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Current Issue. Articles

4(60) // 2017

 

 

1. Original researches

 

Features of different phenotypes development worsening kidney function in acute decompencated heart failure depending on the changes in neutrophil gelatinase-associated lipocalin and initial kidney function (UKR)

K. M. Amosova 1, I. I. Gorda 1, A. B. Bezrodnyi 1, G. V. Mostbauer 1, Yu. V. Rudenko 1, A. V. Sablin 2, N. V. Melnychenko 2, Yu. O. Sychenko 1, I. V. Prudkiy 1&a

1 O. O. Bogomolets National Medical University, Kyiv
2 Oleksandrivska Clinical Hospital, Kyiv

The aim — to establish the clinical significance of WRF depending on the presence of an increase in the plasma level of NGAL and CKD in so-called «wet and warm» patients with acute decompensated heart failure (ADHF).
Materials and methods. 141 patients with ADHF at the age of 38 to 85 years old (mean age 66.4 ± 2.2) were involved in the prospective study, they were sequentially hospitalized in the cardiology departments of Oleksandrivska Clinical Hospital in Kyiv during 2012 — 2014. WRF for creatinine took place in 38 (27 %) patients, in 29 of them GFR at admission was less than 60 ml/min/1.73 m2.
Results and discussion. CVP in the group of patients with WRF with increased NGAL was significantly higher in both groups of WRF without increasing NGAL as well as in the group without PFN, both for D1 and D5 (p < 0.05 — 0.01). The E/E′ index when entering patients with elevated NGAL in the group of patients with WRF was significantly higher both for the group of WRF without increasing NGAL and for the group without WRF. But on discharging the reliable difference was preserved only in comparison with the group without WRF (p < 0.05). On the 5th day in the group of patients with GFR < 60 ml/min/1.73 m2, CVP was significantly higher with WRF (by 23 %, p < 0.05). E/E′ and serum NT pro-BNP at D1 differed in patients with and without WRF only in the GFR group less than 60 ml/min/1.73 m2.
Conclusions. WRF in patients with ADHF is associated with a greater severity of symptoms only if NGAL is increased after 48 hours. WRF is associated with more pronounced signs of congestion only if the GFR is reduced.

Keywords: renal function worsening, acute decompensated heart failure, NGAL, decongestion and glomerular filtration rate.

List of references:  
1.    Bellomo R, Ronco C, Kellutn JA et al., the ADQI workgroup. Acute renal failure — definition, outcomes, measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. 2004;8:204-212.
2.    Borg G. Psychophysical bases of perceived exertion. Med Sci Sports Exercise. 1982;14:377-381.
3.    Butler J, Forman DE, Abraham WT et al. Relationship between heart failure treatment and development of worsening renal function among hospitalized patients. Am Heart J. 2004;147:331-338.
4.    Cleland JG.F., Coletta A, Witte K. Practical applications of intravenous diuretic therapy in decompensated heart failure. Am J Med. 2006;119:26–S36.
5.    Cleland JG, Carubelli V, Castiello T et al. Renal dysfunction in acute and chronic heart failure: prevalence, incidence and prognosis. Heart Fail Rev. 2012;17:133-149.
6.    Cowie MR, Komajda M, Murray-Thomas T et al. Prevalence and impact of worsening renal function in patients hospitalized with decompensated heart failure: results of the prospective outcomes study in heart failure (POSH). Eur Heart J. 2006;27:1216-1222.
7.    Damman K.., Valente MA, Voors AA et al. Renal impairment, worsening renal function, and outcome in patients with heart failure: an updated meta-analysis. Eur Heart J. 2014;35 (7):455-469.
8.    Felker GM, O’Connor CM, Braunwald E.; Heart Failure Clinical Research Network I. Loop diuretics in acute decompensated heart failure: Necessary? Evil? A necessary evil?. Circ Heart Fail. 2009;2:56-62.
9.    Fonarow GC, Stough WG, Abraham WT et al. Characteristics, treatments, and outcomes of patients with preserved systolic function hospitalized for heart failure: a report from the OPTIMIZE-HF registry. J Am Coll Cardiol. 2007;50:768-777.
10.    Gottlieb S, Abraham WT, Butler J et al. The prognostic importance of different definitions of worsening renal function in congestive heart failure. J Card Fail. 2002;8 (3):136-141.
11.    Gheorghiade M, Abraham W, Albert N et al. Systolic blood pressure at admission, clinical characteristics, and outcomes in patients hospitalized with acute heart failure. J Am Med Assoc. 2006;296:2217-2226.
12.    Hunt SA, Abraham WT, Chin MH et al. 2009 focused update incorporated into the / 2005 guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2009;53:el-90.
13.    Inohara T, Kohsaka S, Sato N et al. Prognostic impact of renal dysfunction does not differ according to the clinical profiles of patients: Insight from the Acute Decompensated Heart Failure Syndromes (ATTEND) Registry. Plos One. 2014;9:1-9.
14.    Kidney Disease: Improving Global Outcomes (KD1GO). KDIGO clinical practice guidelines for the prevention, diagnosis, evaluation, and treatment of hepatitis C in chronic kidney disease. Kidney lnt Suppl. 2008;109:51-59.


15.    Lanfear DE, Peterson EL, Campbell J et al. Relation of worsened renal function during hospitalization for heart failure to longterm outcomes and rehospitalization. Am J Cardiol. 2011;107:74-78.
16.    Legrand M, De Berardinis B, Gaggin HK. Evidence of uncoupling between renal dysfunction and injury in cardiorenal syndrome: insights from the BIONICS study. PLoS One. 2014;11. 9 (11).
17.    Liang KV, Williams AW, Greene EL, Redfia MM. Acute decompensated heart failure and the cardiorenal syndrome. Crit Care Med. 2008;36:575-588.
18.    Levey AS, Stevens LA et al. A new equation to estimate glomerular filtration rate. Ann Intern Med. 2009;150:604-612
19.    Logeart D, Tabet JY, Hittinger L et al. Transient worsening of renal function during hospitalization for acute heart failure alters outcome. Int J Cardiol. 2008;127:228-232.
20.    Metra M, Davison B, Bettari L et al. Is worsening renal function an ominous prognostic sign in patients with acute heart failure? The role of congestion and its interaction with renal function. Circ Heart Fail. 2012;5:54-62.
21.    Metra M, Nodari S, Parrinello G et al. Worsening renal function in patients hospitalised for acute heart failure: Clinical implications and prognostic significance. Eur J Heart Fail. 2008;10:188-195.
22.    Núñez J, Garcia S, Núñez E et al. Early serum creatinine changes and out-comes in patients admitted for acute heart failure: the cardiorenal syndrome revisited. Eur Heart J Acute Cardiovasc Care. 2014;30.
23.    Nunez J, Minana G, Santas E, Bertomeu-Gonzalez V. Cardiorenal syndrome in acute heart failure: revisiting paradigms. Rev Esp Cardiol. 2015;68:426-435.
24.    O’Connor CM, Miller AB, Blair JE et al. Causes of death and rehospitalization in patients hospitalized with worsening heart failure and reduced left ventricular ejection fraction: results from Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan (EVEREST) program. Am Heart J. 2010;159:841-849.
25.    Ommen SR, Nishimura RA, Appleton CP et al. Clinical utility of doppler echocardiography and tissue doppler imaging in the estimation of left ventricular filling pressures. Circulation. 2000;102:1788-1794.
26.    Ponikowski P, Voors AA, Anker SD 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)Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur Heart J. 2016;37:2129-2200.
27.    Singh G, Peterson EL, Wells K et al. Comparison of Renal Predictors for In-Hospital and Post-Discharge Mortality after Hospitalized Heart Failure. J Cardiovasc Med. 2012;13 (4):246-253.
28.    Tang WH.W., Mullens W. Cardiorenal syndrome in decompensated heart failure. Heart. 2010;96:255-260.
29.    The Criteria Committee of the New York Heart Association. Nomenclature and riteria for diagnosis of diseases of the heart and great vessels. 9th ed. Boston, Mass: Little, Brown & Co; 1994:253-256.

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Original language: Ukrainian

2. Original researches

 

Predictors of sinus rhythm restoration in patients with persistent atrial flutter (UKR)

U. P. Chernyaha-Royko 1, O. J. Zharinov 2, A. V. Aker 3

1 Danylo Halytskiy Lviv National Medical University
2 P. L. Shupyk National Medical Academy f Postgraduate Education, Kyiv
3 Lviv Regional State Clinical Medical and Diagnostic Cardiology Center

The aim — to compare clinical, electrocardiographic characteristics, myocardial structure and function in patients with non-valvular atrial flutter (AFL) with and without restoration and maintenance of sinus rhythm during short-term hospital follow-up.
Materials and methods. The one-center study included 105 patients with documented persistent AFL, among them 73 (69.5 %) men and 32 (30.5 %) women, median age — 66 (quartiles 56 — 73) years. All patients were retrospectively divided into two groups depending on restoration and maintenance of the sinus rhythm (SR) during short-term follow-up. The first group (n = 70) included patients with restored and maintained SR, second group (n = 35) — patients without SR restoration or with conversion to atrial fibrillation. Demographic parameters, risk factors, concomitant diseases, ECG data, laboratory tests, echocardiography, drug therapy were compared in two groups.
Results and discussion. There were no significant differences between two groups regarding age, gender and prevalence of concomitant diseases. Patients with restored SR had higher left ventricular ejection fraction compared to patients whose rhythm was restored (49 (40 — 58) % vs 40 (30 — 49) %, = 0.001). The episode duration of AFL was significantly shorter in groups with and without SR restoration (10 (1 — 96) vs 48 (10 — 240) weeks, p = 0.048). Heart rate and frequency of the atrial wave were larger in the SR restored group (respectively, 136 (107 — 150) vs 115 (84 — 136) per minute, p = 0.001 and 300 (272 — 300) against 272 (250 — 300) per minute, p = 0.041). Warfarin use was less frequent in patients with recovered SR (19 (27.1 %) vs 21 (60.0 %), p = 0.001).
Conclusions. The restoration and maintenance of sinus rhythm in patients with persistent AFL were associated with shorter duration of arrhythmia, higher frequency of its first episode, less severe manifestations of heart failure and left ventricular dysfunction, as well as less frequent features of atypical AFL by ECG characteristics.

Keywords: atrial flutter, cardioversion, efficiency.

