18 (14.2 %) of 127 children with VM with slow blood flow received conservative treatment, 97 (76.4 %) had sclerotherapy, 5 (3.9 %) had surgery and 7 (5.5 %) — a combination of medical manipulations. 2 (22.2 %) of 9 patients with VM with fast blood flow had endovascular embolization, 5 (55.6 %) — embolization and sclerotherapy and 2 (22.2 %) — combined embolization, sclerotherapy and surgical removal. Complications occurred in 2 (1 %) patients: one child had skin allergic reaction after sclerotherapy with OK-432, the other — transient hypoglycemia against conservative treatment with β-blockers.
Conclusions. The introduction of diagnostic and treatment algorithm based on the approved protocol in a multidisciplinary hospital had positive results with an acceptable level of complications in pediatric patients with vascular anomalies.

Keywords: vascular malformations, infantile hemangiomas, treatment protocol, sclerotherapy, children.

List of references:  
1.    Adams MT, Saltzman B, Perkins JA. Head and Neck Lymphatic Malformation Treatment. A Systematic Review. Otolaryngol Head Neck Surg. 2012;147:627-639.
2.    Burrows PE. Percutaneous Treatment of Slow-Flow Vascular Malformations. Mulliken & Young’s Vascular anomalies hemangiomas and malformations / Ed by J B Mulliken, P E Burrows, S J Fishman. New York, United States of America: Oxford University Press, 2013:661-709.
3.    Del Pozo J, Gómez-Tellado M, López-Gutiérrezc JC. Vascular malformations in childhood. Actas Dermosifiliogr. 2012;103(8) — P. 661-678.
4.    Elluru RG, Friess MR, Richter GT et al. Multicenter evaluation of the effectiveness of systemic propranolol in the treatment of airway hemangiomas. Otolaryngol Head Neck Surg. 2015;153(3) — P. 452-460.
5.    Elluru RG, Balakrishnan K, Padua HM. Lymphatic malformations: Diagnosis and management. Sem Pediatr Surg. 2014;23 — P. 178-185.
6.    Fishman SJ. Slow-flow vascular malformations. Mulliken & Young’s Vascular anomalies hemangiomas and malformations / Eds J B Mulliken, P E Burrows, S J Fishman. New York, United States of America: Oxford University Press, 2013:562-594.
7.    Greene AK, Liu AS, Mulliken JB et al. Vascular anomalies in 5621 patients: guidelines for referral. J Pediatr Surg. 2011;46:1784-1789.
8.    Kulungowski AM, Alomarib AI, Chawlaa A et al. Lessons from a liver hemangioma registry: subtype classification. J Pediatr Surg. 2012;47:165-170.
9.    Lee BB, Baumgartner I, Berlien HP et al. Consensus Document of the International Union of Angiology (IUA)-2013. Current concepts on the management of arterio-venous malformations. Intern Angiol. 2013;32(1):9-36.
10.    Lee BB, Baumgartner I, Berlien P et al. Guideline. Diagnosis and treatment of venous malformations. Consensus Document of the International Union of Phlebology (IUP): Updated-2013. Int Angiol. 2015;34(2):97-149.
11.    McRae MY, Adams S, Pereira J et al. Venous malformations: clinical course and management of vascular birthmark clinic cases. Australas J Dermatol. 2013;54:22-30.
12.    Mulliken JB, Glowacki J. Hemangiomasand vascular malformations in infants and children: a classification based on endothelial characteristics. Plast Reconstr Surg. 1982;69:412-422.
13.    Ogita S, Tsuto T, Tokiwa K, Takahashi T. Intracystic injection of OK-432: a new sclerosing therapy for cystic hygroma in children. Br J Surg. 1987;74(8):690-691.
14.    Upton J, Taghinia A. Special considerations in vascular anomalies: operative management of upper extremity lesions. Clin Plast Surg. 2011;38(1):143-151.
15.    Wassef M, Blei F, Adams D et al. Vascular Anomalies Classification: Recommendations From the International Society for the Study of Vascular Anomalies. Pediatrics. 2015;136(1). P. 203-215.
16.    Yamaki T, Nozaki M, Sakurai H et al. Prospective randomized efficacy of ultrasound-guided foam sclerotherapy compared with ultrasound-guided liquid sclerotherapy in the treatment of symptomatic venous malformations. J Vasc Surg. 2008;47:578-584.

