The aim — to improve the results of treating patients with chronic lower limb ischemia (CLLI) using autologous mesenchymal stem cells (AMSC).
Materials and methods. The study involved 41 patients with CLLI (22 (53.6 %) men and 19 (46.4 %) women). We studied the methods of stem cell injection and their impact on microcirculation.
Results and discussion. The developed technique of using dosed physical training improved the effect of therapy with AMSC. There was a significant increase in the microcirculation of patients treated with AMSC, compared with patients treated with prostaglandins E1 (p = 0.037). The positive dynamics of microcirculation index while using prostaglandins E1 is observed during 1.8 ± 0.3 a month. When using AMSC, a significant increase in the microcirculation is observed in 2.7 ± 0.4 months and lasts for 1 year follow-up.
Conclusions. Therapy with AMSC significantly increases the level of microcirculation in the background of dosed physical load (p = 0.043) in patients with CLLI.

Keywords: chronic lower limb ischemia, mesenchymal stem cells, laser Doppler flowmetry.

List of references:  
1.    Абышов Н. С. Ближайшие результаты «больших» ампутаций у больных с окклюзионными заболеваниями артерий нижних конечностей // Хирургия. — 2005. — 11. — Р. 15—19.
2.    Белов Ю. В. Хирургическое лечение больных с множественным поражением артерий нижних конечностей // Ангиол. и сосуд. хирург. — 2002. — № 1. — С. 78 — 81.
3.    Бокерия Л. А. Первый опыт комбинированного лечения ХИНК с использованием стимуляторов неоангиогенеза // Ангиол. и сосуд. хирург. — 2006. — Т. 7. — С. 73 — 80.
4.    Константинов Б. А. Возможности и перспективы лечения ХИНК с использованием генно-инженерных технологий // Ангиол. и сосуд. хирург. — 2003. — Т. 9. — С. 14 — 18.
5.    Asahara Т., Murohara Т. Isolation of putative progenitor cells for angiogenesis // Science. — 275. — P. 964 — 967.
6.    Huang P. P., Li S. Z. Autologous transplantation of peripheral blood stem cells as an effective therapeutic approach for severe arteriosclerosis obliterans of lower extremities // Thromb. Haemostas. — 2004. — Vol. 91. — P. 606 — 609.
7.    Semenza G. L. Vasculogenesis, angiogenesis, and arteriogenesis: mechanisms of blood vessel formation and remodeling // J. Cell. Biochem. — 2007. — Vol. 102. — P. 840 — 847.
8.    TASC. Management of peripheral arterial disease. TransAtlantic Inter-Society Consensus // Eur. J. Vasc. Endovasc. Surg. — 2000. — P. 208 — 290.
9.    Tateishi-Yuyama E., Matsubara H. Therapeutic Angiogenesis using Cell Transplantation Study Investigators // Lancet. — 2002. — 360. — P. 427 — 435.

Additional: P. 25-29.

Article received on February 22, 2016

The aim — to determine the type of structure of the left ventricle (LV) by calculating the angle of the ventricular-septal angle (VSA) at hypoplastic left heart syndrome (HLHS), to evaluate the possibility of introducing this method in ultrasonic scanning (US) and the process of selecting treatment tactics.
Materials and methods. The hearts of fetuses of 19 — 21 weeks of gestation and newborns with HLHS (n = 49) and without cardiopathology (n = 54) were studied. ZHPU measured in different types of LV structure. VSA was measured in different types of LV structure.
Results and discussion. VSA differs from the norm in all types of LV in case of HLHS: upwards — in «spongy», «trabecular» and «cylindrical» types (from 60.7° to 85.5°) and downwards — in «hypertrophic gap» or «hypoplastic gap» types (from 11.9° to 27.1°).
Conclusions. VSA value depends on the type of the left ventricle at HLHS. The introduction of the angle measurement method in ultrasonic scanning will allow determining the type of the left ventricle in vivo and correcting the medical tactics.

Keywords: hypoplastic left heart syndrome, left ventricular structure types, morphometric studies, ventricular-septal angle.

List of references:  
1.    Бураковский В. И., Бухарин В. А., Подзолков В. П. и др. Врожденные пороки сердца // Сердечно-сосудистая хирургия / Под ред. В. И. Бураковского, Л. А. Бокерия. — М.: Медицина, 1989. — С. 345 — 382.
2.    Савчук Т. В., Захарова В. П. Синдром гіпоплазії лівих відділів серця: особливості будови лівого шлуночка // Вісник серцево-судинної хірургії. — 2014. — С. 307 — 310.
3.    Савчук Т. В., Захарова В. П., Лещенко І. В., Приходько Т. О. Спосіб визначення міжшлуночкового індексу серця. Патент 91803 Україна, МПК А61В 1/002. Київ. Державна установа «Національний інститут серцево-судинної хірургії ім. М. М. Амосова» АМН України, заявл. 18.03.2014, опубл. 10.07.2014.
4.    Савчук Т. В., Захарова В. П., Лещенко І. В., Приходько Т. О. Спосіб визначення «робочої» площі правого шлуночка серця при синдромі гіпоплазії лівих відділів серця. Патент 109840 Україна, МПК G01N33/48 G01N21/00 Київ. Державна установа «Національний інститут серцево-судинної хірургії ім. М. М. Амосова» АМН України, заявл. 29.05.2014, опубл. 12.10.2015.
5.    Allan L. D., Sharland G., Tynan M. J. The natural history of the hypoplastic left heart syndrome // Int. J. Cardiol. — 1989. — Р. 341 — 343.
6.    Cole C. R., Yutzey K. E., Brar A. K. et al. Congenital Heart Disease Linked to Maternal Autoimmunity against Cardiac Myosin // J. Іmmunol. — 2014. — Vol. 194, N 9. — Р. 4074 — 4082.
7.    Fyler D. C. Report of the New England Regional Infant Cardiac Program // Pediatrics. — 1980. — N 65. — Р. 376 — 472.
8.    Haber I., Metaxas D. N., Geva T., Axel L. Three-dimensional systolic kinematics of the right ventricle // Am. J. Physiol. Heart Circ. Physiol. — 2005. — Р. H1826 — 1833.
9.    Kleinman C. S. Fetal Cardiac Intervention Innovative Therapy or a Technique in Search of an Indication // Circulation. — 2006. — N 113. — P. 1378 — 1381.
10.    Miyamoto S. D., Stauffer B. L., Polk J. et al. Gene expression and β- adrenergic signaling are altered in hypoplastic left heart syndrome // J. Heart Lung Transplant. — 2014. — N 33. — P. 785 — 793.
11.    Munn M. B. Prenatally diagnosed hypoplastic left heart syndrome — outcomes after postnatal surgery // J. Matern. Fetal Med. — 1999. — N 8 (4). — Р. 147 — 150.
12.    Pedra C. A. Fetal interventions for congenital heart disease in Brazil // Pediatr. Cardiol. — 2014. — N 35. — Р. 399 — 405.
13.    Xiaoqin L., Shazina S., You L. et al. A Multigenic Etiology of Hypoplastic Left Heart Syndrome: An Analysis Based on Three Novel Mutant Mouse Models of Hyoplastic Left Heart Syndrome // Circulation. — 2012. — N 126.
14.    Zakharova V., Savchuk T., Rudenko О. Hypoplastic left heart syndrome: Structural changes of the left ventricular myocardium // Virchows. Arch. — 2013. — N 463. — P. 198.

Additional: P. 30-34.