List of references:  
1.    Ardashev AV. Tipichnoe trepetanie predserdiy: klassifikatsiya, klinicheskie proyavleniya, diagnostika i lechenie. Kardiologiya. 2010;4:57-65.
2.    Dziak HV, Zharinov OI. Fibryliatsiia peredserd. K.: Chetverta khvylia, 2011:192.
3.    Zharinov OI, Kuts VO, Hrytsai OM. Diahnostyka ta likuvannia tripotinnia peredserd. Medytsyna svitu. 2010;10:21-26.
4.    Zinchenko YuV. Optymizatsiia taktyky likuvannia khvorykh z typovym tripotinniam peredserd neklapannoho henezu v zalezhnosti vid klinichnykh ta elektrofiziolohichnykh kharakterystyk arytmii: avtoref. dys. na zdobuttia nauk. stupenia dok. med. nauk za spetsialnistiu 14.01.11 «kardiolohiia» / YuV Zinchenko. Kyiv, 2015:38.
5.    Rukovodstvo po kardiologii. Pod red. VN Kovalenko. Kyiv: Morion, 2008:1424.
6.    Alam M, Bandeali S, Shahzad SA, Lakkis N. Real-life global survey evaluating patients with atrial fibrillation (REALISE-AF): results of an international observational registry. Exp Rev Cardiovasc Ther. 2012;10(3):283-291.
7.    Barbato G, Carinci V, Tomasi C et al. Is electrocardiography a reliable tool for identifying patients with isthmus-dependent atrial flutter?. Europace. 2009;11:1071-1076.
8.    Bianconi L, Castro A, Dinelli M et al. Comparison of intravenously administered dofetilide versus amiodarone in the acute termination of atrial fibrillation and flutter. A multicentre, randomized, double-blind, placebocontrolled study. Eur Heart J. 2000;2:1265-1273.
9.    Brembilla-Perrot B, Girerd N, Sella JM et al. Risk of atrial fibrillation after atrial flutter ablation. J Cardiovasc Electrophysiol. 2014;25(8):813-820.
10.    Cosío F. Atrial flutter, typical and atypical: a review. Arrhythm Electrophysiol Rev. 2017;6(2):55-62.
11.    Da Costa A, Thévenin J, Roche F et al. Loire-Ardèche-Drôm Isère-Puy-de-Dôme Trial of Atrial Flutter Investigators. Results from the Loire-Ardèche-Drôme-Isère-Puy-de-Dôme (LADIP) trial on atrial flutter, a multicentric prospective randomized study comparing amiodarone and radiofrequency ablation after the first episode of symptomatic atrial flutter. Circulation. 2006;114:1676-1681.
12.    De Loma-Osorio F, Diaz-Infante E, Gallego M. Spanish Catheter Ablation Registry. 12th Official Report of the Spanish Society of Cardiology Working Group on Electrophysiology and Arrhythmias (2012). Rev Esp Cardiol (Engl Ed). 2013;66:983-992.
13.    Ellis K, Wazni O, Marrouche N et al. Incidence of atrial fibrillation post-cavotricuspid isthmus ablation in patients with typical atrial flutter: left-atrial size as an independent predictor of atrial fibrillation recurrence. J Cardiovasc Electrophysiol. 2007;18:799-802.
14.    Granada J, Uribe W, Chyou P et al. Incidence and predictors of atrial flutter in the general population. J Am Coll Cardiol. 2000;36:2242-2246.
15.    Kafkas N, Patsilinakos S, Mertzanos G et al. Conversion efficacy of intravenous ibutilide compared with intravenous amiodarone in patients with recent-onset atrial fibrillation and atrial flutter. Int J Cardiol. 2007;118:321-325.
16.    Kirchhof P, Benussi S, Kotecha D et al. 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. Eur Heart J. 2016;37:2893-2962.
17.    Lee K, Yang Y, Scheinman M. Atrial flutter: A review of its history, mechanisms, clinical features, and current therapy. Current Problems in Cardiology. 2005;30:121-167.
18.    Mareedu RK, Abdalrahman IB, Dharmashankar KC et al. Atrial flutter versus atrial fibrillation in a general population: differences in comorbidities associated with their respective onset. Clin Med Res. 2010;8(1):1-6.
19.    Natale A, Newby KH, Pisanó E et al. Prospective randomized comparison of antiarrhythmic therapy versus first-line radiofrequency ablation in patients with atrial flutter. J Am Coll Cardiol–2000;35:1898-1904.
20.    Peters R, Shorofsky S, Pelini M et al. Overdrive atrial pacing for conversion of atrial flutter: comparison of postoperative with nonpostoperative patients. Am Heart J. 1999;137:100-103.
21.    Page R, Joglar J, Caldwell M et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia. J Am Coll Cardiol. 2016;67 (13):1575-1623.
22.    Rahman F, Wang N, Yin X et al. Atrial flutter: Clinical risk factors and adverse outcomes in the Framingham Heart Study. Heart Rhythm. 2016;13(1):233-240.
23.    Schmieder S, Ndrepepa G, Dong J et al. Acute and long-term results of radiofrequency ablation of common atrial flutter and the influence of the right atrial isthmus ablation on the occurrence of atrial fibrillation. ur eart J. 2003;24 (10):956-962.
24.    Spector P, Reynolds M, Calkins H et al. Meta-analysis of ablation of atrial flutter and supraventricular tachycardia. Am J Cardiol. 2009;104:671-677.
25.    Saoudi N, Cosío F, Waldo A et al. A classification of atrial flutter and regular atrial tachycardia according to electrophysiological mechanisms and anatomical bases. Eur Heart J. 2001;22:1162-1182.

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3. Original researches

 

Long-term observation results of patients with atherosclerosis of the peripheral arteries of the lower extremities (UKR)

V. I. Tseluyko 1, O. D. Yarova 2

1 Kharkiv Medical Academy of Postgraduate Education
2 Sumy Regional Cardiology Dispanser

The aim — to investigate the factors influencing the nature of the course and long-term prognosis of patients with atherosclerosis of the peripheral arteries of the lower extremities (APALE).
Materials and methods. 100 people with APALE were surveyed, average age 60.7 ± 5.8 years. Patients underwent a transthoracic echo-cardiographic examination, doppler-ultrasound examination of arteries of the lower extremities and carotid arteries, Holter monitoring of the electrocardiogram, DNA determination by the polymerase chain reaction. The average age of onset APALE demonstration is 53.76 ± 0.67 years. Blood hypertension was observed in 55 (55 %), obesity — 42 (42 %), type 2 diabetes mellitus — 28 (28 %), tobacco smoking — 54 (54 %), hereditary tainted for early development of cardiovascular diseases — 60 (60 %), hyperlipidemia before the prescription of lipid-lowering therapy was registered in 73 (73 %) patients, acute cerebral circulation disturbances in anamnesis presented in 13 (13 %), ischemic heart disease was diagnosed in 37 (37 %). The observation period lasted 29 months.
Results and discussion. Patients were divided into 2 groups depending on the presence of end points: 1st group (average age 55.81 ± 5.86 years) — 16 patients with cardiovascular events 1 (1 %) cardiovascular death, 2 (2 %) — myocardial infarction (MI), 7 (7 %) — unstable angina, 6 (6 %) — acute cerebral circulation disturbances, 1 (1 %) — myocardial revascularization. The 2nd group (average age 61.68 ± 8.35 years) — 84 patients without end points. Patients of the Ist group were younger (p = 0.009), had an early APALE manifestation (p = 0.004), more severe ischemic affect of the arteries of the lower extremities (p = 0.0005) and involvement of three vascular pools (p = 0.000001), more often Ischemic heart disease (IHD) (p = 0.00001) was manifested, atherosclerotic vascular disease (p = 0.000001) and data about the past of acute cerebral circulation disturbances (p = 0.049). In group I, carriers of C allele (p = 0.001) and SS genotype (p = 0.02) prevailed according to genetic analysis of the gene of the eNOs promoter gene C(–786)T polymorphism. According to the regression data, a connection between the development of adverse cardiovascular events in patients with APALE with the presence of MI (p = 0.005) in anamnesis, atherosclerotic affect of arteria carotis (p = 0.0000001) and feedback with the age of the examined patients (p = 0.001).
Conclusions. An unfavorable prognosis in the examined patients with APALE is related to the aggressiveness of the atherosclerotic process: an early manifestation of the disease (p = 0.004), more significant ischemic affect of the arteries of the lower extremities (p = 0.0005), involvement of three vascular pools (p = 0.000001); the presence of coronary artery disease (p = 0.00001) with MI (p = 0.003) and reduction in GFR (≤ 60 ml/min/1.73 m2) (p = 0.03), C allele (p = 0.001) and CC genotype (p = 0.02) of the C(–786)T polymorphism of the eNOs promoter gene. In the long-term observation of patients with APALE, according to regression analysis, a direct connection was established between the occurrence of adverse cardiovascular events with the presence of atherosclerotic affect of arteria carotis (p = 0.0000001), having in the anamnesis MI (p = 0.005) and feedback with middle age of patients (p = 0.001).

Keywords: peripheral artery disease, ischemic heart disease, polymorphism of endothelial NO-synthase gene, cardiovascular events.

List of references:  
1.    Grigoryev SG, Lobzin YV, Skripchenko NV. The role and place of logistic regression and ROC analysis in solving medical diagnostic problems. Journal Infectology. 2016;8(4):36-45. (In Russian) DOI:10.22625/2072-6732-2016-8-4-36-45.
2.    Nechesova TA, Korobko Y.Ju., Kuznecova NY. Remodeling of the left ventricle: pathogenesis and methods of evaluation. Medical News 2008;11 : 7-13. (In Russian).
3.    Aboyans V, Ricco J. B., Bartelink M. L. et al. Guidelines on the Diagnosis and Treatment of Peripheral Arterial Diseases, in collaboration with the European Society for Vascular Surgery (ESVS). Eur Heart J. 2017;00:1-60.
4.    Bhatt D, Eagle K, Ohman E et al. REACH Registry Investigators. Comparative determinants of 4-year cardiovascular event rates in stable outpatients at risk of or with atherothrombosis. JAMA. 2010;304 (12):1350-1357.
5.    Criqui M, Aboyans V. Epidemiology of peripheral artery disease. Circ Res. 2015;116:1509-1526.
6.    Fowkes F, Murray G, Butcher I et al. Ankle brachial index combined with Framingham Risk Score to predict cardiovascular events and mortality: a meta-analysis. JAMA. 2008;300:197-208.
7.    Gallino A, Aboyans V, Diehm C et al. Non-coronary atherosclerosis. Eur Heart J. 2014;35:1112-1119.
8.    Hur D, Kizilgul M, Aung W et al. Frequency of coronary artery disease in patients undergoing peripheral artery disease surgery. Am J Cardio. 2012;110:736-740.
9.    Lang R, Badano L, Mor-Avi V et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American society of echocardiography and the European association of cardiovascular imaging. Eur Heart J. 2015;16:233-271.
10.    Levey A, Greene T, Kusek J et al. Dietary protein restriction and the progression of chronic renal disease: What have all of the results of the MDRD study shown?. J Am Soc Nephrol. 1999;10 (11):2426-2439.
11.    Nigam PK. Calculated low density lipoprotein-cholesterol: Friedewald’s formula versus other modified formulas. International journal of life science and medical research. 2014;4, Iss. 2:25-23.
12.    Peach G, Griffin M, Jones K et al. Diagnosis and management of peripheral arterial disease. The British Medical Journal. 2012;345:36-41.
13.    Rossi G, Cesari M, Zanchetta M et al. The T-786C endothelial nitric oxide synthase genotype is a novel risk factor for coronary artery disease in Caucasian patients of the GENICA study. J Amer Coll Cardiology. 2003;41(6):930-937.
14.    Thygesen K, Alpert J, Jaffe A et al. Third universal definition of myocardial infarction. Circulation. 2012;126:2020-2035.
15.    Tosaka A, Ishihara T, Iida O et al. Angiographic evaluation and clinical risk factors of coronary artery disease in patients with peripheral artery disease. J Am Coll Cardiol. 2014;63 (12).