The aim — to estimate the health-related quality of life (QL) and physical work capacity in adults after pulmonary autograft operation (PAO).
Materials and methods. From 01 Jan. to 31 Dec 2016 we examined 46 adults over the age of 18. Group I included 22 patients after PAO (subgroup 1A — 8 patients with heart failure (CF) of I functional class (FC) by NYHA, and subgroup 1B — 14 patients with CF of II — III FC by NYHA). Group II consisted of 24 practically healthy adults.
Results and discussion. Health-related quality of life (HRQoL) analysis showed quite good performance indexes on basic research criteria. The six-minute walk test was performed worse in group I (group I — 429.6 ± 22.2 m, group II — 593.3 ± 7.6 m; p <0.01). Exercise tolerance in patients of subgroup 1B was significantly reduced compared with subgroup 1A and group II. Thus, the physical development index (PWC170) in absolute value and in terms of body weight (PWC170/kg) in subgroup 1B was lower in comparison with subgroup 1A (p <0.05) and group II (p < 0.05 and p <0.01, respectively). Maximum oxygen consumption (MOC) in subgroup 1B was statistically significantly lower compared to group II. Evaluation of right ventricular function (RV) showed statistically significantly lower movement of the tricuspid valve ring (TAPSE) in subgroup 1B compared to subgroup 1A and group II (p <0.05), indicating a decrease in systolic function of the RV. In subgroup 1B, the SF-36 questionnaire, reflecting physical functioning (PF) 78.6 ± 5.0, pain intensity 66.0 ± 6.9, general health 59.8 ± 5.7, and social function (SF) 70.5 ± 6.5, were statistically significantly worse than those of group II (p <0.05). Patients of subgroup 1A registered significantly better QoL and deterioration in only one indicator — PF 83.1 ± 4.0 compared with group II (p <0.05). Differences between subgroups 1A and 1B were noted only in SF (90.6 ± 3.9 and 70.5 ± 6.5, respectively, p <0.05).
Conclusions. In adult patients with congenital aortic valve malformations in 5.8 years after PAO, CF of II and III FC by NYHA was associated with worsening of PWC170 and MOC, decrease of RV contractility according to TAPSE index and was combined with significantly higher gradient through pulmonary artery conduit compared with NYHA I. Decrease of QoL in patients with NYHA II — III was characterized by significantly worse indexes of physical component of health and good mental health component indexes compared to patients with NYHA I.

Keywords: quality of life, physical work capacity, congenital heart disease, reconstructive surgery, adults.

List of references:  
1.    Aronov DM, Lupanov VP. Geotar-Media (Russian). 2015:95-103.
2.    Voronkov LG, Amosova KM, Bagriy AE, Dziak GV, Dyadik OI, Zharinov OY, Knishov GV, Kovalenko VM, Korkushko OV. Guidelines of the Ukrainian Association of Cardiology of the diagnosis, treatment and prevention of chronic heart failure in adults (shortversion). Shidnoevr. z. vnutr. simejnoimed (Ukrainian). 2015;1:65-71.
3.    Zharinov OY, Kuts VO, Tkhor NV. Medytsynasvitu (Ukrainian), 2006:90.
4.    KaraskovA. M., SharifulinR. M., Bogachev-ProkofevA. V., Demin II, Zheleznev SI, Open AB. Patologiya krovoobrashcheniya i kardiokhirurgiya – Circulation Pathology and Cardiac Surgery (Russian). 2015;19(3):50-57.
5.    Lebid IH, Razinkina AO, Klymyshyn YI, Pozniak Yu.V., Stohova OV, Khanenova VA, Rudenko NM. Patent na korysnu model #112844UA (Ukrainian).
6.    Luk’yanovA. A. Otdalennye rezul’taty autotransplantatsii klapana legochnoi arterii (protsedury Rossa) u patsientov pediatricheskoi gruppy s vrozhdennym porokom aortal’nogo klapana: dis.... kand. med. nauk: 14.01.26 / Luk’yanov Anton Aleksandrovich. Novosibirsk (Russian). 2016:173.
7.    Rybakova MK, Mitkov VV, Baldin DG. Vidar (Russian), 2016:600.
8.    Sergienko LP. Slobozhanskyi naukovo-sportyvnyi visnyk — Slobozhanskyi herald of science and sport (Russian). 2015;1(45):109-122.
9.    Chernov II, Kozmin D.Yu., Makeev SA, Demetskaya VV, Tarasov DG. Patologiya krovoobrashcheniya i kardiokhirurgiya — Circulation Pathology and Cardiac Surgery (Russian). 2016;20(1):12-18.
10.    Lebid IH, Rudenko NM, Sydorenko A.Yu. Yakist zhyttia u patsiientiv iz vrodzhenymy vadamy sertsia. Praktychnyi posibnyk. Kyiv (Ukrainian), 2016:49.
11.    Baumgartner H. Bonhoeffer P, De Groot NM et al. ESC Guidelines for the management of grown-up congenital heart disease (new version 2010). Eur Heart J. 2010;P.ehq249.
12.    Becker O. Gesundheitsbezogene Lebensqualität und funktionelles Outcome bei Patienten nach Ross-Operation im Vergleich zur Normbevölkerung (Health-related quality of life and functional outcome in patients after Ross surgery compared to the norm population). 2016;118 р.
13.    David TE, David C, Woo A et al. The Ross procedure: outcomes at 20 years. J Thorac Cardiovasc Surg. 2014;147(1):85-93.
14.    Etnel JR, Elmont LC, Ertekin E et al. Outcome after aortic valve replacement in children: A systematic review and meta-analysis. J Thorac Cardiovasc Surg. 2016;151(1):143-152.
15.    Inner-cyte medical art studios. Trial Exhibits [Електронний ресурс]. URL: http://www.innercyte.com/trialexhibits.html.
16.    Kalfa D, Mohammadi S, Kalavrouziotis D et al. Long-term outcomes of the Ross procedure in adults with severe aortic stenosis: single-centre experience with 20 years of follow-up. Eur J Cardio-Thorac Surg. 2015;47(1):159-167.
17.    Mastrobuoni S, de Kerchove L, Solari S et al. The Ross procedure in young adults: over 20 years of experience in our Institution. Eur J Cardio-Thorac Surg. 2016;49, N2:507-513.
18.    Pauliks LB, Clark JB, Rogerson A et al. Exercise stress echocardiography after childhood Ross surgery: functional outcome in 26 patients from a single institution. Pediatr Cardiol. 2012;33(5):797-801.
19.    Ringle A, Richardson M, Juthier F et al. Ross procedure is a safe treatment option for aortic valve endocarditis: Long-term follow-up of 42 patients. Int J Cardiol. 2016;203:62-68.