Article received on February 17, 2016

The aim — to compare the changes in brachial blood pressure (BP) and indexes of central hemodynamics according to applanation tonometry in patients younger than 75 years of age with uncomplicated arterial hypertension (AH), depending on age, gender, heart rate (HR) and define independent determinants of pulse pressure amplification.
Materials and methods. Continuous prospective analysis was conducted of 91 patients aged 35 — 75 years (mean age 56.0 ± 10.3 years, 40.7 % men) with uncomplicated essential hypertension of stage I — II, 1 — 3 degrees, with office BP 160/100 brahial — 200/120 mm Hg in the absence of antihypertensive treatment or 140/90 — 200/120 mm Hg against a background of antihypertensive treatment and sinus rhythm with a heart rate of 50 — 100 beats/min. All patients underwent general clinical and laboratory examinations, ECG in 12 leads and echocardiography. Parameters of central hemodynamics were determined using applanation tonometry of radial artery on SphygmoCor (AtCor Medical, Australia) device: central systolic, diastolic and pulse pressure (cSBP, cDBP, cPBP), augmentation pressure (AP), augmentation index (AIx) and AIx for heart rate of 75 beats/min. (AIx75), pulse pressure amplification (PPA). Patients were divided into groups according to median age (58 years), gender, median heart rate which was registered at the time of applanation tonometry.
Results and discussion. Older patients (≥ 58 years) compared to younger ones (< 58) had higher levels of brachial (SBР: 157.5 ± 19.7 and 148.6 ± 16.5 mm Hg, p < 0.05, respectively; bPBp : 62.8 ± 13.8 and 54.8 ± 11.0 mm Hg, p < 0.01), central SBP (145.0 ± 18.6 and 136.1 ± 14.97 mm Hg, respectively, p < 0.05) and PBP (49.3 ± 12.3 and 40.9 ± 9.0 mm Hg, respectively, p < 0.01), AP (13.7 ± 8.5 and 10.5 ± 6.3 mm Hg, respectively, p < 0.05) and lower PPA (127.7 ± 15.1 and 135 ± 17.1, respectively, p < 0.01). Significant differences in levels of brachial and central SBP, DBP and PBP depending on gender was not revealed, however, women had higher AP than men (14.6 ± 7.3 vs 8.6 ± 6.6 mm Hg, respectively, p < 0.01), AIx (30.3 ± 11.9 vs 18.4 ± 12.2 %, respectively, p < 0.01), AIx75 (27 .0 ± 10.7 vs 16.1 ± 9.4 %, respectively, p < 0.01) and lower levels of PPA (127.6 ± 15.2 vs 139.2 ± 19.2 %, respectively, p < 0.01). At the same levels of brachial and central SBP, DBP, PBP, patients with a heart rate < 70 beats/min had lower PPA (125.6 ± 16.3 and 138.9 ± 17.2 %, respectively, p < 0.01) and higher AIx (28.3 ± 13.2 and 22.6 ± 12.9, p < 0.05) and AP (13.9 ± 7.7 and 10.4 ± 7.2 mm Hg, respectively, p < 0.05). According to univariate regression analysis, patients with higher heart rates, regardless of age and sex, had better indicators of AP and PPA (p < 0.01). Using multivariate logistic regression analysis,
we identified predictors of statistical model of PPA value prognosis with consideration of sex (A), HR (B), and age (C):
Y = 4.358 + 1.236 · А – 0.102 · B + 0.020 · C (R2 = 0.33), with the probable frequency of faultless prognosis of 72.8 % (95 % confidence interval (CI) 64.8 — 79.6), sensitivity of 71.6 % (95 % CI 59.9 — 81.0) and specificity of 73.9 % (95 % CI 62.5 — 82.8).
Conclusions. In patients with uncomplicated hypertension aged < 75 years, female sex and increase in age are associated with increased pulse wave augmentation, which promotes rise of cSBP, cPBP and bPBP. Increase in HR ≥ 70 beats/min is associated with a reduction of augmentation, regardless of age and gender. Use of these independent determinants in a logistic regression model allows predicting unfavorable as to cardiovascular risk reduction in PPA < 130 % with accuracy of 72.8 %.

Keywords: central blood pressure, arterial hypertension, pulse pressure amplification.

List of references:  
1.    Agabiti-Rosei E., Mancia G., O’Rourke M. F. et al. Central blood pressure measurements and antihypertensive therapy: a consensus document // Hypertension. — 2007. — Vol. 50. — P. 154 — 160.
2.    Avolio A., Van Bortel L., Boutouyrie P. et al. The role of pulse pressure amplification in arterial hypertension: experts’ opinion and review of the Data // Hypertension. — 2009. — Vol. 54. — P. 375 — 383.
3.    Benetos A., Thomas F., Joly L. Pulse pressure amplification: a mechanical biomarker of cardiovascular risk // J. Am. Coll. ­Cardiol. — 2010. — Vol. 55. — Р. 1032 — 1037.
4.    Carnethon M. R., Golden S. H., Folsom A. R. et al. Prospective investigation of autonomic nervous system function and the development of type 2 diabetes: the Atherosclerosis Risk In Communities study, 1987 — 1998 // Circulation. — 2003. — Vol. 107 (17). — Р. 2190 — 2195.
5.    Chirinos A., Townsend R. Pulse pressure amplification as a predictor of cardiovascular risk // J. Am. Coll. Cardiol. — 2010. — Vol. 56. — P. 744.
6.    ESH/ESC Guidelines for the management of arterial hypertension: the Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC) // J. Hypertens. — 2013. — Vol. 31 (7). — Р. 1281 — 1357.
7.    Fantin F. , Mattocks A. , Bulpitt C. J. et al. Is augmentation index a good measure of vascular stiffness in the elderly? // Age and Ageing. — 2007. — Vol. 36. — Р. 43 — 48.
8.    Franklin S. S. Hypertension in older people: part 1 // J. Clin. Hypertens. — 2006. — Vol. 8 (6). — Р. 444 — 449.
9.    Gatzka C. D., Kingwell B. A., Cameron J. D. et al. The ANBP2 investigators. Gender differences in the timing of arterial wave reflection beyond differences in body height // J. Hypertens. — 2001. — Vol. 19. — Р. 2197 — 2203.
10.    Grundy S. M., Cleeman J. I. et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement // Circulation. — 2005. — Vol. 112 (17). — Р. 2735 — 2752.
11.    Laurent P., Albaladejo P., Blacher J. et al. Heart rate and pulse pressure amplification in hypertensive subjects // Am. J. Hypertens. — 2003 — Vol. 16 (5 Pt 1). — Р. 363 — 370.
12.    Lemogoum D., Flores G., Vanden Abeele W. et al. Validity of pulse pressure and augmentationindex as surrogate measures of arterial stiffness during beta-adrenergic stimulation // J. Hypertens. — 2004. — Vol. 22 (3). — Р. 511 — 517.
13.    McEniery C. M., Yasmin, Hall I. R., Qasem A. et al. Normal vascular aging: differential effects on wave reflection and pulse wave velocity. The Anglo-Cardiff Collaborative Trial (ACCT) // J. Am. Coll. Cardiol. –2005. — Vol. 46. — Р. 1753 — 1760.
14.    McEniery C. M., Yasmin, McDonnell B. et al. Central pressure: variability and impact of cardiovascular risk factors: the Anglo-Cardiff Collaborative Trial II // Hypertension. — 2008. — Vol. 51. — Р. 1476 — 1482.
15.    Noon J. P., Trischuk T. C., Gaucher S. A. et al. The effect of age and gender on arterial stiffness in healthy Caucasian Canadians // J. Clin. Nurs. — 2008. — Vol. 17, N 17. — P. 2311 — 2317.
16.    Otsuka T., Kawada T., Ibuki C. et al. Obesity as an independent infl uential factor for reduced radial arterial wave refl ection in a middleaged Japanese male population // Hypertens. Res. — 2009. — Vol. 32, N 5. — P. 387 — 339.
17.    Protogerou A. D., Blacher J., Mavrikakis M. et al. Increased pulse pressure amplification in treated hypertensive subjects with metabolic syndrome // Am. J. Hypertens. — 2007. — Vol. 20. — P. 127 — 133.
18.    Segers P., Mahieu D. et al. Amplification ofthe pressure pulse in the upper limb in healthy, middle-aged men and women // Hypertension. — 2009. — Vol. 54. — P. 414 — 420.
19.    Vergnaud A. C., Protogerou A. D., Li Y. et al. Pulse pressure amplification, adiposity and metabolic syndrome in subjects under chronic antihypertensive therapy: the role of heart rate // Atherosclerosis. — 2008. — Vol. 199. — P. 222 — 229.
20.    Wilkinson I. B., MacCallum H., Flint L. et al. The influence of heart rate on augmentation index and central arterial pressure in humans // J. Physiol. — 2000. — Vol. 525. — P. 263 — 270.
21.    Wykretowicz A., Agnieszka R. et al. Pulse pressure amplification in relation to body fatness // Br. J. Clin. Pharmacol. —2011. — Vol. 73, N 4. — P. 546 — 552.