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4. Original researches

 

Communication parameters of pulse wave and vitamin D3 in elderly patients with uncomplicated hypertension (UKR)

K. M. Amosova 1, V. V. Povoroznyuk 2, O. I. Nishkumay 1, K. P. Lazareva 1, G. V. Mostbauer 1, P. O. Lazarev 1, Yu. V. Rudenko 1

1 O. O. Bogomolets National Medical University, Kyiv
2 SI «D. F. Chebotarev Institute of Gerontology of NAMS of Ukraine», Kyiv

The aim  —  carry out a comparative analysis of the central aortic pressure, pulse wave parameters, and levels of parathyroid hormone and 25 (OH) vit D in elderly female patients with uncomplicated essential hypertension and in healthy female of the control group.
Materials and methods. The study included 28 women mean age of 69.2 ± 0.9 years with postmenopausal duration 17.4 ± 1.1 years with essential hypertension II stage 2 degrees and 25 practically healthy women mean age of 65.6 ± 1.6 years, BMI 27.7 ± 0.8 kg/m2, the duration of the postmenopausal period is 15.0 ± 1.6 years. All patients underwent general clinical and laboratory examination, daily monitoring of blood pressure (BP) and echocardiography. Parameters of central hemodynamics and arterial stiffness were measured using SphygmoCor device (AtCor Medical, Australia). All patients were tested for the level of 25(OH) vit D, ionized calcium, blood phosphorus, parathyroid hormone (PTH), creatinine clearance.
Results and discussion. Patients with hypertension and control groups were matched with age, BMI, brachial indexes and central blood pressure (as at that study stage we achieved target blood pressure against the background of hypotensive therapy). Analyzing parameters of the pulse wave, we detected a significant increase in the augmentation index, including normalized for heart rate of 75 beats per min and augmentation pressure (AP) in the main group on (46 %, 35 %, 29.8 %, p < 0.001, p < 0.001, p < 0.001 respectively) compared with the control. Amplification pressure (PPampl.) in the main group was significantly lower (16.4 %, p < 0.001). Pulse wave velocity through the muscular type arteries (PWVrad.) and the arteries of the elastic type (PVW fem.) in the study group were higher (40 %, 17.7 %, p < 0.001, p < 0.01). The average level of 25(OH)D in patients in the main group is lower compared to the control group (23.1 ± 1.29 and 29.13 ± 1.5 ng/ml, p < 0.01). The deficiency of 25(OH)D among the patients in the main group was detected in 12 patients (42.9 %), insufficiency — 10 (35.7  %), normal level — 6 (21.4 %), compared with patients in the control group: deficiency 25(OH)D — 4 (12  %), level insufficiency — 3 (16 %). In 14 (50 % %) of the examined patients of the main group with a deficiency of 25(OH)D the secondary hyperparathyroidism was diagnosed. There was a positive correlation between the level of 25(H)D, parathyroid hormone (PTH) and PWV fem. and brachial pulse AP (bPAP). There were negative statistically significant correlations between PWV fem and a level of 25(OH)D (r = –0.39, p < 0.05) and an indicator of vitamin D level with PTH (r = –0.53, p < 0.01). There were positive correlation links between PWV fem. with bSAP (r = 0.69), bPAP (r = 0.58), cSAP (r = 0.68), cDAP (r = 0.39), cPAP (r = 0.46).
Conclusions. Elderly female patients with controlled uncomplicated hypertension, compared with healthy women, demonstrated the increase in arterial rigidity rates according to the pulse wave which is associated with secondary hyperparathyroidism against the backdrop of vitamin D insufficiency. The correlation between level 25(OH)D and carotid-femoral pulse rate may indicate the importance of vitamin D deficiency in the pathogenesis of arterial stiffness, which is probably mediated by increased calcification of intima and/or media, and determine the need for selection of combined therapy to correct the revealed violations.

Keywords: arterial hypertension, osteoporosis, arterial stiffness, vitamin D.

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5. Original researches

 

linical symptoms of carotid body tumor (UKR)

I. I. Kobza, . . Savchenko

Danylo Halytsky Lviv National Medical University

The aim — to identify basic symptoms for the diagnosis of carotid body tumor.
Materials and methods. The analysis of the clinical symptoms of 56 patients who were hospitalized in the department of vascular surgery Lviv regional hospital for the period 1995 to 2016 in this group of patients in the 31 case diagnosed tumor of the carotid body (study group) and 25 cases of tumors of other oncogenesis in section of carotid arteries (control group).
Results and discussion. In the group of carotid body tumor (CBT) main symptom is the appearance of painless, round, tight elastic consistency, formation of the neck in the projection of the bifurcation of the common carotid artery, which slowly increased in size 25 (81 %) patients with CBT. The episodes of vertigo were in history of 9 (17 %) of clinical cases, headache — 7 (23 %), episodes of fainting — 5 (16 %), the appearance of a painful lesion on his neck — 6 (19 %), lymphadenopathy — 5 (16 %), amnesia — 2 (6 %), dysphagia — 2 (6 %), dysarthria — 2 (6 %), cough, ear disorder — 1 (3 %). 5 (16 %) patients with CBT from the study group we diagnosed the syndrome of carotid node. The basis for the diagnosis of this syndrome in patients was the presence of bradycardia and hypotension, which regressed after removal of CBT. Based on the comparative analysis between the frequency of symptoms in study groups by Fisher test we identified that in the study group a statistically significant lesion is the emergence of asymptomatic lesion in the neck in the projection of carotid arteries in 81 % of patients (p = 0.0021), dizziness in 29 % of patients (p = 0.0489) syndrome of carotid node in 16 % (p = 0.0445).
Conclusions. Analysis of the clinical picture in patients with carotid body tumor showed that this disease is marked by the appearance of painless, oval-shaped, tight elastic consistency lesion in the neck in the projection of the bifurcation of the common carotid artery, which is accompanied by vertigo syndrome and syndrome of carotid node.

Keywords: carotid body tumor, carotid artery, tumor.

List of references:  
1.    Shidlovs’kyy VO, Shidlovs’kyy OV. Shyyni parahanhliomy [Neck paraganglia]. Visnyk naukovykh doslidzhen. 2012;1:4-7. (In Ukr)
2.    Amato B, Bianco T, Compagna R et al. Surgical resection of carotid body paragangliomas: 10 years of experience. Am J Surg. 2014;207:293-298.
3.    Boscarino G, Parente E, Minelli F et al. An evaluation on management of carotid body tumour (CBT). A twelve years’ experience. G Chir. 2014;35:47-51.
4.    Beigi AA, Ashtari F, Salari M, Norouzi R. Convulsive syncope as presenting symptom of carotid body tumors: case series. J Res Med Sci. 2013;18(2):164-166.
5.    Devender S, Jaydip R, Rajani. Management for carotid body tumors: a single center experience. Indian J Vasc Endovasc Surg. 2014;1(1):8-11.
6.    Dixon JL, Atkins MD, Bohannon WT et al. Surgical management of carotid body tumors: a 15-year single institution experience employing an interdisciplinary approach. Proc (Bayl Univ Med Cent). 2016;29(1):16-20.
7.    Gwon JG, Kwon TW, Kim H, Cho YP. Risk factors for stroke during surgery for carotid body tumors. World J Surg. 2011;35:2154-2158.
8.    Sethi RV, Sethi RK, Herr MW, Deschler DG. Malignant head and neck paragangliomas: treatment efficacy and prognostic indicators. Am J Otolaryngol. 2013;34:431-438.

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6. Original researches

 

Allele status of single nuclear polymorphism 1166 of ATIIR1 gene and cardiac remodeling after ST segment elevation myocardial infarction (UKR)

O. V. Petyunina, M. P. Kopytsya

SI «L. T. Mala National Therapy Institute of NAMS of Ukraine», Kharkiv

The aim — to analyse the dynamics of miocardium structural and functional parameters, to demonstrate the heart rate variability in patients with miocardial infarction with ST segment elevation depending on polymorphism 1166 of ATIIR1 gene.
Materials and methods. 87 patients with STEMI, 70 (80 %) male and 17 (20 %) female average age 58.94 ± 10.16 years were examined. Patients were hospitalized to SI «L. T. Mala National Therapy Institute of NAMS of Ukraine» during first three days after selective coronary angiography and infarct-related artery stenting were performed. After 6-month observation period 57 patients were examined. Allele polymorphism A1166C of ATIIR1 gene was determined by polymerase chain reaction in real time, heart rate variability (HRV) — Cholter 24-hour monitoring, morpho-functional data — ultrasound research.
Results and discussion. In patients with and -genotypes compared with on 1 — 3 day of STEMI higher level of LVEDD (p = 0.004), LVESD (p = 0.043), LVMM (p = 0.041), frequency of mitral regurgitation (p = 0.028), the tendency to higher LVEDV (p = 0.089) were revealed. These means unfavorable structure of early post infarction myocardial remodeling (RM). After 6 month patients with and -genotypes compared with demonstrated higher LVEDD (p = 0.083), left atrium (p = 0.091), LVMM (p = 0.081). When analysed echocardiographic data in acute period of STEMI and after 6-month observation, groups with and and -genotypes demonstrated significant increasing or growth tendency to higher level of LVEDV (p = 0.06, p = 0.034), LVEDD (p = 0.057, p = 0.01), LVEF (p = 0.037, p = 0.07) respectevly. In patients with AC and CC-genotypes compared with AA were lower level of SDNN (p = 0.049), HF (p = 0.053), higher level of LF (p = 0.069) and LF/HF-index (p = 0.046).
Conclusions. Polymorphic and -genotype cariers compared with -genotype of ATIIR1 gene demonstrated more relevant increase of left ventricular diameters and volume, left atrium and LV myocardial mass in acute period of STEMI. After 6-month period in both groups LV dilatation and LVEF were observed. These data refer to the similar with Frank — Starling law dynamic of compensation. Patients with and -genotypes compared with A demonstrate unfavorable structure of LV CR which is associated with more expressed sympathic-vagous dysbalance.