The aim — to determine the main changes in the arterial bed depending on the state of the gallbladder (GB) in patients with coronary heart disease (CHD) who underwent coronary artery bypass grafting.
Materials and methods. We analyzed data of 98 patients (40 % — with acute myocardial infarction, 60 % — with unstable angina).
Results and discussion. Patients with intact GB were characterized by minimal frequency of stenosis of anterior interventricular branch (AIVB) of left coronary artery (LCA), minimal frequency and grade of affection of right coronary artery (RCA), minimal grade of stenosis of left circumflex artery (LCA). Patients with sludge differed by higher grades of stenosis of AIVB and RCA, most frequent affection of both coronary arteries (CA) and absence of right type of blood supply. Bent of GB body was accompanied by minimal frequency of stenosis of LCA and the least frequent affection of two CA. Patients with GB neck deformations had maximal frequency and grade of RCA affection. Patients with cholelithiasis most frequently had lesion of AIVB of LCA (100 %) and the highest frequency of left type of blood supply. Patients with cholelithiasis were characterized by the most frequent trivascular lesion of CA, maximal frequency of stenosis of all CA, the highest grade of LCA stenosis (92.5 %).
Conclusions. Increase of grade of GB affection is accompanied by augmentation of frequency and grade of coronary arteries affection and also incidence of multivessel stenoses which correlate with coagulation and lipid metabolism parameters.

Keywords: anterior interventricular branch of left coronary artery, right and left coronary arteries, circumflex left coronary artery, gallbladder.

List of references:  
1.    Stebelskyj SY, Kulchytskyj KI, Kozlov VO ta in. Shlyakhy krovopostachannya sercya.Dnipropetrovsk (Ukrainian), 1993:8-10.
2.    Brooks N, Cattell M, Jennings K et al. Isolated disease of left anterior descending coronary artery. Angiocardiographic and clinical study of 218 patients. Br Heart J. 1982;47:71-77.
3.    Jiang Z.-Y., Sheng X, Xu C.-Y. et al. Gallbladder Gallstone Disease Is Associated with Newly Diagnosed Coronary Artery Atherosclerotic Disease: A Cross-Sectional Study. PLoS One. 2013;8 (9). e75400. Doi: 10.1371/journal.pone.0075400.
4.    Kim K.-W., Kim HY, Chun J.-K. et al. Relationship between gallbladder distension and lipid profiles in Kawasaki disease. Korean Circ J. 2010;40:137-140.
5.    Lv J, Qi L, Yu C et al. Gallstone disease and the risk of ischemic heart disease. Arterioscler Thromb Vasc Biol. 2015;Oct; 35 (10):2232-2237. Doi: 10.1161/ATVBAHA.115.306043.
6.    Targher G, Byrne CD. Gallstone disease and increased risk of ischemic heart disease: сausal association or epiphenomenon?. Arterioscler Thromb Vasc Biol. 2015;35:2073-2075. Doi: 10.1161/ATVBAHA.115.306339.

The aim — to conduct a comparative evaluation of central hemodynamics and aortic stiffness parameters in patients with hypertension depending on the presence or absence of metabolic syndrome (MS).
Materials and methods. The study included 100 patients with uncomplicated essential hypertension of I — II stage, 1 — 3 degrees, aged 35 — 70 years, with blood pressure (BP) ≥ 160/100 mmHg in patients who had not previously been treated or BP ≥ 140/90 mmHg in those who had had antihypertensive treatment, and heart rate of 60 — 100 beats/min. MS was diagnosed in 40 % of them. The diagnosis of MS was based on the guidelines of the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III). All patients underwent general clinical and laboratory examinations, 24hours ambulatory BP monitoring and echocardiography. Brachial BP was measured followed by determination of arterial stiffness and parameters of central hemodynamics with the use of SphygmoCor system (AtCor Medical, Australia).
Results and discussion. Patients in groups with and without MS were comparable in blood pressure according to the results of 24hours ambulatory BP monitoring and in parameters of echocardiography and central and brachial systolic (SBP), diastolic (DBP), pulse pressure (PP) and mean BP (p > 0.05). However difference between the brachial and central SBP (ΔSBP = 15.2 ± 5.7 vs 12.2 ± 5.7 mm Hg), difference between the brachial and central PP (ΔPP = 16.6 ± 6.0 vs 13.5 ± 5.7 mm Hg) and PP amplification (РРA = (141.0 ± 16.6) to (132.1 ± 17.5 %, respectively) were higher, and augmentation index (AIx) and augmentation pressure (AP) ((19.0 ± 12.8) and (25.5 ± 13.8) % vs (8.2 ± 6.3) and (12.1 ± 8.0) mm Hg, respectively) were lower in patients with MS (all p < 0.05). AIx75 ((19.1 ± 8.5) vs (24.3 ± 10.9) mm Hg; p > 0.05) did not significantly differ between the groups. Carotid-radial pulse wave velocity (PWV) was not significantly different in the two groups, but patients with MS in contrast to patients without MS had higher carotid-femoral PWV ((9.0 ± 1.5) vs (7.9 ± 1.6) m/s; p < 0.05). A comparative analysis of parameters of central hemodynamics in patients with hypertension with or without MS depending on gender found that women had lower ΔSBP, ΔPP, PPA and higher AIx, AIx75, AP. Moreover, in women with MS, the carotid-femoral PWV was statistically significantly different from that in patients without MS.
Conclusions. In patients with hypertension and metabolic syndrome in contrast to hypertensive patients without MS matched by age, the difference between brachial and central SBP and PP, as also carotid-femoral PWV were higher, while augmentation index and augmentation pressure were lower, central and brachial SBP, DBP, mean BP and PP were comparable. Among age-matched hypertensive patients with or without MS, female gender is associated with a smaller difference between brachial and central SBP and PP, PPA, higher AIx, AIx75, AP. In women with MS, the carotid-femoral PWV statistically significantly differs from that in women without MS.