Additional: P. 37-45.

Article received on March 5, 2016

The aim — to determine the peculiarities of the hemodynamic response in healthy subjects and in patients with acute stroke while the motor task execution by the analysis of the functional MRI data.
Materials and methods. Routine MRI examination was performed for the examination and evaluation of the ischemic brain regions. Diffusion-weighted MRI was used for the localization of the ischemic regions. Three groups of patients were studied by the fMRI for the evaluation of stroke related motor cortex mapping peculiarities. 1st group included 18 healthy subjects with no signs of neurological disorders; 2nd group included 3 stroke patients with white matter ischemic lesion located in the left hemisphere and 3rd group included 3 stroke patients with ischemic lesion located in central sulcus of the left hemisphere. During fMRI procedure, patients performed right hand motor task. fMRI data analysis was done by the general linear modelling method using FSL software.
Results and discussion. The analysis of the fMRI data revealed activation of the primary sensory-motor areas, additional motor area and ventral premotor part of the cortex of brain contralateral hemisphere, and ipsilateral cerebellar hemisphere. In stroke patients, ipsilateral primary sensory-motor cortex, fronto-parietal and premotor cortex and both hemispheres of cerebellum were activated by the motor task execution. It has been revealed that average indexes of BOLD-signal progressively change in the surveyed groups: 1st group (1.1 %) < 2nd group (1.8 %) < 3rd group (3.6 %). Correlation of maximal BOLD-signal change amplitude with the general volume of brain activation was found in all groups: (1st group: R = 0.84; 2nd group: R = 0.82; 3rd group: R = 0.86).
Conclusions. Phenomenon of high correlation (R > 0.82) of maximal BOLD fMRI signal change and volume of brain activation in the surveyed groups was found. An increase was demonstrated in the mean BOLD changes of fMRI signal in stroke patients compared with healthy volunteers (1st group (1.1 %) < 2nd group (1.8 %) < 3rd group (3.6 %)). Compensatory changes in motor brain network in stroke patients resulting from primary functional zones dysfunction were shown.

Keywords: brain, neurovascular hemodynamic response, acute stroke, functional magnetic resonance imaging, motor cortex.

List of references:  
1.    Гусев Е. И. Проблема инсульта // Журн. неврол. и психиатр. — 2003. — 9. — С. 3 — 6.
2.    Кузнецова С. М., Юрченко Ф. В. Влияние тиоцетама на функциональное состояние ЦНС у больных перенесших ишемический инсульт // Мед. неотл. сост. — 2007. — 5 (12). — С. 122 — 126.
3.    Нечипуренко Н. И., Пашковская И. Д., Мусиенко Ю. И. Основные патофизиологические механизмы ишемии головного мозга // Мед. новости. — 2008. — 1. — С. 7 — 13.
4.    Friston K. J., Holmes A. P., Worsley K. J. et al. Statistical parametric maps in functional imaging: a general linear approach // Hum. Brain Mapp. — 1994. — 2 (4). — P. 189 — 210.
5.    Gelderen P., Ramsey N. F., Liu G. Three-dimensional functional magnetic resonance imaging of human brain on a clinical 1.5-T scanner // Proc. Natl. Acad. Sci. — 1995. — 92 (15). — P. 6906 — 6910.
6.    Heerden J., Desmond P. M., Phal P. M. Functional MRI in clinical practice: a pictorial essay // J. Med. Imaging Radiat. Oncol. — 2014. — 58 (3). — P. 320 — 326.
7.    Jackman K., Iadecola C. Neurovascular regulation in the ischemic brain // Antiox & Redox Signal. — 2015. — 22 (2). — P. 149 — 160.
8.    Jueptner M., Weiller C. Review: does measurement of regional cerebral blood flow reflect synaptic activity? — Implications for PET and fMRI // Neuroimage. — 1995. — Vol. 2 — P. 148 — 156.
9.    Mazzetto-Betti K. C., Leoni R. F., Pontes-Neto O. M. The stability of the BOLD fMRI response to motor tasks is altered in patients with chronic ischemic stroke // Stroke. — 2010. — 41 (9). — P. 1921 — 1926.
10.    Moonen C. T. W., Bandettini P. A. Functional MRI. — Berlin: Springer, 2000 — 575 p.
11.    Ogawa S., Lee T., Kay A. et al. Brain magnetic resonance imaging with contrast dependent on blood oxygenation // Proc. Natl. Acad. Sci. — 1990. — 87 (24). — P. 9868 — 9872.
12.    Rijntjes M., Dettmers C., Büchel C. et al. A blueprint for movement: functional and anatomical representations in the human motor system // J. Neurosci. — 1999. — 19 (18). — P. 8043 — 8048.
13.    Sibson N. R. et al. Stoichiometric coupling of brain glucose metabolism and glutamatergic neuronal activity // PNAS. — 1998. — Vol. 95 — P. 316 — 321.
14.    Srinivasan A., Goyal M., Al-Аzri F. et al. State-of-the-art imaging of acute stroke // Radiographics. — 2006. — 26 (suppl. 1). — P. S75 — 95.
15.    Weimar C., Kurth T., Kraywinkel K. et al. Assessment of functioning and disability after ischemic stroke // Stroke. — 2002. — 33 (8). — P. 2053 — 2059.

Additional: P. 46-52.