Keywords: STEMI, single nuclear polymorphism 1166 of ATIIR1, cardiac remodeling.

List of references:  
1.    Alieva AM, Bulaeva NI, Gromova OI, Goluchova EZ. Heart rhythm variability in assessment of clinical state and prognosis in congestive heart failure. Kreativnaia Kardiologiia 2015; 3 : 42-55 doi: 10.15275/kreatkard.2015.03.04 [Russian].
2.    Zhebel VM, Starzhynska OL, Hefter Yu.O. ta in. Genotype of angiotensin II type 1 receptor as a factor of influence on myocardials structure and function in patients with essential hypertension of different severity. Arterial’naya Hipertenziya [Hypertension]. 2009. 1 (3). C.24-29. (Ukrainian).
3.    Svirshevski EB, Ianov AA, Michailov Yu.N., Popov SO. Kolichestvennaia otsenka socratitelnoi activnosti miocarda [Quantitative estimate of contractile myocardial activity]. Kardiologiia I serdechno-sosudistaia hirurgia 2010; 3 (4): 69-74. (Russian).
4.    Tseluyko VY, Yakovleva LM, Popova KI. Faktory, shcho vplyvayut’ na perebih infarktu miokarda u khvorykh na ishemichnu khvorobu sertsya [Factors that influence a myocardial infarction current in patients with ischemic heart disease]. Liky Ukrayiny [Medications of Ukraine]. 2013. 3-4 (16-17). .19-23. (Ukrainian).
5.    Ceolotto G, Papparella I, Bortoluzzi A et al. Interplay between miR-155, AT1R A1166C polymorphism, and AT1R expression in young untreated hypertensives. Am J Hypertens. 2011;24:241-246. doi: 10.1038/ajh.2010.211
6.    ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2012;33: 2569-2619. DOI:10.1093/eurheartj/ehs215
7.    Huikuri HV, Stein PK. Clinical applicarion of heart rate variability after acute myocardial infarction. Frontiers in Physiology. 2012;3, suppl. 41. doi: 10.3389/fphys.2012.00041
8.    Kruzliak P, Kovacova G, Pechanova O, Balogh S. Association between angiotensin II type I receptor polimorghism and sudden cardiac death in myocardial infarction. Dis Markers. 2013;35, suppl. 5:287-293. http://dx.doi.org/10/1155/2013/73609
9.    Li Y, Li X, Jia N et al. Meta-analysis of the association between angiotensin II receptor, type 1 gene A1166C polymorphism and coronary artery disease in Chinese populations. J Renin-Angiotensin-Aldosterone Syst. 2013;14, suppl. 1:82-90. doi: 10.1177/1470320312450599 jra.sagepub.com
10.    Martin MM, Buckenberger JA, Jiang J et al. The human angiotensin II type 1 receptor +1166 A/C polymorphism attenuates microrna-155 binding. J Biol Chem. 2007;282:24262-24269. DOI: 10.1074/jbc.M701050200.
11.    Martinez-Quintata E, Chirino R, Nieto-Lago V et al. Prognostic value of ACE I/D, AT1R A1166C, PAI-1 3G/5G and GPIIIa a1/a2 polymorphisms in myocardial infarction. Cardiol J. 2014;21, suppl. 3:229-237. doi: 10.5603/CJ.a2013.0107.
12.    Mishra A, Srivasava A, Kumar S et al. Role of angiotensin II type I (AT1 A1166C) receptor polymorphism in susceptibility of left ventricular dysfunction. Ind Heart J. 2015;67:214-221.
13.    Nossent AY, Hansen JL, Doggen C et al. SNPs in microRNA binding sites in 3-UTRs of RAAS genes influence arterial blood pressure and risk of myocardial infarction. Am J Hypertens. 2011;24:999-1006. doi: 10.1038/ajh.2011.92.
14.    Ozdemir M, Arslan U, Turkoglu S et al. Losartan improves heart rate variability and heart rate turbulence in heart failure due to ischemic cardiomyopathy. J Cardiac Fail. 2007;13:812-817. doi: 10.1016/j.cardfail.2007.08.002
15.    Ozturk O, Ozturk U, Negriz S et al. The relationship between angiotensin-II type I receptor gene polymorphism and repolarization parametres after a first anterior acute myocardial infarction. Korean Circ J. 2016;46, suppl. 6: 791-797. doi: 10.4070/kcj.2016.46.6.791.
16.    Paradis P, Dali-Youcef N, Paradis FW et al. Overexpression of angiotensin II type I receptor in cardiomyocytes induces cardiac hypertrophy and remodeling. Proc Natl Acad Sci USA. 2000;97:931-936. PMC 15433.
17.    Sethupathy P, Bore C, Gagnebin M et al. Human microRNA-155 on Chromosome 21 Differentially Interacts with Its Polymorphic Target in the AGTR1 3′ Untranslated Region: A Mechanism for Functional Single-Nucleotide Polymorphisms Related to Phenotypes. Am J Hum Genet. 2007;Vol. 81, suppl. 2: 405-413. doi: 10.1086/519979.
18.    Song T, Qu XF, Zhang YT et al. Usefullness of heart-rate variability complex for predicting cardiac mortality after acute myocardial infarction. BMS Cardiovascular disorders. 2014;14:59. doi: 10.1186/1471- 2261-14-59.
19.    Tian J, Hu S, Wang F et al. PPARG, AGTR1, CXCL16 and LGALS2 polymorphisms are correlated with the risk for coronary heart disease. Int J Clin Exp Pathol. 2015;8, suppl. 3:3138-3143. www.ijcep.com/ISSN: 1936-2625/IJCEP0005186
20.    Townend JN, al-Ani M, West JN et al. Modulation of cardiac autonomic control in humans by angiotensin II. Hypertension. 1995;25:1270-1275. doi: https:. doi.org/10.1161/01.HYP.25.6.1270.
21.    Zhang K, Zhou B, Zhang L. Association study of angiotensin II type 1 receptor: A1166C (rs5186) polymorphism with coronary heart disease using systematic meta-analysis. J Renin-Angiotensin-Aldosterone Syst. 2013;14, suppl. 2:181-188. DOI: 10.1177/1470320312447652 jra.sagepub.com.

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7. Original researches

 

Surgical treatment of venous thromboses of lower extremities (UKR)

V. I. Rusyn, V. V. Korsak, Ya. M. Popovich, S. O. Boiko

Uzhhorod National University

The aim —  to improve the results of treatment of deep vein tromobosis (DVT) in the system of vena cava inferior.
Materials and methods. 678 patients with DVT in the system of vena cava inferior were treated in the surgical clinic of the Regional Clinical Hospital A. Novak. Considering the method of treatment, the patients were divided into two groups. The first (main) group consisted of 443 (65.3 %) patients with deep vein thrombosis (DVT) in the system of the vena cava inferior (VCI), who underwent an open full or partial thrombectomy. The second (control) group included 235 (33.7 %) patients with DVT in the VCI system receiving only conservative treatment.
Results and discussion. Surgical treatment of deep vein thrombosis according to the cumulative analysis allowed to achieve a positive result of treatment in 89.5 % of patients, and with conservative treatment — only in 48.8 % of patients. At the end of 3 years of observation, the marked signs of chronic venous insufficiency in patients in the control group were observed in 51.6 % of patients, and in the main group — only in 13.1 %.
Conclusions. Surgical lumen restoration of deep veins in the system of the vena cava inferior allows to preserve vein valves, prevent postthrombophlebitic syndrome with following chronic venous insufficiency occurrence, to improve treatment results in patients with DVT.

Keywords: deep vein thrombosis, vena cava inferior, thrombectomy, conservative treatment.

List of references:  
1.    Gudz IM. Diagnostyka ta likuvannja gostrogo trombozu glybokyh ven nyzhnih kincivok i tazu. Rekomendacii’ Tovarystva sudynnyh hirurgiv Nimechchyny (Ukrainian). Serce i sudyny [Heart and vessels] (Ukrainian). 2006;2 (14):34-36.
2.    Kobza II, Gavryliv BM, Orel Ju.G., R.A. Zhuk, M.G. Orel, A.T. Kihtjak, S.A. Lebedjeva, V.D. Luzhans’kyj Likuvannja flebotromboziv systemy nyzhn’oi’ porozhnystoi’ veny, uskladnenyh flotacijeju verhivky trombu (Ukrainian). Nauk. visnyk Uzhgorods’kogo universytetu, serija «Medycyna» [Scientific Bulletin of Uzhgorod University Medical Series] (Ukrainian). 2012;2 (44):52-53.
3.    Pokrovskyj AV. Sostojanye sosudystoj hyrurgyy v Rossyy v 2007 godu (Russian). Moskva, 2008:46.
4.    Sergejev OO, Kutovyj OB, Ljul’ko I.V., Habarlak V, vsjukov SV. , Sokolov A,  El’hash O. V. Hirurgichne likuvannja gostryh venoznyh klubovo-stegnovyh tromboziv (Ukrainian). Shpytal’na hirurgija [Hospital Surgery] (Ukrainian). 2009;4:27-29.
5.    Comerota AJ. Treatment of acute iliofemoral deep venous thrombosis: a strategy of thrombus removal. Eur J Vasc Endovasc Surg. 2007;33(3):351-360.
6.    Bergan John J. The vein book: monograph. London-Oxford: Elsevier Academic Press, 2007:617.
7.    Ekloef B. Aggressive treatment of proximal deep venous thrombosis: 6th North Sea Meeting on Venous Diseases. Antwerpen, 2007:15-17.
8.    Geier B, Asciutto G, Strohmann B et al. Long-term results after transfemoral venous thrombectomy for iliofemoral deep venous thrombosis. Abstracts XXIII Annual Meeting European Society for Vascular Surgery (3-6 September 2009, Oslo, Norway):148.
9.    Pillny M, Sandmann W. Deep venous thrombosis: surgical options. Minimally invasive venous surgery. Turin: Edizioni Minevra Medica S.p.A., 2008:93-98.
10.    Rosales A, Sanbæk G, Jørgensen JJ. Stenting for chronic postthrombotic cava and iliofemoral occlusions. clinical outcome and midterm patency. Abstracts XXIII Annual Meeting European Society for Vascular Surgery (3-6 September 2009, Oslo, Norway):59.