Keywords: arterial stiffness, metabolic syndrome, arterial hypertension, gender features.

List of references:  
1.    Alberti KG, Eckel RH, Grundy SM et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120:1640-1645.
2.    Ben-Shlomo Y, Spears M, Boustred C et al. Aortic pulse wave velocity improves cardiovascular event prediction: an individual participant meta-analysis of prospective observational data from 17,635 subjects. J Am Coll Cardiol. 2014;63:636-646.
3.    Blacher J, Guerin AP, Pannier B et al. Impact of aortic stiffness on survival in end-stage renal disease. Circulation. 1999;99:2434-2439.
4.    Chirinos JA, Zambrano JP, Chakko S et al. Aortic pressure augmentation predicts adverse cardiovascular events in patients with established coronary artery disease. Hypertension. 2005;45:980-985.
5.    Dimitriadis K, Tsioufis C, Andrikou E et al. Metabolic syndrome is associated with increased sympathetic nervous system activity and arterial stiffness in resistant hypertensive patients. Hypertension. 2016;34. P. e86.
6.    Gami AS, Witt BJ, Howard DE et al. Metabolic syndrome and risk of incident cardiovascular events and death: a systematic review and meta-analysis of longitudinal studies. J Am CollCardiol. 2007;49:403-414.
7.    Grundy SM, Cleeman JI, Daniels SR et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation. 2005;112:2735-2752.
8.    Grundy SM. Metabolic syndrome pandemic. Arterioscler Thromb Vasc Biol. 2008;28:629-636.
9.    Kangas P, Tikkakoski A, Tahvanainen A et al. Metabolic syndrome may be associated with increased arterial stiffness even in the absence of hypertension: a study in 84 cases and 82 controls. Metabolism. 2013;62(8):1114-1122.
10.    KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl. 2013;3(1):1-150.
11.    Kovaite M, Petrulioniene Z, Ryliskyte L. Systemic assessment of arterial wall structure and function in metabolic syndrome. Proc WestPharmacol Soc. 2007;50:123-130.
12.    Lang RM, Bierig M, Devereux RB et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2005;18:1440-1463.
13.    Lee Ho-Joong Youn et al. Effects of metabolic syndrome on aortic pulse wave velocity. Clin Hypertens. 2017;23(1):1-7.
24.    Mahmud A, Feely J. Effect of smoking on arterial stiffness and pulsepressure amplification. Hypertension. 2003;41:183-187.
15.    Mancia G, Fagard R, Narkiewicz K et al. 2013 ESH/ESC guidelines for the management of arterial hypertension. Hypertension. 2013;Vol. 31:1281-1357.
16.    Orshal JM, Khalil RA. Gender, sex hormones, and vascular tone. Am J Physiol Regul Integr Comp Physiol. 2004;286:233-249.
17.    Paratia G, Stergiouc G, O’Briend Е et al. European Society of Hypertension practice guidelines for ambulatory blood pressure monitoring. J Hypertens. 2014;32:1359-1366.
18.    Protogerou AD, Blacher J, Mavrikakis M et al. Increased pulse pressure amplification in treated hypertensive subjects with metabolic syndrome. Am J Hypertens. 2007;20(2):127-133.
19.    Protogerou AD, Blacher J, Aslangul E et al. Gender influence on metabolic syndrome’s effects on arterial stiffness and pressure wave reflections in treated hypertensive subjects. Atherosclerosis. 2007;193:151-158.
20.    Radhakrishnan J, Swaminathan N, Pereira NM et al. Acute changes in arterial stiffness following exercise in people with metabolic syndrome. Diab Met Syndr: Clin Res Rev. 2016;DOI: 10.1016/j.dsx.2016.08.013.
21.    Rundek T, White H, Boden-Albala B et al. The metabolic syndrome and subclinical carotid atherosclerosis: the Northern Manhattan study. J Cardiometab Syndr. 2007;2:24-29.
22.    Safar ME, Balkau B, Lange C et al. Hypertension and vascular dynamics in men and women with metabolic syndrome. J Am Coll Cardiol. 2013;61:12-19.
23.    Scuteri A, Cunha PG, Rosei EA et al. MARE Consortium. Arterial stiffness and influences of the metabolic syndrome: a cross-countries study. Atherosclerosis. 2014;233:654-60.
24.    Scuteri A, Najjar SS, Morrell CH et al. Cardiovascular Health Study. The metabolic syndrome in older individuals: prevalence and prediction of cardiovascular events: the Cardiovascular Health Study. Diabetes Care. 2005;28:882-887.
25.    Smulyan H, Asmar RG, Rudnicki A et al. Comparative effects of aging in men and women on the properties of the arterial tree. J Am Coll Cardiol. 2001;37:1374-1380.
26.    Steinberg HO, Brechtel G, Johnson A et al. Іnsulinmediated skeletal muscle vasodilatation is nitric oxide dependent: a novel action of insulin to increase nitric oxide release. J Clin Invest. 1994;94:1172-1179.
27.    Vágovičová P, Mlíková Seidlerová J, Mayer O. Jr. et al. Differential effect of metabolic syndrome on various parameters of arterial stiffness. Blood Press. 2015;24(4):206-211.
28.    Vergnaud AC, Athanase D. Protogerou, Yan Li et al. Pulse pressure amplification, adiposity and metabolic syndrome in subjects under chronic antihypertensive therapy: The role of heart rate. Atherosclerosis. 2008;199(1):222-229.
29.    Vyssoulis GP, Pietri PG, Karpanou EA et al. Differential impact of metabolic syndrome on arterial stiffness and wave reflections: Focus on distinct definitions. Int J Cardiol. 2010;138:119-125.
30.    Westerbacka J, Seppala-Lindroos A, Yki-Jarvinen H. Resistance to acute insulin induced decreases in large artery stiffness accompanies the insulin resistance syndrome. J Clin Endocrinol Metab. 2001;86:5262-5268.
31.    Westerbacka J, Wilkinson I, Cockcroft J et al. Diminished wave reflection in the aorta. A novel physiological action of insulin on large blood vessels. Hypertension. 1999;33:1118-1122.