Article received on December 17, 2015

The aim — to analyse cardiovascular (CV) risk factors, antihypertensive therapy regimes, levels of adherence to treatment in patients with uncomplicated uncontrolled arterial hypertension (AH) in general outpatient cardiology practice in Kyiv.
Materials and methods. The study involved 407 patients aged from 35 to 75 years with uncontrolled uncomplicated essential AH. They took antihypertensive treatment for at least 1 month prescribed by cardiologists of medical institutions in Kiev. The 1st group included 122 (30 %) patients with probable resistance to AH treatment, that is, with «office» arterial pressure (AP) of ≥ 140/90 mm Hg, despite the prescription of three or more drugs; the 2nd group consisted of 285 (70 %) patients with uncontrolled AP, despite the use of one or two drugs. We conducted general clinical examination, assessed cardiovascular risk factors, the 10-year risk of cardiovascular events by Framingham scale, the number and doses of antihypertensive agents, the level of adherence to treatment according to X. Girerd questionnaire.
Results and discussion. Patients of group 1 more frequently suffered from stable angina of I — II functional class, type 2 diabetes, had cardiovascular complications in the family history and a larger average body mass index than patients of group 2. There were 78.9 % people with a high cardiovascular risk in 1st group, 75.9 % (p > 0.05) — in the 2nd group. In group 1, the average risk of cardiovascular events was higher than in group 2 (36.9 ± 10.1 and 30.7 ± 9.3, respectively; p < 0.05). For antihypertensive treatment of patients of 1st and 2nd groups we used angiotensin-converting enzyme (ACE) inhibitors (82.8 and 71.9 %, respectively; p > 0.05), β-blockers (86.9 and 42.6 %, respectively; p < 0.001), calcium channel blockers (46.7 and 13.3 %, respectively; p < 0.001) and diuretics (82.7 and 24.2 %, respectively; p < 0.001), including the optimal doses : ACE inhibitors — in 49.2 and 44.6 % (p > 0.05), β-blockers — in 51.6 and 27.4 % (p < 0.01), calcium channel blockers — in 38.5 and 10.1 % (p < 0.001), diuretics — in 53.3 and 10.5 %, respectively, (p < 0.001). The proportion of people with a low level of compliance was 54.1 and 51.6 %, with a moderate one — 24.6 and 28.8 %, and with a high one — 21.3 and 19.6 % in the 1st and 2nd groups, respectively, (all p > 0.05).
Conclusions. More than 75 % of patients with complicated uncontrolled AH without concomitant coronary artery disease, who are treated on an outpatient basis in Kiev, have been at high risk of cardiovascular events on the Framingham scale over the next 10 years. Among patients with uncomplicated AH and «office» blood pressure ≥ 140/90 mm Hg, the frequency of resistant to the treatment uncontrolled AH is 30 %. At comparable levels of AP and adherence to treatment, this category of patients differed from those whose antihypertensive therapy included one or two drugs. Particularly, they had a larger by 16.8 % average risk of cardiovascular events for 10 years due to a higher value of body mass index, frequency of type 2 diabetes and cardiovascular diseases in the family history. The proportion of patients who have probably resistant to treatment uncontrolled AH and are prescribed the optimal antihypertensive therapy, is 23 %, among which 57.2 % patients have a low commitment to treatment.

Keywords: essential arterial hypertension, antihypertensive therapy, uncontrolled arterial hypertension, stroke, resistant arterial hypertension, adherence to treatment.

List of references:  
1.    Амосова К. М., Руденко Ю. В., Рокита О. І., Кацитадзе І. Ю. Ефективність уніфікованого покрокового алгоритму лікування для забезпечення контролю артеріального тиску у хворих з артеріальною гіпертензією в амбулаторній практиці: результати дослідження ПЕРФЕКТ // Серце і судини. — 2014. — № 1. — С. 34 — 46.
2.    Горбась І. М. Эффективный контроль артеріального давления: как достичь успеха? // Здоров’я України. — 2013. — № 1 (26). — С. 16 — 17.
3.    Сіренко Ю. М., Радченко Г. Д., Казмирук В. І. Оцінка ефективності лікування хворих на артеріальну гіпертензію: результати однорічної диспансеризації у Черкаській області // Серце і судини. — 2007. — № 2. — С. 47 — 54.
4.    Calhoun D. A., Jones D., Textor S. et al. Resistant hypertension: diagnosis, evaluation, and treatment. A scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research // Hypertension. — 2008. — Vol. 51. — P. 1403 — 1419.
5.    Ceral J., Habrdova V., Vorisek V. et al. Difficult-tocontrol arterial hypertension or uncooperative patients? The assessment of serum antihypertensive drug levels to differentiate non-responsiveness from non-adherence to recommended therapy // Hypertens. Res. — 2011. — Vol. 34. — P. 87 — 90.
6.    D’Agostino R. B., Vasan R. S., Pencina M. J. et al. General Cardiovascular Risk Profile for Use in Primary Care The Framingham Heart Study // Circulation. — 2008. — Vol. 117. — P. 743 — 753.
7.    de Souza F., Muxfeldt F., Fiszman R., Salles G. Efficacy of Spironolactone Therapy in Patients With True Resistant Hypertension // Hypertension. — 2010. — Vol. 55. — P. 147 — 152.
8.    Egan B. M., Zhao Y., Axon R. N. et al. Uncontrolled and apparent treatment resistant hypertension in the United States, 1988 to 2008 // Circulation. — 2011. — Vol. 124. — P. 1046 — 1058.
9.    Egan B. M., Zhao Y., Li J. et al. Prevalence of optimal treatment regimens in patients with apparent treatment-resistant hypertension based on office blood pressure in a community-based practice network // Hypertension. — 2013. — Vol. 62. — P. 691 — 697.
10.    Ernst M. E. Resistant hypertension or resistant prescribing? // Hypertension. — 2011. — Vol. 58. — P. 987 — 988.
11.    Girerd X., Fourcade J., Brillet G. et al. The compliance evaluation test: a validated tool for detection of nonadherence among hypertensive treated patients // J. Hypertens. — 2001. — Vol. 19. — P. 74 S.
12.    Grassi G., Cifkova R., Laurent S. et al. Blood pressure control and cardiovascular risk profile in hypertensive patients from central and eastern European countries: results of the BP-CARE study // Eur. Heart J. — 2011. — Vol. 32. — P. 218 — 225.
13.    Grigoryan L., Pavlik V. N., Hyman D. J. Characteristics, drug combinations and dosages of primary care patients with uncontrolled ambulatory blood pressure and high medication adherence // JASH. — Vol. 7. — P. 471 — 476.
14.    Gupta A. K., Arshad S., Poulter N. R. Compliance, Safety, and Effectiveness of Fixed-Dose Combinations of Antihypertensive Agents: A Meta-Analysis // Hypertension. — 2010. — Vol. 55. — P. 399 — 407.
15.    Gupta A. K., Nasothimiou E. G., Chane C. L. et al. on behalf of the ASCOT investigators. Baseline predictors of resistant hypertension in the Anglo-Scandinavian Cardiac Outcome Trial (ASCOT): a risk score to identify those at high-risk // J. Hypertens. — 2011. — Vol. 29. — P. 2004 — 2013.
16.    Lim S. S., Vos T., Flaxman A. D. et al. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990 — 2010: a systematic analysis for the Global Burden of Disease Study 2010 // Lancet. — 2013. — Vol. 380. — P. 2224 — 2260.
17.    Mancia G., Fagard R., Narkiewicz K. et al. 2013 ESH/ESC Guidelines for themanagement of arterial hypertension TheTask Force for the management ofarterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC) // J. Hypertens. — 2013. — Vol. 31. — P. 1281 — 1357.
18.    Okonofua E. C., Simpson K. N., Jesri A. et al. Therapeutic Inertia Is an Impediment to Achieving the Healthy People 2010 Blood Pressure Control Goals // Hypertension. — 2006. — Vol. 47. — P. 345 — 351.
19.    Persell S. D. Prevalence of resistant hypertension in the United States, 2003 — 2008 // Hypertension. — 2011. — Vol. 57. — P. 1076 — 1080.
20.    Sarafidis P. A., Bakris G. L. Resistant hypertension: an overview of evaluation and treatment // J. Am. Coll. Cardiol. — 2008. — Vol. 52. — P. 1749 — 1757.
21.    Weber M. A., Schiffrin E. L., White W. B. et al. Clinical Practice Guidelines for the Management of Hypertension in the Community A Statement by the American Society of Hypertension and the International Society of Hypertension // J. Clin. Hypertens. — 2014. — Vol. 16. — P. 14 — 26.
22.    Weitzman D., Chodick G., Shalev V. et al. Prevalence and factors associated with resistant hypertension in a large health maintenance organization in Israel // Hypertension. — 2014. — Vol. 64. — P. 501 — 507.
23.    World Health Organization. A global brief on hypertension: silent killer, global public health crisis. World Health Day 2013. Report, 1 — 39. — Geneva, Switzerland; World Health Organization, 2013.