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8. Original researches

 

The state of the proteolytic system by the example of neutrophil elastase in patients with trophic ulcers of arterial and venous genesis (UKR)

I. D. Duzhiy, A. S. Nikolaienko, V. M. Popadynets, I. M. Medvedeva

Sumy State University

The aim — to establish features of the proteolytic system by the example of neutrophil elastase in patients with trophic ulcers of arterial and venous genesis.
Materials and methods. We examined and treated 38 patients with vascular disease of arterial and venous nature. The patients were divided into 2 groups. The first group consisted of 20 patients with trophic ulcers against the background of postthrombophlebitic syndrome and venous varices. In the second group, there were patients with trophic ulcers (n = 18) with diabetic angiopathy and obliterating atherosclerosis of the arteries of the lower extremities. The control group comprised 20 practically healthy individuals. The activity of neutrophil elastases was measured in nmol/min/ml.
Results and discussion. In the study of the proteolytic system by the example of neutrophil elastase in  patients with trophic ulcers of arterial genesis, it was shown that the average level of the enzyme was 286.17 ± 2.00 nmol/min/ml, which was  71.10 ± 0.52 nmol/min/ml in the control group. That was 4 times more. In patients with trophic ulcers of the venous genesis the average level of this indicator was 229.55 ± 0.55 nmol/min/ml. Compared with the control group), it was 3.2 times more. Comparing the results obtained in patients of both groups, we noted that the level of neutrophil elastases was significantly higher (1.2 times) in patients with trophic ulcers of the arterial genesis than the venous genesis. The difference between these groups was 56.62 nmol/min/ml.
Conclusions. The level of neutrophil elastase in patients with trophic ulcers of the lower extremities of the arterial and venous genesis is higher in comparison with the control group. After a more detailed study of the level of neutrophilic elastases, this data may be included in the standard laboratory test in the future.

Keywords: trophic ulcers, elastase, atherosclerosis, venous varice.

List of references:  
1.    Arefeva M. Osobennosti konservativnoy terapii troficheskih yazv smeshanoy etiologii. Praktichna angIologIya. (Russian). 2015;2 (69):33-38.
2.    Golubnichiy SO, Golubnicha VM, PIddubna GP, Gupalo MV. OsoblivostI spontannogo pnevmotoraksu tuberkuloznogo ta nespetsifIchnogo Genezu. Tuberkuloz v suchasnomu svItI – chastota, simptomi , lIkuvannya: stattI. LyublIn. (Ukrainian), 2013:129-140.
3.    Kudyikin MN. Kompleksnoe lechenie troficheskih yazv. Flebologiya. (Russian). 2008;3:16-20.
4.    Schupakova AN, Okulich VK, Belyaeva LE, Prudnikova AR.. Proteoliticheskaya aktivnost neytrofilnoy elastazyi kak prognosticheskiy faktor razvitiya zabolevaniy serdechno-sosudistoy sistemyi. Vesnik VGMU. (Russian). 2016;2:17-26.
5.    El-Eshmawy M.M, El-Adawy EH, Mousa AA et al. Elevated serum neutrophil elastase is related to prehypertension and airflow limitation in obese women. BMC Womens Health. 2011;N 11:1.
6.    Khokha R, Murthy A, Weiss A. Metalloproteinases and their natural inhibitors ininflammation and immunity. Nat Rev Immunol. 2011;13(9):649-665.
7.    Liu Z, Shapiro S. A critical role for neutrophil elastase in experimental bullous pemphigoid. J Clin Invest. 2000;105(1):113-123.
8.    Rahman GA, Adigun IA, Fadeyi A. Epidemiology, etiology, and treatment of chronic leg ulcer: experience with sixty patients. Ann Afr Med. 2010;9(1):1-4.

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9. Original researches

 

Effect of combination therapy with alpha-lipoic acid on the arterial lesion in patients with coronary artery disease (RUS)

L. V. Zhuravlyova, N. A. Lopina

Kharkiv National Medical University

The aim — to evaluate the carotid-femoral pulse wave velocity (cfPWV) and the intima media thickness of the common carotid artery (TIM CCA) in patients with coronary artery disease (CAD), depending on the presence of type 2 diabetes mellitus (T2DM), lesions of the coronary arteries (CA) prior to therapy and in the process of standard and combined therapy with the addition of alpha-lipoic acid (ALA).
Materials and methods. 131 patients with CAD (89 men, 42 women), mean age of 59.6 ± 9.11 years were examined. Depending on the presence of T2DM patients with CAD were divided into 2 groups: 1st group (n = 70) — patients with concomitant T2DM, 2nd group (n = 61) — patients with CAD and without T2DM. All patients were performed coronary angiography to verify the diagnosis of CAD. All  patients depending on the nature of the therapy were divided into 2 subgroups — subgroup IA (standard therapy) and the subgroup IB (combined therapy). Also cfPWV and TIM CCA were assessed before treatment and after 3 month of treatment.
Results and discussion. The study demonstrated that in patients with CAD, the values of cfPWV were significantly increased in comparison with the control group (p < 0.05). In the 1st group patients, in comparison with the 2nd group, the values of cfPWV (12.29 ± 2.10 m/s vs 11.02 ± 2.15 m/s, p = 0.0009) were significantly increased. In the 1st group of patients TIM CCA was significantly higher in comparison with the control (1.22 ± 0.10 mm vs 0.89 ± 0.06 mm, p = 0.00001), in the 2nd group patients also TIM CCA was significantly higher in comparison with the control group (1.11 ± 0.15 mm vs 0.89 ± 0.06 mm, p = 0.00001). In addition, in the 1st group patients TIM CCA was significantly higher in comparison with patients of the 2nd group (1.22 ± 0.10 mm vs 1.11 ± 0.15 mm, p = 0.00001). In the 1st group patients of standard therapy, after 3 months of treatment, an unreliable decrease cfPWV (10.60 ± 2.26 m/s vs 10.23 ± 2.16 m/s, p > 0.05) and TIM CCA (1.11 ± 0.07 mm vs 1.07 ± 0.07 mm, p > 0.05). In the 2nd group patients of standard therapy, after 3 months of treatment, there was a slight decrease cfPWV (9.85 ± 2.10 m/s 9.49 ± 2.10 m/s), TIM CCA (1.07 ± 0.10 mm vs 1.05 ± 0.10 mm, p > 0.05), but there was no significant difference (p > 0.05). In the 1st group patients of combined therapy, after 3 months of treatment, an unreliable decrease in the value of cfPWV was noted (12.64 ± 1.87 m/s vs 12.12 ± 1.88 m/s, p > 0.05), a significant decrease TIM CCA (1.24 ± 0.08 mm vs 1.21 ± 0.09 mm, p = 0.0302). In the 2nd group patients of combined therapy, after 3 months of treatment, an unreliable decrease cfPWV was noted (11.37 ± 2.10 m/s vs 10.83 ± 2.07 m/s, p > 0.05), and TIM CCA (1.11 ± 0.14 mm vs 1.08 ± 0.14 mm, p > 0.05).
Conclusions. For patients with CAD accompanied with T2DM, opposite to patients without T2DM, the addition of ALA to recommended therapy during 3 months was associated with decrease of TIM CCA. Addition of ALA to therapy for patients with CAD during 3 months was associated with decrease of TIM CCA as well as cfPWV.

Keywords: carotid-femoral pulse wave velocity, arterial stiffness, intima media thickness of the common carotid artery, atherosclerosis, coronary heart disease, type 2 diabetes mellitus, a marker of endothelial dysfunction, alpha-lipoic acid.