The aim —  to study the age-related changes of ECG findings in rats.
Materials and methods. ECG was registered in male Wistar rats, 8 and 24 months of age, under anesthesia; the amplitude and direction of the waves, the duration of the waves and intervals, and the stroke volume index were calculated.
Results and discussion. A number of differences between the ECG of rats and humans were revealed, namely: presence of a notch on the downward knee of the R wave on the ECG for both adult and old rats in 100 % of cases, absence of pronounced ST segments, a direct transition of the T wave into the R wave or its duration is 0.0 — 0.05 sec. A common feature of the human and rat ECG is the direction of the waves and the amplitude of most of them. The following age-specific features of the ECG of rats were revealed: in adult rats, the duration of the QT interval is 0.08 ± 0.00 sec, in aging rats, it is 0.10 ± 0.01 sec. In adult rats, the heart rate is 368.22 ± 6.39 beats per minute, and in old rats, it is 354.25 ± 17.56 beats per minute. The amplitude of the QRS complex is 21.86 ± 0.75 mm in adult rats and 14.88 ± 1.33 mm in aging rats, the amplitude of the T wave is 2.75 ± 0.07 and 2.02 ± 0.06 mm, and the systolic index is 0.49 ± 0.01 and 0.55 ± 0.02 sec, respectively (all р < 0.05) for adult and aging rats.
Conclusions. The ECG of old rats differs from the ECG of adults by a smaller heart rate, longer duration of RR, QT intervals, smaller total QRS tooth amplitude and a larger systolic index, as also by the presence of cardiac rhythm disturbances at the beginning of ECG recording

Keywords: ECG waves and intervals, stroke volume index, aging rats.