Additional: P. 53-62.

Article received on July 16, 2015

The aim — to investigate serum levels of fibronectin and endothelin-1 in patients with metabolic syndrome (MS), diagnosed with the use of various criteria.
Materials and methods. The study involved 93 people, including 71 patients with MS and 22 individuals without MS (control group). Patients were divided into three groups according to the MS criteria described in three different classifications: WHO, Adult Treatment Panel III (ATP III) of the National Cholesterol Education Program and the International Diabetes Federation (IDF). The first group (patients with MS, defined according to WHO criteria) included 23 persons (mean age — 51.91 ± 5.55 years), the second group (MS defined by IDF criteria) — 18 people (50.33 ± 4.57 years), the third group (ATP III criteria) — 30 people (51.33 ± 5.11 years). The contents of fibronectin and endothelin-1 were determined by ELISA.
Results and discussion. Serum level of fibronectin was 367.40 ± 44.04 pmol/ml, and endothelin-1 — 8.09 ± 0.91 pmol/ml in the first group of patients; 346.63 ± 76.01 and 7.63 ± 1.01 pmol/ml, respectively, in the second group; 343.05 ± 61.26 and 7.81 ± 1.26 pmol/ml, respectively, in the third group. These indices are significantly higher in all patients with metabolic syndrome than in those of the control group (226.17 ± 21.35 and 4.38 ± 0.81 pmol/ml, respectively), regardless of criteria by which MS was diagnosed.
Conclusions. Metabolic syndrome is accompanied by an increase of serum content of fibronectin and endothelin-1, which may be a manifestation of endothelial dysfunction in this pathological condition. Increased fibronectin and endothelin-1 are observed in all groups of people with metabolic syndrome regardless of criteria by which it was diagnosed. Criteria for determining MS by ATP III cover a wider range of persons who have predisposition to the development of cardiovascular disease.

Keywords: metabolic syndrome, fibronectin, endothelin-1, endothelial dysfunction.

List of references:  
1.    Alberti K. G., Zimmet P., Shaw J. The metabolic syndrome: a new worldwide definition // Lancet. — 2005. — Vol. 366. — Р. 1059 — 1062.
2.    Bauters C., Marotte F., Hamon M. et al. Accumulation of fetal fibronectin mRNAs after balloon denudation of rabbit arteries // Circulation. — 2005. — Vol. 92. — P. 904 — 911.
3.    Campia U., Tesauro M., Di Daniele N., Cardillo C. The vascular endothelin system in obesity and type 2 diabetes: Pathophysiology and therapeutic implications // Life Sci. — 2014. — Vol. 7. — Р. 24 — 32.
4.    Chan D. T., Watts G. F., Irish A. B. et al. Insulin resistance and the metabolic syndrome are associated with arterial stiffness in patients with chronic kidney disease // Am. J. Hypertens. — 2013. — Vol. 26 (9). — P. 1155 — 1161.
5.    Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III) // JAMA — 2001. — Vol. 285. — P. 2486 — 2497.
6.    Figueiredo V. N., Yugar-Toledo J. C., Martins L. C. Vascular stiffness and endothelial dysfunction: Correlations at different levels of blood pressure // Blood Press. — 2012. — Vol. 21 (1). — P. 31 — 38.
7.    Hirahatake K. M., Slavin J. L., Maki K. C., Adams S. H. Associations between dairy foods, diabetes, and metabolic health: Potential mechanisms and future directions // Metabolism. — 2014. — Vol. 17. — P. 26 — 49.
8.    Hirota A. H., Rodrigues C. J., Borges R. L. et al. Performance of two metabolic syndrome definitions in the estimation of cardiovascular disease among hypertensive patients // J. Clin. Hypertens — 2010. — Vol. 2 (8). — P. 588 — 596.
9.    Hynes R. O. Fibronectins // Sci. Am. — 2006. — Vol. 254. — P. 42 — 51.
10.    Green J., Yurdagul A.Jr., McInnis M. C. et al. Flow patterns regulate hyperglycemia-induced subendothelial matrix remodeling during early atherogenesis // Atherosclerosis. — 2014. — Vol. 232 (2). — P. 277 — 284.
11.    Levesque J., Lamarche B. The metabolic syndrome: definitions, prevalence and management // J. Nutrigenet Nutrigenomics. — 2008. — Vol. 1 (3). — P. 100 — 108.
12.    Lin J. D., Chang J. B., Wu C. Z. et al. Identification of insulin resistance in subjects with normal glucose tolerance // Ann. Acad. Med. Singapore. — 2014. — Vol. 43 (2). — P. 113 — 119.
13.    Mangiapane H. Cardiovascular disease and diabetes // Adv. Exp. Med. Biol. — 2012. — Vol. 771. — Р. 219 — 228.
14.    Nevelsteen I., Van den Bergh A., Van der Mieren G. et al. NO–dependent endothelial dysfunction in type II diabetes is aggravated by dyslipidemia and hypertension, but can be restored by angiotensin-converting enzyme inhibition and weight loss // J. Vasc. Res. — 2013. — Vol. 50 (6). — P. 486 — 497.
15.    Polovina M. M., Potpara T. S. Endothelial dysfunction in metabolic and vascular disorders // Postgrad. Med. — 2014. — Vol. 126 (2). — P. 38 — 53.
16.    Rana J. S., Nieuwdorp M., Jukema J. W., Kastelein J. J. Cardiovascular metabolic syndrome — an interplay of obesity, inflammation, diabetes and coronary heart disease // Diabetes Obes. Metab. — 2007. — Vol. 9. — P. 218 — 232.
17.    Reaven G. M. Banting lecture 1988. Role of insulin resistance in human disease // Diabetes. — 1988. — Vol. 37. — P. 1595 — 1607.
18.    Rizzoni D., Porteri E., Guelfi D. et al. Structural alterations in subcutaneous small arteries of normotensive and hypertensive patients with non-insulin-dependent diabetes mellitus // Circulation. — 2011. — Vol. 103. — P. 1238 — 1244.
19.    Takata H., Fujimoto S. Metabolic syndrome // Nihon. Rinsho. — 2013. — Vol. 71 (2). — P. 266 — 269.
20.    World Health Organization. Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications: report of a WHO Consultation. Part 1: diagnosis and classification of diabetes mellitus. — Geneva, Switzerland: World Health Organization, 1999.

Additional: P. 63-68.

Article received on February 14, 2016

The aim — to compare the effect of two methods of reperfusion therapy on the course and hospital consequences of acute coronary syndrome (ACS) with ST segment elevation, depending on the time of ischemia, the degree of risk on TІMІ and the type of primary percutaneous coronary intervention (PCI) in the clinical practice.
Materials and methods. A retrospective analysis was conducted of case histories of 286 patients with acute myocardial infarction (MI) with ST-segment elevation who were treated at Alexander Hospital in Kyiv in 2009 and 2011 —2013 and underwent PCI (171 patients) and thrombolytic therapy (TT) (115 patients). The patients were divided according to the risk on TІMІ, ischemia time and the type of PCI. The influence of these factors on hospital mortality, complications of MI and combined endpoints was analyzed.
Results and discussion. The groups had no differences in gender, age, comorbidities, MI localization. Time of ischemia was significantly longer in the PCI group — 8.4 ± 1.3 hours than in the TT group — 5.4 ± 0.8 h (p < 0.05). Significant differences were found between the groups in time «03 — balloon/needle»: it was 198.0 ± 10.7 min in the PCI group, which was significantly higher than in the TT group — 103.0 ± 14.1 min (p < 0.001). Patients of PCI group had significantly higher average risk on TІMІ 5.8 ± 0.2 than those of TT group 3.8 ± 0.2 (p < 0.001). The number of patients at risk of more than 5 points on TІMІ was bigger in the PCI group (102 (59.6 %) patients) than in the TT group (51 (44.3 %) patients, (p < 0.05)). Patients after PCI had a higher risk, longer time before hospitalization and ischemia, underwent reperfusion later than those after TT. When comparing the complications and mortality, primary PCI were more effective in patients with longer time of ischemia and higher risk. Hospital mortality was more dependent on the time of ischemia than on the risk. The highest mortality rate was in patients at high risk (TІMІ more than 5), with time of ischemia exceeding 4 hours who underwent TT — 12.9 %. The lowest mortality rate was in PCI and TT groups, among patients with a low risk, early hospitalization — 2.5 and 2.6 %, respectively.
Conclusions. In clinical practice, the primary PCI showed significant advantage over TT regarding hospital mortality and ischemic complications, mainly in patients hospitalized late and at high risk. Hospital mortality of patients with acute coronary syndrome with ST segment elevation without shock after primary PCI in clinical practice is more largely dependent on the time of ischemia than the risk. After TT it depends on both of these factors.