List of references:  
1.    Biduchak AS, Shkrobanets ID, Leonets SI. Epidemiolohichni osoblyvosti khvorob systemy krovoobihu v Ukrainianaini i Chernivetskii oblasti. [Epidemiological features of cardiovascular diseases Ukrainianaine in Chernivetskii region]. Bukovynskyi medychnyi visnyk (Ukrainian). 2013;17, 3 (67). . 2:100-103.
2.    Zhuravlyova LV, Lopina NA Value of carotid-femoral pulse wave velocity in prediction of atherosclerotic lesions of the coronary vessels depending on presence of type 2 diabetes mellitus (Russian). Ukrainianayinskiy Kardiologichniy Zhurnal [Ukrainian cardiology journal] (Ukrainian). 2017;1:43-50.
3.    Zhuravleva LV, Lopina NA, Kuznetsov IV  Method of carotid-femoral and aorto-femoral wave velocity measurement using rheography (Russian). Liki Ukrainianayini [Medications of Ukrainianaine] (Ukrainian). 2016;10:22-32.
4.    Zhuravleva LV, Lopina NA, Kuznetsov IV  Comparative evaluation of pulse wave velocity measurement with the use of reography and Doppler ultrasound (Russian). Serce i sudyny [Heart and vessels] (Ukrainian). 2016;4:72-79.
5.    Moskalenko VF, Hulchii OP, Holubchykov MV, Liedoshchuk BO, Liekhan VM, Ohniev VA, Lytvynova LO, Maksymenko OP, Tonkovyd OB, authors; Moskalenko VF, editor. Biostatystyka. [Biostatistics]. .: Knyha plius (Ukrainian), 2009:184.
6.    Rekomendatsii po diabetu, prediabetu i serdechno-sosudistyim zabolevaniyam [Recommendations for diabetes, prediabetes and cardiovascular diseases. EASD/ESC] (Russian). Rossiyskiy Kardiologicheskiy Zhurnal [Russian Cardiology Journal] (Russian). 2014;3 (107):6-70.
7.    Stabilna ishemichna khvoroba sertsia: adaptovana klinichna nastanova, zasnovana na dokazakh. [Stable ischemic heart disease: adapted, evidence based, clinical guidelines] (Ukrainian). Kyiv, 2016:177.
8.    Unifikovanyi klinichnyi protokol pervynnoi ta vtorynnoi (spetsializovanoi) medychnoi dopomohy: Stabilna ishemichna khvoroba sertsia. [Unified clinical protocols of primary and secondary (specialized) care: Stable ischemic heart disease]. Nakaz MOZ Ukrainianainy vid 02.03.2016 152. [Order of MOH Ukrainianaine from 02.03.2016 152.] (Ukrainian):61.
9.    Unifikovanyi klinichnyi protokol pervynnoi ta vtorynnoi (spetsializovanoi) medychnoi dopomohy: tsUkrainianoviy dIabet 2 tipu. [Unified clinical protocols of primary and secondary (specialized) care: Diabetes mellitus type 2].115.
10.    Chang JW, Lee EK, Kim TH et al. Effects of alpha-lipoic acid on the plasma levels of asymmetric dimethylarginine in diabetic end-stage renal disease patients on hemodialysis: a pilot study. Am J Nephrol. 2007;27:70-74.
11.    Dworacka M, Iskakova S, Krzyżagórska E et al. Alpha-lipoic acid modifies circulating angiogenic factors in patients with type 2 diabetes mellitus. Diab Res Clin Pract. 2015;107, suppl. 2:273-279.
12.    Gianturco V, Bellomo A et al. Impact of therapy with alpha-lipoic acid (ALA) on the oxidative stress in the controlled NIDDM: a possible preventive way against the organ dysfunction?. Arch Gerontol Geriatr. 2009;49, suppl. 1:129-133.
13.    Harding SV, Rideout TC, Jones PJ. Evidence for using alpha-lipoic acid in reducing lipoprotein and inflammatory related atherosclerotic risk. J Diet Suppl. 2012;9, suppl. 2:116-127.
14.    Heinisch BB, Francesconi M, Mittermayer F et al. Alpha-lipoic acid improves vascular endothelial function in patients with type 2 diabetes: a placebo-controlled randomized trial. Eur J Clin Invest. 2010;40:148-154.
15.    Holme I, Faergeman O, Fayyad R et al. Prognostic model of residual risk for major cardiovascular events in statin-treated coronary patients: a combined analysis of the IDEAL and TNT trials. J Am Coll Cardiol. 2012;59, suppl. 13:E1495–E1495.
16.    Huang Y, Cai X, Chen P et al. Associations of prediabetes with all-cause and cardiovascular mortality: A meta-analysis. Ann Med. 2014;46:684-692.
17.    Kim HS, Kim HJ, Park KG et al. Alpha-lipoic acid inhibits matrix metalloproteinase-9 expression by inhibiting NF-kappaB transcriptional activity. Exp Mol Med. 2007;39:106-113.
18.    Liao YF, Feng Y, Chen LL et al. Coronary heart disease risk equivalence in diabetes and arterial diseases characterized by endothelial function and endothelial progenitor cell. J Diabetes Complications. 2014;28, suppl. 2:214-218.
19.    Lim SY, Bae EH et al. The effect of alpha lipoic acid in a porcine in-stent restenosis model. J Cardiol. 2009;54, Iss. 3:375-385.
20.    McMackin CJ, Widlansky ME, Hamburg NM et al. Effect of combined treatment with alpha lipoic acid and acetyl-l-carnitine on vascular function and blood pressure in coronary artery disease patients. J Clin Hypertens (Greenwich). 2007;9, suppl. 4:249-255.
21.    Mitchell GF, Hwang Sh.-J., Vasan RS. Arterial stiffness and cardiovascular events: The Framingham Heart Study. Circulation. 2010;121(4):505-511.
22.    Mittermayer F, Pleiner J, Francesconi M, Wolzt M. Treatment with alpha-lipoic acid reduces asymmetric dimethylarginine in patients with type 2 diabetes mellitus. Translat Res. 2010;155:6-9.
23.    Morcos M, Borcea V, Isermann B et al. Effect of alpha-lipoic acid on the progression of endothelial cell damage and albuminuria in patients with diabetes mellitus: an exploratory study. DiabRes Clin Pract. 2001;52:175-183.
24.    Moreau R et al. Lipoic acid improves hypertriglyceridemia by stimulating triacylglycerol clearance and downregulating liver triacylglycerol secretion. Arch Biochem Bioph. 2009;485, suppl. 1:63-71.
25.    Park S, Karunakaran U, Jeoung NH et al. Physiological effect and therapeutic application of alpha lipoic acid. Curr Med Chem. 2014;21, suppl. 32:3636-3645.
26.    Sadeghi R, Adnani N, Erfanifar A et al. Premature coronary heart disease and traditional risk factors-can we do better?. Int Cardivasc Res J. 2013;7, suppl. 2:46-50.
27.    Scaramuzza A, Giani E, Redaelli F et al. Alpha-lipoic acid and antioxidant diet help to improve endothelial dysfunction in adolescents with type 1 diabetes: a pilot trial. J Diab Rese. 2015. Epub 2015 Jun 16.
28.    Sena CM, Nunes E, Louro T et al. Effects of alpha-lipoic acid on endothelial function in aged diabetic and high-fat fed rats. Br J Pharmacol. 2008;153:894-906.
29.    Skibska B, Goraca A. The protective effect of lipoic acid on selected cardiovascular diseases caused by age-related oxidative stress. Oxidative Medicine and Cellular Longevity. 2015;313021. doi: 10.1155/2015/313021. Epub 2015 Apr 8.
30.    Sola S, Mir MQ, Cheema FA et al. Irbesartan and lipoic acid improve endothelial function and reduce markers of inflammation in the metabolic syndrome: results of the Irbesartan and Lipoic Acid in Endothelial Dysfunction (ISLAND) study. Circulation. 2005;111:343-348.
31.    Standards of medical care in diabetes — 2016. American Diabetes Association. Diab Care. 2016;39, suppl. 1. S.1–S.109.
32.    Townsend RR, Wilkinson IB, Schiffrin EL et al. Recommendations for Improving and Standardizing Vascular Research on Arterial Stiffness: A Scientific Statement from the American Heart Association. Hypertension. 2015;66(3):698-722.
33.    Van Bortel L et al. Expert consensus document on arterial stiffness: methodological issues and clinical applications. Eur Heart J. 2006;27, suppl. 21:2588-2605.
34.    Van Bortel LM, Laurent S, Boutouyrie P et al. Expert consensus document on the measurement of aortic stiffness in daily practice using carotid-femoral pulse wave velocity. J Hypertens. 2012;30, suppl. 3:445-448.
35.    Wollin SD, Wang Y, Kubow S, Jones PJ. Effects of a medium chain triglyceride oil mixture and alpha-lipoic acid diet on body composition, antioxidant status, and plasma lipid levels in the Golden Syrian hamster. J Nutr Biochem. 2004;15, suppl. 7:402-410.
36.    Xiang GD, Sun HL, Zhao LS et al. The antioxidant alpha-lipoic acid improves endothelial dysfunction induced by acute hyperglycemia during OGTT in impaired glucose tolerance. Clin Endocrinol (Oxford). 2008;68:716-723.
37.    Xu J, Yang W, Deng Q et al. Flaxseed oil and α-lipoic acid combination reduces atherosclerosis risk factors in rats fed a high-fat diet. Lipids in Health and Disease. 2012;11:148.
38.    Yi X, Maeda N. Lipoic acid prevents the increase in atherosclerosis induced by diabetes in apoliprotein E-deficient mice fed high-fat/low-cholesterol diet. Diabetes. 2006;55:2238-2244.
39.    Yi X, Xu L, Hiller S et al. Reduced alpha-lipoic acid synthase gene expression exacerbates atherosclerosis in diabetic apolipoprotein E-deficient mice. Atherosclerosis. 2012;223, suppl. 1:137-143.
40.    Ying Z, Kampfrath T, Sun Q et al. Evidence that α-lipoic acid inhibits NFκ-B activation independent of its antioxidant function. Inflamm Res. 2011;60:219-225.
41.    Zhang Y, Han P, Wu N et al. Amelioration of lipid abnormalities by α-lipoic acid through antioxidative and anti-inflammatory effects. Obesity (Silver Spring). 2011;19:1647-1653.
42.    Zulkhairi A, Zaiton Z, Jamaluddin M et al. Alpha lipoic acid possess dual antioxidant and lipid lowering properties in atherosclerotic-induced New Zealand White rabbit. Biomed Pharmacother. 2008;62, suppl. 10:716-722.

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10. Original researches

 

The role of mitral valve reconstructive surgery in primary mitral regurgitation treatment (UKR)

O. A. Myshakivskyy 1, V. G. Averchuk 1, I. I. Kobza 2

1 Lviv Regional Clinical Hospital
2 Danylo Halytsky Lviv National Medical University

The aim —  to evaluate features and results of surgery for patients with primary mitral regurgitation by using the method of mitral plasty compared with mitral prosthesis method.
Materials and methods. We have analyzed results of treatment of 72 patients with primary MR (PMR) who were subjected to MVR or MVRe performed in the Department of cardiac surgery affiliated with Lviv regional clinical hospital (Ukraine) since October, 2013 till February, 2016.
Results and discussion. Males prevailed in the MVRe group — 12 persons (66.67 %), female prevailed in the MVR group — 29 persons (53.7 %). Before surgery in the group with MVRe and MVR all patients had moderate MR. After performed MVRe 16 patients (88.89 %) did not demonstrated MR and light MR was revealed in2 patients (11.11 %). In the group with performed MVR 100 % patients had no MR after surgery. The predominant correction method of MR was MVR — 54 patients (75 %). The most often etiological factor of MR were MV degenerative changes — 41 patient (56.9 %). The most often direct cause of MR was chordal rupture — 43 cases (59.7 %). In the MVRe group predominantly posterior cusp was involved — 11 patients (61.1 %), in the MVR group two cusps were affected — 20 patients (37.04 %). During MVRe, additional to valvuloplasty ring, more often wedge-shaped resection was used in 7 patients. Amount of early postsurgical complications was significantly higher in MVR group — 5 patients, compared to MVRe — 1 patient. The mortality was higher in MVR group — 3 patinets, compared to MVRe — none.
Conclusions. Key direct cause of MR is the chordal rupture of MV cusps (59.7 %), etiological factor in the majority of advanced countries is degenerative changes (56.9 %). Principal method of MR surgical correction in out center is MVR (54 patients, 75 %), though the preferable global trend is MVRe. Complications and lethality percentages in our study were higher among the patients from MVR group. This corresponds to results of other studies and guidelines that recommend MVRe as optional method for MR correction.

Keywords: primary mitral regurgitation, mitral valve replacement, mitral valve repair.

List of references:  
1.    Adams DH, Rosenhek R, Falk V. Degenerative mitral valve regurgitation: best practice revolution. Eur Heart J. 2010;31:1958-1966.
2.    Enriquez-Sarano M, Akins C, Vahanian A. Mitral regurgitation. Lancet. 2009;373:1382-1394.
3.    Enriquez-Sarano M, Basmadjian AJ, Rossi A et al. Progression of mitral regurgitation: a prospective Doppler echocardiographic study. J Am Coll Cardiol. 1999;34:1137-1144.
4.    Gammie J, Sheng S, Griffith B et al. Trends in mitral valve surgery in the united states: results from the society of thoracic surgeons adult cardiac database. Ann Thorac Surg. 2009;87 (5):1431-1439.
5.    Gillinov AM, Cosgrove D, Blackstone E et al. Durability of mitral valve repair for degenerative disease. J Thorac Cardiovasc Surg. 1998;116 (5):734-743.
6.    Iung B. A prospective survey of patients with valvular heart disease in Europe: The Euro Heart Survey on Valvular Heart Disease. Eur Heart J. 2003;24:1231-1243.
7.    Ling LH., Enriquez-Sarano M, Seward JB. Early surgery in patients with mitral regurgitation due to flail leaflets: a long-term outcome study. Circulation. 1997;96:1819-1825.
8.    Mirabel M, Iung B, Baron G et al. What are the characteristics of patients with severe, symptomatic, mitral regurgitation who are denied surgery?. Eur Heart J. 2007;28 (11):1358-1365.
9.    Otto C. Evaluationand management of chronic mitral regurgitation. New Eng J Med. 2001;345:740-746.