List of references:  
1.    Davis M. Canine and feline geriatry. Practice of veterinarium. — Moscow: Akvarium-Print, 2002:256. (Russian)
2.    Zapadnyuk IP, Zapadnyuk VI, Zakhariya Ye.A. et al. Laboratory animals. Breeding, keeping, use in the experiment. Kyiv: Vyshcha shkola, 1983:383. (Russian)
3.    Korolenko ТК. Features of heavy metals cardiotoxic action of lead, mercury and manganese, taking into account age reactions. Actual problems of transport medicine. 2010;4:131—138. (Ukrainian)
4.    Kraynova IN, Demin AV, Moroz TP. Bioelectric activity of the heart in women with severe postural instability. Arctic environment Res Series: natural science. 2013;4:64-69. (Russian)
5.    Kulik VL, Yabluchansky NI. QT interval in cardio clinic. J of V N Karazin KhNU. 2009;879, series «Medicine». 18:73-96. (Ukrainian)
6.    Mahanova NA, Antonov AR, Markel AL et al. Ontogenetic dynamics of blood pressure and characteristics of ECG in hereditary hypertrnsive NISAG rats. Bull Experimental biology and medicine. 1997;123:709-713. (Russian)
7.    Mikhailov VM, Mamaeva GI. NADP+ influence for electrophysiological properties of cardiomyocytes of C57BL/6 and MDX mice. Cell and tissue biology. 2013;Т.55:815—820. (Russian)
8.    Prokopjuk OS, Chizhevsky VV, Prokopjuk VY. Effects of cryopreserved chorionic tissue implantation on the morphofunctional state of myocardium of old rats. Medicine today and tomorrow. 2011;1—2:242-245. (Ukrainian)
9.    Prokopieva SN, Movchan LA, Iskhakova GG et al. Features of elektrocardiografical diagnosis among persons of older age groups. Practical medicine. 2008;Т. 28:21—29. (Russian)
10.    Frol’kis V. V. Aging and life expectancy. Leningrad: Nauka, 1988:239. (Russian)
11.    Abhishekh HA, Nisarga P, Kisan R et al. Influence of age and gender on autonomic regulation of heart. Int J Clin Monit Comp. 2013;27:259-264. DOI: 10.1007/s10877-012-9424-3.
12.    Ai J, Gozal D, Li L et al. Degeneration of vagal efferent axons and terminals in cardiac ganglia of aged rats. J Comp Neurol. 2007;504:74-88. DOI: 10.1002/cne.21431.
13.    Agudelo CF, Scheer P, Tomenendalova J. How to approach the QT interval in dogs — state of the heart: a review. Veterin Med. 2011;56:14-21.
14.    Annila P, Jäntti V, Lindgren L et al. Changes in the T-wave amplitude of ECG during isoflurane anaesthesia. Acta Anaesthesiol Scand. 1993;37. P. 611—615.
15.    Bacharova L, Kyselovic J, Klimas J. QRS voltage-duration product and left ventricular hypertrophy in rats. Arq Bras Cardiol. 2002;79:143 —148. http://dx.doi.org/10.15 90/S0066-782X2002001100006
16.    Bachman S, Sparrow D, Smith LK. Effect of aging on the electrocardiogram. Am J Cardiol. 1981;48:513-516.
17.    Battler А, Froelicher V, Slutsky R et al. Relationship of QRS amplitude changes during exercise to left ventricular function and volumes and the diagnosis of coronary artery disease. Circulation. 1979;60:1004-1013
18.    Baumert M, Czippelova В, Porta А et al. Decoupling of QT interval variability from heart rate variability with ageing. Physiol Meas. 2013;34:1435-1448. DOI: 10.1088/0967-3334/34/11/1435.
19.    Berg BN. The electrocardiogram in aging rats. J Gerontol. 1955;10:420-423.
20.    Bonilha AM.M., Saraiva RM, Kanashiro RM et al. A routine electrocardiogram cannot be used to determine the size of myocardial infarction in the rat. Braz J Med Biol Res. 2005;38:615-619. DOI: /S0100-879X2005000400016.
21.    Boyle PM, Massé S, Nanthakumar К et al. Transmural IK (ATP) heterogeneity as a determinant of activation rate gradient during early ventricular fibrillation: mechanistic insights from rabbit ventricular models. Heart Rhythm. 2013;10:1710-1717. DOI: 0.1016/j.hrthm.2013.08.010.
22.    Brisinda D, Caristo МЕ, Fenici R. Contactless magnetocardiographic mapping in anesthetized Wistar rats: evidence of age-related changes of cardiac electrical activity. Am J Physiol Heart Circ Phys. 2006;291:368-378. DOI: 10.1016/j.hrthm.2013.08.010.
23.    Chen YC, Huang JH, Lin YK et al. Gender modulates the aging effects on different patterns of early repolarization. Heart Vess. 2014;29:249-255. DOI: 10.1007/s00380-013-0352-z.
24.    Dias da Silva VJ, Ferreira Neto E, Salgado HC et al. Chronic converting enzyme inhibition normalizes QT interval in aging rats. Braz J Med Biol Res. 2002;35:1025-1031.
25.    Edwards IJ. Highlights in basic autonomic neurosciences: changes to the autonomic nervous system associated with healthy aging. Autonom Neurosci. 2014;183:1—3. DOI: 10.1016/j.autneu.2014.04.004.
26.    Fasdellia N, Tontodonati М, Dorigatti R. An improved method of electrode placement in configuration Lead II for the reliable ECG recording by telemetry in the conscious rat. J Pharm Tox Meth. 2011;63:1-6. DOI: 0.1016/j.vascn.2010.03.001.
27.    Gandhi DK, Singh J. Ageing аnd аutonomic nervous system аctivity. J Phys Pharm Adv. 2012;2:307-311.
28.    Gordon CJ. Cardiac and thermal homeostasis in the aging brown Norway rat. J Gerontol A Biol Sci Med Sci. 2008;63:1307-1313. DOI: https:. doi.org/10.1093/gerona/63.12.1307.
29.    Hamlin RL, Kijtawornrat А, Keene BW et al. QT and RR intervals in сonscious and аnesthetized guinea рigs withhighly varying RR intervals and given QT clengthening test аrticles. Toxicol Sci. 2003;76:437-442. DOI: 10.1093/toxsci/kfg254.
30.    Huang JH, Lin Y.Q, Pan NH et al. Aging modulates dispersion of ventricular repolarization in the very old of the geriatric population. Heart Vessels. 2010;25:500-508. DOI: 10.1007/s00380-010-0026-z.
31.    Kharin SN, Krandycheva VV, Shmakov DN. Depolarization pattern of ventricular epicardium in two-kidney one-clip hypertensive rats. Exp Phys. 2005;90:621— 626. DOI: 10.1113/expphysiol.2004.029785.
32.    Klimas J, Vaja V, Vercinska M et al. Discrepant regulation of QT (QTc) interval duration by calcium channel blockade and angiotensin converting enzyme inhibition in experimental hypertension. Bas Clin Pharmacol Toxicol. 2012;111:279-288. DOI: 10.1111/j.1742-7843.2012.00901.x