Keywords: acute coronary syndrome, primary coronary interventions, thrombolytic therapy, time of ischemia, risk stratification.

List of references:  
1.    Дзяк Г. В. Тромболитическая терапия при остром коронарном синдроме с элевацией сегмента ST: необходимо ли изменить стандарт реперфузионной терапии? // Укр. кардіол. журн. — 2004. — № 1. — С. 15 — 21.
2.    Нетяженко В. З., Мальчевська Т. Й., Ликов О. В. Реваскуляризаційні методи лікування гострого коронарного синдрому з елевацією сегмента ST // Внутр. медицина. — 2008. — № 3. — С. 50 — 54.
3.    Пархоменко А. Н., Лутай Я. М., Даншан Н. Украинский регистр острого инфаркта миокарда как фрагмент Европейского: характеристика больных, организация медицинской помощи и госпитальная терапия // Укр. мед. часопис. — 2011. — № 1. — С. 20 — 24.
4.    Соколов М. Ю. Реестр перкутанных коронарных вмешательств: сравнительный анализ, реперфузионная терапия в Украине, Сервей ПКВ — 2015 // Серце і судини. — 2015. — № 3 (51). — С. 7 — 30.
5.    Соколов Ю. Н., Терентьев В. Г., Соколов М. Ю. Интервенционные методы обследования и лечения больных с острой и хронической формами коронарного атеросклероза // Укр. кардіол. журн. — 2007. — № 5. — С. 26 — 36.
6.    Эрлих А. Д., Грацианский Н. А. Регистр Рекорд. Лечение больных с острыми коронарными синдромами в стационарах, имеющих и не имеющих возможности выполнения инвазивных коронарных процедур // Кардиол. — 2010. — № 7. — C. 8 — 14.
7.    Andersen H. R., Nielsen T. T., Rasmussen K. et al. A comparison of coronary angioplasty with fibrinolytic therapy in acute myocardial infarction // New Engl. J. Med. — 2003. — Vol. 349. — P. 733 — 742.
8.    Andersen H. R., Nielsen T. T., Vesterlund T. et al. Danish multicenter randomized study on fibrinolytic therapy versus acute coronary angioplasty in acute myocardial infarction: rationale and design of the Danish Trial in Acute Myocardial Infarction-2 (DANAMI-2) // Am. Heart J. — 2003. — Vol. 146. — P. 234 — 241.
9.    Aversano T., Aversano L. T., Passamani E. et al. Thrombolytic therapy vs primary percutaneous coronary intervention for myocardial infarction in patients presenting to hospitals without on-site cardiac surgery: a randomized controlled trial // JAMA. — 2002. — Vol. 287. — P. 1943 — 1951.
10.    Dharma S., Andriantoro H., Dakota I. et al. Organisation of reperfusion therapy for STEMI in a developing country // Open Heart. — 2015. — Vol. 2 (10). — P. 1136.
11.    Eagle K. A., Nallamothu B. K., Mehta R. H. et al. Trends in acute reperfusion therapy for ST-segment elevation myocardial infarction from 1999 to 2006: we are getting better but we have got a long way to go // Eur. Heart J. — 2008. — Vol. 29 (5). — P. 609 — 617.
12.    Grines C. L., Browne K. F., Marco J. et al. A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. The Primary Angioplasty in Myocardial Infarction Study Group // New Engl. J. Med. — 1993. — Vol. 328. — P. 673 — 679.
13.    Management of Acute Myocardial Infarction in patients presenting with ST-segment elevation // EHJ. — 2008. — Vol. 29. — P. 2909 — 2945.
14.    Melikian N., Morgan K., Beatt K. J. Can the published cost analysis data for delivery of an efficient primary angioplasty service be applied to the modern National Health Service? // Heart. — 2005. — Vol. 91. — P. 1262 — 1264.
15.    Morrow D. A. et al. Application of the TIMI Risk Score for ST-Elevation MI in the National Registry of Myocardial Infarction 3 // JAMA. — 2000. — Vol. 286. — P. 1356 — 1359.
16.    Morrow D. A. et al. TIMI Risk Score for ST-Elevation Myocardial Infarction: A Conveniet, Bedside, Clinical Score for Risk Assessment at Presentation: An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy // Circullation. — 2000. — Vol. 102. — P. 2031 — 2037.
17.    Nallamothu B. K., Antman E. M., Bates E. R. Primary percutaneous coronary intervention versus fibrinolytic therapy in acute myocardial infarction: does the choice of fibrinolytic agent impact on the importance of time-to-treatment? // Am. J. Cardiol. — 2004. — Vol. 94. — P. 772 — 774.
18.    Nallamothu B. K., Bates E. R., Herrin J. et al. Times to treatment in transfer patients undergoing primary percutaneous coronary intervention in the United States: National Registry of Myocardial Infarction (NRMI)-3/4 analysis // Circulation. — 2005. — Vol. 111 (6). — P. 761 — 767.
19.    Ratcliffe A. T., Pepper C. Thrombolysis or primary angioplasty? Reperfuion therapy for myocardial infarction in the UK // Postgrad. Med. J. — 2008. — Vol. 84. — P. 73 — 77.
20.    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 // J. Am. Soc. Echocardiogr. — 2005. — 18. — P. 1440 — 1463.
21.    Tarantini G. Acceptable reperfusion delay to prefer primary angioplasty over fibrin-specific thrombolytic therapy is affected (mainly) by the patient’s mortality risk: 1 h does not fit all // Eur. Heart J. — 2010. — Vol. 31. — 676 — 683.
22.    The GUSTO IIb investigators. A clinical trial comparing primary coronary angioplasty with tissue plasminogen activator for acute myocardial infarction. The Global Use of Strategies to Open Occluded Coronary Arteries in Acute Coronary Syndromes (GUSTO 838 lib) Angioplasty Substudy Investigators // New Engl. J. Med. — 1997. — Vol. 336. — P. 1621 — 1628.
23.    Thune J. J., Hoefsten D. E., Lindholm M. G. et al. Simple Risk Stratification at Admission to Identify Patients With Reduced Mortality From Primary Angioplasty // Circulation. — 2005. — Vol. 112 (13). — P. 2017 — 2021.
24.    Widimsky P., Budesinsky T., Vorac D. et al. Long distance transport for primary angioplasty vs results of the randomized national multicentre trial — PRAGUE-2 // Eur. Heart J. — 2003. — Vol. 24. — P. 94 — 104.
25.    Widimsky P., Groch L., Zelizko M. et al. Multicentre randomized trial comparing transport to primary angioplasty vs immediate thrombolysis vs combined strategy for patients with acute myocardial infarction presenting to a community hospital without a catheterization laboratory. The PRAGUE study // Eur. Heart J. — 2000. — Vol. 21. — P. 823 — 831.
26.    Zahn R., Schiele R., Schneider S. et al. Primary angioplasty versus intravenous thrombolysis in acute myocardial infarction: can we define subgroups of patients benefiting most from primary angioplasty? Results from the pooled data of the Maximal Individual Therapy in Acute Myocardial Infarction Registry and the Myocardial Infarction Registry // J. Am. Coll. Cardiol. — 2001. — Vol. 37 (7). — P. 1827 — 1835.
27.    Zijlstra F., Patel A., Jones M. et al. Clinical characteristics and outcome of patients with early (< 2 h), intermediate (2 — 4 h) and late (> 4 h) presentation treated by primary coronary angioplasty or thrombolytic therapy for acute myocardial infarction // Eur. Heart J. — 2002. — Vol. 23 (7). — P. 550 — 557.