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11. Original researches

 

Osteoprotegerin as marker of treatment of patients with diabetic foot syndrome (UKR)

. V. Pyptiuk, V. . Pyptyuk

Ivano-Frankivsk National Medical University

The aim — to study OPG as indicator in complex treatment of patients with diabetic foot syndrome (DFS).
Materials and methods. Under our observation there were 118 patients with diabetic foot syndrome (F. W. Wagner II—V stage), 59.4 ± 8.3 years old. 86 % of patients had purulent-necrotic process of II—IV stages according to F. W. Wagner. Two patients groups were compared, the groups were age, gender and diabetes duration (from 5 till 15 years) matched. In 74 % of them the level of HbA1c was 7.9 ± 1.39 % (7.5—8.0). Patients with purulent-necrotic process of II—IV stages according to F. W. Wagner (86 patients) were divided into two groups. First experimental group was formed with 49 patients who were operated on purulent-necrotic form of DFS. Comparing group contained 37 patients whom, additionally osteoperforation of tibia, at the side of damaged foot was performed. Control group was formed with 32 patients who had diabetes mellitus II with peripheral form of atherosclerosis without purulent-necrotic complications. We observed the dynamics of OPG level in blood by means of immune enzyme analysis. Severity of ischemic lesion of an extremity was evaluated by determination of transcutaneous oxygen pressure measurements (TcPO2) with TCM4 device.
Results and discussion. Levels of OPG in a control group was 8.2 pmol/L, at TcPO2 27.4 ± 5.2 mmHg. On 10th day after operation we saw the positive dynamic of TcPO2 accretion up to 40 — 50 %. At the moment, levels of OPG was 7.54 pmol/L. Patients with F. W. Wagner II—V stage (86 patients), at the moment of hospitalization, OPG blood serum level was 17.5 pmol/L (p Kruskal — Wallis — 0.012). The elevation of TcPO2 up to 30 % was observed in the first group on the 10th day after an operation and weakly positive dynamic of pathological process. OPG level in this case was 16.1 pmol/L (p Kruskal — Wallis  — 0.006). In group , elevation of TcPO2 on 10th day was 43 %. OPG levels was 20.7 pmol/L (p Kruskal — Wallis 0.006). The support function of foot was saved in 88.3 % of patients.
Conclusions. OPG serum concentration increases at patients with DFS (F. W. Wagner II—V stage) by 113 % comparing with patients with DFS without destructive processes. Increasing of OPG levels up to 18.1 %, comparing with hospitalization (p < 0.01), in patients who had osteoperforation in addition to small amputation because of DFS (W. Wagner II—V stage), in case of positive progress of pathological  process, it can be a marker of neoangiogenesis.

Keywords: diabetic foot syndrome, osteoperforation, osteoprotegerine.

List of references:  
1.    Augoulea , Vrachnis N, Lambrinoudaki  et al. Osteoprotegerin as a marker of atherosclerosis in diabetic patients. Int  J Endocrinol. 2013;N 10:1155-1161.
2.    Cassiano F,  Weege R, Barroso R, Luiz M. Immunohistochemical analysis of bone resorption regulators (RANKL and OPG), angiogenic index, and myofibroblasts in syndrome and non-syndrome odontogenic keratocysts. Arch Oral Biol.  2012.  Vol. 57, iss. 3:230-237.
3.    Esteghamati , Aflatoonian , Rad  et al. Association of osteoprotegerin with peripheral artery disease in patients with type 2 diabetes. Arch Cardiovasc Dis. 2015;N 108:412-419.
4.    Grigoropoulou P, Eleftheriadou I, Zoupas C, Tentolouris N. The role of the osteoprotegerin/RANKL/RANK system in diabetic vascular disease. Curr Med Chem. 2011;18(31):4813-4819.
5.    Huang K, Ma Y, Wang J et al. The correlation between transcutaneous oxygen tension and microvascular complications in type 2 diabetic patients. J Diabetes Complications. 2017;N 5:886-890.
6.    International Diabetes Federation. IDF Diabetes Atlas. 7th Edition [Internet]. BRussiansels, Belgium: IDF; 2015. Available from http://www.diabetesatlas.org/ Accessed 20 February 2016.
7.    Kiechl S, Werner P, Knoflach M et al. The osteoprotegerin/RANK/RANKL system: a bone key to vascular disease. Exp Rev Cardiovasc Ther. Published online: 10 Jan 2014:801-811.
8.    Kobayashi-Sakamoto M, Tamai R. Beyond bone remodeling–emerging functions of osteoprotegerin in host defense and microbial infection. Integr Mol Med. 2015;2(6):384-390.
9.    Lipsky , Aragón-Sánchez J, Diggle  et al. IWGDF guidance on the diagnosis and management of foot infections in persons with diabetes. Diabetes/Metabolism Research and Reviews. 2016;32:45-74.
10.    Norgren L, Hiatt WR, Dormandy JA et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J Vasc Surg. 2007;N 45:5-67.
11.    Selvin E, Parrinello CM, Sacks DB, Coresh J. Trends in prevalence and control of diabetes in the United States, 1988-1994 and 1999 — 2010. Ann Intern Med. 2014;160(8):517-525.
12.    Tuttolomondo , Maida , Pinto . Diabetic foot syndrome: Immune-inflammatory features as possible cardiovascular markers in diabetes. World J Orthop. 2015;18; 6 (1):62-76.
13.    Volmer-Thole M, Lobmann R. Neuropathy and diabetic foot syndrome. Int J Mol Sci. 2016;N6:917-921.
14.    Xu L, Kanasaki R. Diabetic angiopaty and angiogenic defects. Fibrogenesis Tissue Repair. 2012;N5:1-13.

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12. Original researches

 

The case of systemic amyloidosis with heart damage (RUS)

O. E. Zaitseva 1, E. A. Dyadyk 2, L. V. Kushnir 3, T. Raad 4

1 O. O. Bogomolets National Medical University, Kyiv
2 P. L. Shupyk National Medical Academy f Postgraduate Education, Kyiv
3 Oleksandrivska Clinical Hospital, Kyiv
4 SI «Medical Scientific and Practical Center of Pediatric Cardiology and Cardiosurgery of Health Ministry of Ukraine», Kyiv

Amyloidosis with the synthesis of light chains of amyloid is a rare and fatal disease for which there are no approved methods of treatment. In patients with amyloidosis, amyloid light chains accumulate in the organs, leading to organ failure, which is especially predictive of seriousness when the heart is involved in the process. The diagnosis of the disease is complex and largely depends on the doctors’ knowledge of this pathology. It includes visualization methods: CT and MRI with contrast, surrogate markers of damage (NT-proBNP) and biopsy with immunohistochemical examination. There are no successful methods of treatment at the moment. However, frequently used treatment options, such as high-dose chemotherapy in combination with autologous stem cell transplantation, a combination of alkylating agents and steroids, proteasome inhibitors and/or immunomodulatory medications, can reduce the production of amyloid precursor protein by plasma cells.

Keywords: cardiomyopathy, restrictive cardiomyopathy, systemic amyloidosis, cardiac amyloidosis, magnetic resonance imaging.

List of references:  
1.    Ardehali H, Qasim A, Cappola T. Endomyocardial biopsy plays a role in diagnosing patients with unexplained cardiomyopathy. Am Heart J. 2004;147, N. 5:919-923.
2.    Banypersad SM, Moon JC, Whelan C. Updates in cardiac amyloidosis: a review. J Am Heart Assoc. 2012;1, N. 2:1847-1852.
3.    Bejar D, Colombo PC, Latif F. Infiltrative Cardiomyopathies. Clin Med Insights Cardiol. 2015;9(2):29-38.
4.    Cantwell RV, Aviles RJ, Bjornsson J. Cardiac amyloidosis presenting with elevations of cardiac troponin I and angina pectoris. Clin Cardiol. 2002;25, N. 1:33-37.
5.    Chew C, Ziady GM, Raphael MJ, Oakley CM. The functional defect in amyloid heart disease: the «stiff heart» syndrome. Am J Cardiol. 1975;36(4):438-444.
6.    Cooper LT, Baughman KL, Feldman AM. American Heart Association, American College of Cardiology, European Society of Cardiology, Heart Failure Society of America, Heart Failure Association of the European Society of Cardiology The role of endomyocardial biopsy in the management of cardiovascular disease a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology Endorsed by the Heart Failure Society of America and the Heart Failure Association of the European Society of Cardiology. J Am Coll Cardiol. 2007;50, N. 19:1914-1931.
7.    Dispenzieri A, Gertz MA, Kyle RA. Serum cardiac troponins and N-terminal pro-brain natriuretic peptide: a staging system for primary systemic amyloidosis. J Clin Oncol. 2004;22(18):3751-3757.
8.    Falk RH, Dubrey SW. Amyloid heart disease. Prog Cardiovasc Dis. 2010;52, N. 4:347-361.
9.    Gertz MA, Dispenzieri A, Sher T. Pathophysiology and treatment of cardiac amyloidosis. Nat Rev Cardiol. 2015;12, N.2:91-102.
10.    Klein AL, Hatle LK, Burstow DJ. Doppler characterization of left ventricular diastolic function in cardiac amyloidosis. J Am Coll Cardiol. 1989;13(5):1017-1026.
11.    Kraemer BF, Seizer P, Geisler T. Persistent troponin elevation in a patient with cardiac amyloidosis. Clin Cardiol. 2009;32(11):39-42.
12.    Kumar S, Dispenzieri A, Lacy MQ. Revised prognostic staging system for light chain amyloidosis incorporating cardiac biomarkers and serum free light chain measurements. J Clin Oncol. 2012;30(9):989-995.
13.    Kushwaha SS, Fallon JT, Fuster V. Restrictive cardiomyopathy. N Engl J Med. 1997;336(4):267-276.
14.    Merlini G, Bellotti V. Molecular mechanisms of amyloidosis. N Engl J Med. 2003;349(6):583-596.
15.    Merlini G, Seldin DC, Gertz MA. Amyloidosis: pathogenesis and new therapeutic options. J Clin Oncol. 2011;29(14):1924-1933.
16.    Mikhael JR, Schuster SR, Jimenez-Zepeda VH. Cyclophosphamide-bortezomib-dexamethasone (CyBorD) produces rapid and complete hematologic response in patients with AL amyloidosis. Blood. 2012;119(19):4391-4394.
17.    Murtagh B, Hammill SC, Gertz MA. Electrocardiographic findings in primary systemic amyloidosis and biopsy-proven cardiac involvement. Am J Cardiol. 2005;95(4):535-537.
18.    Neben-Wittich MA, Wittich CM, Mueller PS. Obstructive intramural coronary amyloidosis and myocardial ischemia are common in primary amyloidosis. Am J Med. 2005;118(11):1287.
19.    Ridolfi RL, Bulkley BH, Hutchins GM. The conduction system in cardiac amyloidosis. Clinical and pathologic features of 23 patients. Am J Med. 1977;62(5):677-686.
20.    Seward JB, Casaclang-Verzosa G. Infiltrative cardiovascular diseases cardiomyopathies that look alike. J Am Coll Cardiol. 2010;55(17):1769-1779.
21.    Shah KB, Inoue Y, Mehra MR. Amyloidosis and the heart: a comprehensive review. Arch Intern Med. 2006;166(17):1805-1813.
22.    Smith RR, Hutchins GM. Ischemic heart disease secondary to amyloidosis of intramyocardial arteries. Am J Cardiol. 1979;44(3):413-417.
23.    Syed IS, Glockner JF, Feng D. Role of cardiac magnetic resonance imaging in the detection of cardiac amyloidosis. JACC Cardiovasc Imaging. 2010;3(2):155-164.
24.    Tsang W, Lang RM. Echocardiographic evaluation of cardiac amyloid. Curr Cardiol Rep. 2010;12(3):272-276.