33.    Kumar R, Kela A, Tayal G et al. Effect оf аcute stress оn rat ECG. The Internet J Pharmacol. 2010;8.
34.    Larson ED, St Clair JR, Sumner WA et al. Depressed pacemaker activity of sinoatrial node myocytes contributes to the age-dependent decline in maximum heart rate. Proc Natl Acad Sci. 2013;110:18011-18016. DOI: 10.1073/ pnas.1308477110.
35.    Li RA, Leppo M, Miki T et al. Molecular basis of electrocardiographic ST-segment elevation. Circ Res. 2000;87:837-839.
36.    Machida K, Doi K, Kaburaki M et al. Electrocardiographical findings of WBN/Kob rats. Laboratory Animals. 1990;24:288-291.
37.    Magnanі JW, Williamson МА, Ellinor РТ et al. P wave indices. Current status and future directions in epidemiology, clinical, and research applications. Circulation: аrrhythmia and еlectrophysiol. 2009;2:72-79. DOI: https://doi.org/10.1161/CIRCEP.108.806828.
38.    Mangoni AA, Kinirons MT, Swift CG et al. Impact of age on QT interval and QTdispersion in healthy subjects: a regression analysis. Age and Аgeing. 2003;32:326-331. DOI: 0.1093/ageing/32.3.326.
39.    Medenwald D, Kors JA, Loppnow H et al. Inflammation and рrolonged QT time: results from the сardiovascular disease, living and ageing in Halle (CARLA) study. PLoS ONE. 2014;9(4). P. e95994. DOI: http://dx.doi.org/ 10.1371/journal.pone.0095994.
40.    Midttun M, Güzel A. Heart rhythm in 90+ years old fallers. European Geriatric Medicine. 2013;4:5-7. DOI: http://doi.org/ 10.1016/j.eurger.2012.08.006.
41.    Milani-Nejad N, Janssen PM.L. Small and large animal models in cardiac contraction research: аdvantages and disadvantages. Pharmacol Therapeut. 2014;141:235-249. DOI: 10.1016/j.pharmthera.2013.10.007.
42.    Mozos I, Serban С. The relation between QT interval and T-wave variables in hypertensive patients. J Pharm Bioallied Sci. 2011;3:339-344. DOI: 10.4103/0975-7406.84433.
43.    Morita Н, Wu J, Zipes DP. The QT syndromes: long and short. Lancet. 2008;372:750—763. DOI: http://dx.doi.org/10.1016/S0140-6736 (08)61307-0.
44.    North BJ, Sinclair DA. The Intersection between аging and сardiovascular disease. Circ Res. 2012;110 — P. 1097-1108. DOI: 10.1161/ CIRCRESAHA.111.246876.
45.    Perrenoud J. -J. Q waves and QS complexes. Eur Geriatr Med. 2010;1:360-368. DOI: 10.1016/j.eurger.2010.09.006.
46.    Pokrovskii VM, Polischuk LV. On the conscious control of the human heart. J Integrat Neurosci. 2012;11:213-223. DOI:10.1142/S0219635212500161.
47.    Rossi S, Baruffi S, Bertuzzi A et al. Ventricular activation is impaired in aged rat hearts. Am J Physiol Heart Circ Physiol. 2008;295:2336-2347. DOI: 10.1152/ajpheart.00517.2008.
48.    Saburkina І, Gukauskiene L, Rysevaite К et al. Morphological pattern of intrinsic nerve plexus distributed on the rabbit heart and interatrial septum. J Anat. 2014;224:583-593. DOI: 10.1111/joa.12166.
49.    Sambhi MP, White FN. The Electrocardiogram of the normal and hypertensive rat. Circ Research. 1960;8:129-134.
50.    Scridon А, Gallet С, Arisha ММ et al. Unprovoked atrial tachyarrhythmias in aging spontaneously hypertensive rats: the role of the autonomic nervous. Am J Physiol Heart Circ Physiol. 2012;303:386—392. DOI: 10.1152 /ajpheart. 00004.2012.
51.    Silva L, Castania J, Salgado H et al. Vagus nerve morphology in elderly spontaneously hypertensive rats. The FASEB J —2014;28. Suppl.728.23/ www.fasebj.org/content/28/1_Supplement/728.23.short.
52.    Shankar V, Veeraiah S. Age related сhanges in the рarasympathetic сontrol of the heart. International J Sci Res Publ. 2012;2:1-6.
53.    Slove S, Lannoy M, Behmoaras J et al. Potassium channel openers increase aortic elastic fiber formation and reverse the genetically determined elastin deficit in the BN rat. Hypertension. 2013;62:794-801. DOI: 10.1161/ HYPERTENSIONAHA.113.01379.
54.    Strait JB, Lakatta EG. Aging-associated cardiovascular changes and their relationship to heart failure. Heart Fail Clin. 2012;8:143-164. DOI:10.1016/j.hfc.2011.08.011
55.    Su НМ, Chiu HC, Lin TH et al. Longitudinal study of the ageing trends in QT interval and dispersion in healthy elderly subjects. Age and Ageing. 2006;35 — Р. 636—638. DOI: 10.1093/ageing/afl114.
56.    Tanabe S, Bunag RD. Age-related central and baroreceptor impairment in female Sprague-Dawley rats. Am J Physiol. 1989;256:1399-1406.
57.    Tellez JO, Mączewski M, Yanni J et al. Ageing-dependent remodelling of ion channel and Ca2+ clock genes underlying sino-atrial node pacemaking. Exp Physiol. 2011;96 — Р.1163-1178. DOI: 10.1113/expphysiol.2011.057752.
58.    Terho HK, Tikkanen JT, Junttila JM. Prevalence and рrognostic significance of fragmented QRS сomplex in middle-аged subjects with and without сlinical or еlectrocardiographic еvidence of сardiac disease. J Cardiol. 2014;114 — Р.141—147. DOI: 10.1016/j.amjcard.2014.03.066.
59.    Tontodonati М, Fasdelli N, Repeto P et al. Characterisation of rodent dobutamine echocardiography for preclinical safety pharmacology assessment. J Pharmacol Toxicol Methods. 2011;64:129-133. DOI: http://doi.org/10.1016/ j.vascn.2011.04.005.
60.    Werner А, Irigoyen МС, Moreira ED et al. Aging and baroreflex control of RSNA and heart rate in rats. American J Рhys. 2000;279:1865—1871.
61.    Werner А, Rosa NR, Oliveira AR et al. Changes in blood pressure control in aged rats. Brazilian J Medical Bio Res. 1995;28:603-607.
62.    Vajda S, Baczkó I, Leprán I et al. Selective cardiac plasma-membrane KATP channel inhibition is defibrillatory and improves survival during acute myocardial ischemia and reperfusion. Eur J Pharmacol. 2007;577:115-123. DOI: 10.1016/j.ejphar.2007.08.016.
63.    Xing S, Tsaih S-W., Yuan R et al. Genetic influence on electrocardiogram time intervals and heart rate in aging mice. Am J Physiol Heart Circ Physiol —2009;296 — Р. H1907 — H1913. DOI: 10.1152/ajpheart.00681.2008.
64.    Yanni J, Tellez JO, Sutyagin PV et al. Structural remodelling of the sinoatrial node in obese old rats. J Mol Cell Cardiol. 2010;48:653-662. DOI: 10.1016/j.yjmcc.2009.08.023.