Additional: P. 71-78.

Article received on March 11, 2016

The second part of the review is dedicated to the problem of resistance to antiplatelet effect of acetylsalicylic acid (ASA) with the focus on importance of revealing of pseudoresistance, which, in contrast to its true form, may be overcоme. Special considerations are given for recommendations of ASA use in patients with diabetes according to current 2013 European Society of Cardiology Guidelines on diabetes, pre-diabetes, and cardiovascular diseases with emphasis on ways of overcoming the resistance. Enteric coating formulation of ASA as one of the most significant causes of its reduced antiplatelet effect became main topic for discussion in this part of the review. Influence of enteric coating on ASA absorption is described. The mechanism of influence of enteric coating on ASA absorption is shown. Data from several studies are shown, suggesting that resistance to antiplatelet effect of ASA is caused by enteric coating, underdosing, and modifiable risk factors (e.g., patient’s non-compliance to treatment) rather than genetic factors. The assumption was made that cautious attitude is needed to the enteric coating of ASA formulations during cardiovascular prophylaxis in the context of results from the recent studies.

Keywords: acetylsalicylic acid, resistance, pseudoresistance, modifiable risk factors, enteric coating formulation, bioavailability, clinical study.

List of references:  
1.    Bochner F., Somogyi A. A., Wilson K. M. Bioinequivalence of four 100 mg oral aspirin formulations in healthy volunteers // Clin. Pharmacokinet. — 1991. — Vol. 21. — P. 394 — 399.
2.    Campbell C. L., Smyth S., Montalescot G. et al. Aspirin Dose for the Prevention of Cardiovascular Disease. A systematic Review // JAMA. — 2007. — Vol. 297, N 18. — P. 2018 — 2024.
3.    Cox D., Maree A. O., Dooley M. et al. Effect of enteric coating on antiplatelet activity of low-dose aspirin in healthy volunteers // Stroke. — 2006. — Vol. 37 (8). — P. 2153 — 2158.
4.    DiChiara J., Bliden K. P., Tantry U. S. et al. The effect of aspirin dosing on platelet function in diabetic and nondiabetic patients: an analysis from the aspirin-induced platelet effect (ASPECT) study/ // Diabetes. — 2007. — Vol. 56. — P. 3014 — 3019.
5.    Dillinger J. G., Drissa A., Sideris G. et al. Biological efficacy of twice daily aspirin in type 2 diabetic patients with coronary artery disease // Am. Heart J. — 2012. — Vol. 164. — P. 600 — 606.
6.    Edlund M. Sugar Coating Aspirin / M. Edlund, 18 декабря 2012 [Электронный ресурс]. — Режим доступа: https: // therestdoctor.wordpress.com/2012/12/18/sugar-coating-aspirin-121912/ [Просмотрено 29.05.2015].
7.    Enteric Coating as a Factor in Aspirin Resistance [Электронный ресурс]. — Режим доступа: http://www.druglib.com/trial/62/NCT00531362.html [Просмотрено 29.05.2015].
8.    Evangelista V., de Berardis G., Totani L. et al. Persistent platelet activation in patients with type 2 diabetes treated with low doses of aspirin // J. Thromb. Haemost. — 2007. — Vol. 5. — P. 2197 — 2203.
9.    Gasparyan A. Y., Watson T., Lip G. Y. The role of aspirin in cardiovascular prevention: implications of aspirin resistance // J. Am. Coll. Cardiol. — 2008. — Vol. 51 (19). — P. 1829 — 1843.
10.    Grosser T., Fries S., Lawson J. A. et al. Drug Resistance and Pseudoresistance: An Unintended Consequence of Enteric Coating Aspirin // Circulation. — 2013. — Vol. 127 (3). — P. 377 — 385.
11.    Haastrup P. F., Grønlykke Th., Jarbøl D. E. Enteric сoating can lead to reduced antiplatelet effect of low-dose acetylsalicylic acid // Basic Clin. Pharmacol. Toxicol. — 2015. — Vol. 116. — Р. 212 — 215.
12.    Hankey G. J., Eikelboom J. W. Aspirin resistance // Lancet. — 2006. — Vol. 367. — P. 606 — 617.
13.    Helgason C. M., Tortorice K. L., Winkler S. R. et al. Aspirin response and failure in cerebral infarction // Stroke. — 1993. — Vol. 24 (3). — P. 345 — 350.
14.    Kasotakis G., Pipinos I. I., Lynch T. G. Current evidence and clinical implications of aspirin resistance // J. Vasc. Surg. — 2009. — Vol. 50 (6). — P. 1500 — 1510.
15.    Maree A., Curtin R., Dooley M. et al. Platelet response to low-dose enteric-coated aspirin in patients with stable cardiovascular disease // J. Am. Coll. Cardiol. — 2005. — Vol. 46. — P. 1258 — 1263.
16.    Michelson A. D., Cattaneo M., Eikelboom J. W. et al. Aspirin resistance: position paper of the Working Group on Aspirin Resistnce // J. Thromb. Haemost. — 2005. — Vol. 3 (6). — P. 1309 — 1311.
17.    Mousavi M., Salehimarzijarani B., Dadvar Z. et al. Relationship between continuous use of low-dose enteric-coated aspirin and gastrointestinal injuries in patients with gastrointestinal hemorrhage // Turk. J. Gastroenterol. — 2013. — Vol. 24 (2). — P. 93 — 98.
18.    Muir N., Nichols J. D., Clifford J. M. et al. The influence of dosage form on aspirin kinetics: implications for acute cardiovascular use // Curr. Med. Res. Opin. — 1997. — Vol. 13. — P. 547 — 553.
19.    Murri N. Aspirin “Resistance”: Is There an Elephant in the Room? — 2009 [Электронный ресурс]. — Режим доступа: http://www.medscape.com/viewarticle/702347 [Просмотрено 30.05.2015]
20.    Patrono C., Ciabattoni G., Patrignani P. et al. Clinical pharmacology of platelet cyclooxygenase ingibition // Circulation. — 1985. — Vol. 72. — P. 177 — 184.
21.    Peace A., Mccall M., Tedesco T. et al. The role of weight and enteric coating on aspirin resistance in cardiovascular patients // J. Thromb. Haemost. — 2010. — Vol. 8. — P. 2323 — 2325.
22.    Pulcinelli F. M., Biasucci L. M., Riondino S. et al. COX-1 sensitivity and thromboxane A2 production in type 1 and type 2 diabetic patients under chronic aspirin treatment // Eur. Heart J. — 2009. — Vol. 30. — P. 1279 — 1286.
23.    Rocca B., Santilli F., Pitocco D. et al. The recovery of platelet cyclooxygenase activity explains interindividual variability in responsiveness to low-dose aspirin in patients with and without diabetes // J. Thromb. Haemost. — 2012. — Vol. 10. — P. 1220 — 1230.
24.    Rydén L., Grant P., Anke S. D. et al. 2013 ESC Guidelines on diabetes, pre-diabetes, and cardiovascular diseases developed in collaboration with the EASD/ The Task Force on diabetes, pre-diabetes, and cardiovascular diseases of the European Society of Cardiology in collaboration with the European Association for the Study of Diabetes // Eur. Heart J. — 2013. — Vol. 34. — P. 3035 — 3087.
25.    Sagar K. A., Smyth M. R. A comparative bioavailability study of different aspirin formulations using on-line multidimensional chromatography // J. Pharm. Biomed. Anal. — 1999. — Vol. 21. — P. 383 — 392.
26.    Schwartz K.A., Schwartz D.E., Barber K. et al. Non-compliance is the predominant cause of aspirin resistance in chronic coronary arterial disease patients // J. Transl. Med. — 2008 [Электронный ресурс]. — Режим доступа: http://www.translational-medicine.com/content/6/1/46 [Просмотрено 29.05.2015].