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13. Reviews

 

Strategy for the functional state and quality of life determination in adults with congenital heart defects (UKR)

I. H. Lebid

SI «The Scientific Practical Children’s Cardiac Center», Kyiv

This article provides the literature review which includes an analysis of assessing the severity and functional status of adult patients with congenital heart disease (CHD). Different approaches to assessment the complexity of CHD are outlined. Disease severity index, Index ability to lead a normal life, Congenital heart disease functional index are described, the assessment of heart failure functional class by NYHA and left ventricular contractility (ejection fraction of left ventricle) is presented. Considerable attention is paid to applying the standard questionnaires to determine the Health-related quality of life. The subjective assessment of the health status in CHD should be supported by the analysis of symptoms, the ability to work physically, mood state and also by an objective assessment of satisfaction with environment, social relationships, and the ability to act in accordance with their religious and personal convictions. The complexity of CHD systematization, the problem of an adequate assessment of the severity of CHD cause necessity for studying the effect of this pathology on the quality and life expectancy of such patients with the aim of optimizing the system for providing them with cardiac treatment.

Keywords: congenital heart defects, adults, functional status, quality of life.

List of references:  
1.    Evsina OV. The quality of life in medicine — an important indicator of patient health status (review) Lichnost’ v menyayushchemsya mire: zdorov’e, adaptatsiya, razvitie. [Personality in a changing world: health, adaptation, development] 2013;1 : 119-133. (Russian).
2.    Lebid IH, Rudenko NM, Yemets IM. Bilingual structured nomenclature of diagnoses, cardiological and cardiac surgery, extracardiac anomalies, general pre- and postoperative risk factors in adults with congenital heart disease. Kyiv: UCCC, 2015:72. (Ukrainian).
3.    Lebid IH, Rudenko NM, Sydorenko A.Yu. et all. Quality of life in patients with congenital heart disease. Kyiv: UCCC, 2016:49. (Ukrainian).
4.    Novik , Ionova TI. Manual for Quality of life estimation M. RAEN. 2012:320. (Russian).
5.    Guidelines for the diagnosis and treatment of Chronic Heart Failure by Ukrainian Association of Cardiologists. Heart Failure and co-morbid pathology. 2017; 1 (Suppl.1): 66 (Ukrainian).
6.    Amedro P, Basquin A, Gressin V et al. Health-related quality of life of patients with pulmonary arterial hypertension associated with CHD: the multicentre cross-sectional ACHILLE study. Cardiol Young. 2016;26. (7):1250-1259.
7.    Apers S, Kovacs AH, Luyckx K et al. Quality of Life of Adults With Congenital Heart Disease in 15 Countries: Evaluating Country-Specific Characteristics. J Am Coll Cardiol. 2016;67 (19):2237-2245.
8.    Bay A, Dellborg M, Berghammer M et al. Patient reported outcomes are associated with physical activity level in adults with congenital heart disease. Int J Cardiol. 2017;243:174-179.
9.    Chen CA, Liao SC, Wang JK et al. Quality of life in adults with congenital heart disease: biopsychosocial determinants and sex-related differences. Heart. 2011;97(1):38-43.
10.    Eaton SL, Wang QF, Menahem S. Determinants of quality of life in adults with CHD: an Australian cohort. Cardiol Young. 2017:1-6.
11.    Fteropoulli T. In good heart»: a study of the factors associated with health-related quality of life in adult congenital heart disease: . City University London, 2016:584.
12.    Fteropoulli T, Stygall, J., Cullen, S. et al. Quality of life of adult congenital heart disease patients: a systematic review of the literature. Cardiol Young. 2013;23(4):473-485.
13.    Miller MR, Forrest CB, Kan JS. Parental preferences for primary and specialty care collaboration in the management of teenagers with congenital heart disease. Pediatrics. 2000;106:264-269.
14.    Moons P, Van Deyk K, De Geest S et al. Is the severity of congenital heart disease associated with the quality of life and perceived health of adult patients?. Heart. 2005;91(9):1193-1198.
15.    Ponikowski P, Voors AA, Anker SD et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failureThe Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur Heart J. 2016;37 (27):2129-2200.
16.    Rassart J, Apers S, Kovacs AH et al. Illness perceptions in adult congenital heart disease: A multi-center international study. Int J Cardiol — 2017;244:130-138.
17.    Romero M, Vivas-Consuelo D, Alvis-Guzman N. Is Health Related Quality of Life (HRQoL) a valid indicator for health systems evaluation?. Springer Plus. 2013;2(1):664.
18.    Tyagi M, Fteropoulli T, Hurt CS et al. Cognitive dysfunction in adult CHD with different structural complexity. Cardiol Young. 2016:1-9.
19.    Ware JE. SF-36® Health Survey Update. Available from: http://www.sf-36.org/tools/sf36.shtml.
20.    Warnes CA, Liberthson R, Danielson GK et al. Task force 1: the changing profile of congenital heart disease in adult life. J Am Coll Cardiol. 2001;37:1170-1175.
21.    Warnes CA, Somerville J. Tricuspid atresia in adolescents and adults: current state and late complications. Br Heart J. 1986;56:535-543
22.    WHO: WHOQOL: measuring quality of life. Available from: http://www. who.int/mental_health/media/68.pdf.

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14. Reviews

 

Aneurysmal alteration of different arterial pools (UKR)

S. M. Genyk

Ivano-Frankivsk National Medical University

The high frequency of different arterial pools aneurysms in abdominal aorta aneurysm became known as aneurysmal disease and allows to recommend the patients to be observed for aneurysmal process in all main arteries. The everyday use of mentioned predictors in clinical practice will improve the diagnostic results and surgical treatment of aneurysmal disease. When identifying the different arterial poolls aneurysms, the active surgical treatment is recommended. The choice of treatment strategy depends on the severity of the disease, clinical manifestations, aneurysm localization and its morphology, but always a preference is given to endovascular methods.

Keywords: aneurysmal disease, aorta, arterial pools, main arteries, matrix metalloproteinases.

List of references:  
1.    Arshinov AV, Maslova IG. Role of the infection and inflammation in atherosclerosis development (literature review)/ Angiol. and vascular surgery. 2011;. 17(1):35-41 (Russian).
2.    Bokeria LA, Arakelyan VS, Jane AK, Papitashvili YG, Siradze IV. Remote results of open interventions in treatment of abdominal aortic aneurysms. Angiology and vascular surgery. 2012;18(2):107-115 (Russian).
3.    Bytsay AM. Surgical management of aneurismal disease of main arteries of lower extremities. Heart vessels. 2015;2:107-111 (Russian).
4.    Vachitov D, Suominen V, Korhonen J. and others. Endovascular treatment of mycotic aneuresms of the abdominae aorta and the inferior mesenteric artery. Angiology and Vascular Surgery. 2016;22(1):83-85 (Russian).
5.    Gavrilenko AV, Vakhratyan PE, Kotov AE, Alikin E.Yu. Surgical treatment of an aneurysm of the deep femoral artery. Angiology and vascular surgery. 2013;19(2):139-146 (Russian).
6.    Henyk SM. The role of infection in Atherosclerosis Development. Galician Medical Journal. 2012;1:146-149 (Ukrainian).
7.    Zatevakhin II, Zolkin VH, Matyushkin AV, Tolstov TA, Tishenko IS. On the pathogenesis and risk of abdominal aortic aneurysm rupture.Angiol. and Vascular Surgery. 2006;. 12(1):17-24 (Russian).
8.    Imaev TE, Kuchin IV, Lepilin PM, Kolegaev AS. and others. Use of an iliac branched endoprotheis in endovascular treatment for an abdominal aortic aneurysm combined with aneurysm of both common iliac arteries. Angyology and Vascular Surgery. 2016;22(4):83-86 (Russian).
9.    Irtyuha OB, Vorozhyna IV, Smagina LV. and others. The activity of matrix metalloproteinases in patients with aneurysm of the ascending aorta of various etiologies. Arterial hypertension. 2010;6:587-591 (Russian).
10.    Karpenko AA, Starodubtsev VB, Dynsupov AA et al. Results of endoprosthetic reconstruction in patiens with aneurysm of the intrarenal portion of the aorta. Angiol. and Vascular Surgery. 2013;. 19(4):108-113 (Russian).
11.    Kokov LS, Karmazanovsky GG, Tabaeva NV, Tzygankov VN et al. Radiological endovascular correction of azygous visceral arterial aneurysms. Angiol. and vascular surgery.. 2008;. 14(3):55-61 (Russian).
12.    Kriger AG, Kokov LS, Karmazanovsky GG et al. False arterial aneurysms of celiac trunk system in patients with chronic pancreatitis. N. I. Pirogov Journal of Surgery. 2008;12:17-23 (Russian).
13.    Mischalov VN, Uzhanov OH, Chernyak VA. Clinical and anatomical classification of the aortic aneurysm. Ukrainian balneal magazine. 2004;2:53-54 (Ukrainian).
14.    Nikonenko AA, Makarenkov AO. Diagnostic value of the volume of the aneurysm of the abdominal aorta and intraluminal thrombus for determining the tactic of treatment and predicting the risk of rupture. Heart vessels. 2014;1 (45):69-72 (Russian).
15.    Pokrovskiy AV. Clinical angiology. Guide in 2 parts. M.: Medicine. 2004. . 2:117-122 (Russian).
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4(60) // 2017

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K. M. Amosova 1, I. I. Gorda 1, A. B. Bezrodnyi 1, G. V. Mostbauer 1, Yu. V. Rudenko 1, A. V. Sablin 2, N. V. Melnychenko 2, Yu. O. Sychenko 1, I. V. Prudkiy 1&a

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