Takotsubo syndrome (TS) or Takotsubo cardiomyopathy is an emergency that simulates acute coronary syndrome by clinical symptoms and is often characterized by the development of acute heart failure resulting from reversible violations of contractility of the heart. The causes of TS are not known at present. Among the possible mechanisms of left ventricle contractility disorders are multiple coronary vasospasm, microcirculatory dysfunction and acute catecholaminergic myocardial stunning. Catecholamines appear to have a central role in the pathophysiology of TS, as the trigger is often a sudden, unexpected stress. TS occurs predominantly in post-menopausal women (80 — 90 %). The average age of patients according to various studies is 65 — 68 years. It is believed that TS occurs in approximately in 1 — 2 % of patients with acute coronary syndrome. However, the diagnosis of TS in Ukraine is very rare. This is due to the insufficient knowledge about this disease and to the necessity of using modern methods of cardiovisualization to exclude acute myocardial infarction and to confirm TS in these patients, which, unfortunately, are not always available. The article describes the personal clinical experience in managing patients with Takotsubo syndrome and presents a literature review on this issue.

Keywords: Takotsubo syndrome, Takotsubo cardiomyopathy, clinical case.

One of the most serious complications of diabetes is damage to the vessels and nerves of the lower limbs with the development of the syndrome of the diabetic foot (SDS). Symptoms of ischemia due to neuropathy are often atypical and uncertain, leading to untimely diagnosis. Ulcerative lesions due to neuropathy, infection and damage to the distal arterial peripheral channel often lead to amputation of the lower limb. Significant number of amputations with SDS, complicated by purulent necrotic process, is performed in general surgical departments of hospitals without an attempt of reconstructive vascular surgeries. Therefore, in such patients it is very important to investigate the function of peripheral vessels. The use of revascularization techniques in patients with SDS, complicated by a purulent necrotic process, can save limb or reduce the level of amputation. Performing surgical interventions on the foot or determining the level of amputation is advisable only after a preliminary reconstructive vascular surgery that makes it possible to eliminate ischemia of the lower limbs. Conservative therapy of ischemia in patients with SDS is ineffective and has temporary effect.

Keywords: diabetic foot syndrome, ischemia, amputation, reconstructions.