Additional: P. 73-85.

Article received on January 19, 2016

The article is dedicated to the clinical case of the tactics of endovascular treatment of ischemic heart disease in patient with an allergic reaction to iodinated radiopaque drugs. Efficacy of gadobutrol was demonstrated which is a paramagnetic contrast agent and is used for magnetic resonance imaging. The presented case report demonstrates that all patients before the diagnostic tests, which use contrast agents, require detailed examination, premedication and use of low-osmolar agents.

Keywords: ischemic heart disease, endovascular treatment, iodinated radiopaque agents, gadobutrol, allergic reaction.

List of references:  
1.    Зубарев А. В. Методы медицинской визуализации — УЗИ, КТ, МРТ — в диагностике опухолей и кист печени. — М.: Видар, 1996. — С. 46 — 58.
2.    Клиническая аллергология: Рук-во для практических врачей / Под ред. Р. М. Хаитова. — М.: МЕДпресс-информ, 2002. — С. 624 — 626.
3.    Клиническая иммунология и аллергология / Под ред. Г. Лолора, Т. Фишера, Д. Адельмана. — М.: Практика, 2000. — С. 357 — 393.
4.    Линденбратен. Л. Д., Королюк И. П. Медицинская радиология. — 2-е изд. — М.: Медицина, 2000. — С. 617 — 619.
5.    Терновой С. К., Синицын В. Е., Гагарина Н. В. Неинвазивная диагностика атеросклероза и кальциноза коронарных артерий. — М.: Атмосфера, 2003. — С. 140 — 144.
6.    Akhtar N. J., Markowitz A. H., Gilkeson R. C. Multidetector computed tomography in the preoperative assessment of cardiac surgery patients // Radiol. Clin. North Am. — 2010. — 48 (1). — P. 117 — 139H.
7.    McCullough P. A. Effects of Intra-Arterial and Intravenous Iso-Osmolar Contrast Medium (Iodixanol) on the Risk of Contrast-Induced Acute Kidney Injury: A Meta-аnalysis // Cardiorenal. Med. — 2011. — Vol. 1. — P. 220 — 234.
8.    Strijkers G. J., Mulder W. J., van Tilborg G. A., Nicolay K. MRI contrast agents: current status and future perspectives // Anticancer Agents Med. Chem. — 2007. — 7 (3). — P. 291 — 305.

Additional: P. 86-88.

Article received on March 1, 2016

Multi atherosclerotic lesions of peripheral arteries are the main cause of severe chronic lower limb ischemia. A clinical case is presented of successful endovascular treatment of a patient with chronic occlusion of the external iliac artery and occlusion of the femoral artery from the contralateral side. As a result of the operation, occluded arterial segments were completely canalized and satisfactory therapeutic effect was achieved with minimum operational trauma using one percutaneous access.

Keywords: endovascular recanalization, iliac occlusion.

List of references:  
1.    Белов Ю. В., Степаненко А. Б., Гене А. П., Халилов И. Г. Хирургическое лечение больных с множественным поражением артерий нижних конечностей // Ангиология и сосудистая хирургия. — 2002. — № 1. — С. 72 — 79.
2.    Мишалов В. Г., Черняк В. А. Окклюзионная болезнь периферических артерий: что мы можем сделать для пациента уже сегодня // Практична ангiологiя. — 2011. — № 1. — C. 12 — 19.
3.    Cioppa A., Stabile E., Popusoi G. et al. Combined treatment of heavy calcified femoro-popliteal lesions using directional atherectomy and a paclitaxel coated balloon: one-year single centre clinical results // Cardiovasc. Revasc. Med. — 2012. — 13. — P. 219 — 223.
4.    Egorova N. N., Guillerme S., Gelijns A. et al. An analysis of the outcomes of a decade of experience with lower extremity revascularization including limb salvage, lengths of stay, and safety // J. Vasc. Surg. — 2010. — 51. — P. 878 — 885.
5.    Fanelli F., Cannavale A., Gazzetti M. et al. Calcium burden assessment and impact on drug-eluting balloons in peripheral arterial disease // Cardiovasc. Intervent. Radiol. — 2014. — 37. — P. 898 — 907.
6.    Fowkes F., Leng G. C. Bypass surgery for chronic lower limb ischaemia // Cochrane Vascular Group, The Cochrane Collaboration. — 2008.
7.    Fowkes F. G., Murray G. D., Butcher I. et al. Ankle brachial index combined with Framingham risk score to predict cardiovascular events and mortality: a meta-analysis // JAMA. — 2008. — 300. — P. 197 — 208.
8.    Norgren L., Hiatt W. R., Dormandy J. A. et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II) // Eur. J. Vasc. Endovasc. Surg. — 2007. — Vol. 33. — P. S1 — 75.

Additional:

The variety of diseases, which can be complicated by coronaritis, is a challenge for physicians of different specialties. In practice, the etiology of coronaritis is often difficult to determine because of obscure and atypical clinical symptoms, objective difficulties of diagnosis. Thе article presents an autopsy case of coronaritis in a five-years-old boy with renal hypoplasia and clinical manifestations of acute myocardial infarction. The identity of coronaritis is difficult to verify because of the lack of clinical information on the beginning and progression of the disease. Pathomorphological changes of the coronary arteries are likely to be identified as coronaritis caused by Kawasaki disease.

Keywords: coronaritis, hypoplastic kidneys, Kawasaki disease.

List of references:  
1.    Дядык А. И. Кардиоренальные и ренокардиальные синдромы // Серцева недостатність. — 2009. — № 2. — С. 10 — 19.
2.    Дядык А. И., Холопов Л. С., Зборовский С. Р. и др. Системные васкулиты в современной клинической практике / Под ред. А. И. Дядыка. — Донецк: Издатель Заславский А. Ю., 2013. — 248 с.
3.    Морфологічні аспекти ангіології: Матер. Всеукр. наук.-практ. конф., 24 — 25 жовтня 2013 р. / МОЗ України. — Тернопіль: ТДМУ: Укрмедкнига, 2013. — 207 с.
4.    Стрижаков Л. А. Коронарит при ревматических заболеваниях: обзор литературы // Фарматека. — 2012. — № 6. — С. 16 — 19.
5.    Толстикова Т. В. Поражение сердца при инфекционном мононуклеозе у детей: Автореф. дис. ...канд. мед. наук: спец. 14.00.09 Педиатрия. — Красноярск, 2009. — 20, [1] c.
6.    Eaden J., Peckham D. Myocardial infarction in an adult with cystic fibrosis and heart and lung transplant // Multidisciplin. Resp. Med. — 2013. — № 8. — P. 1 — 5.
7.    Egier D. Kawasaki Disease: A Review of the epidemiology, clinical features, and management of a paediatric condition // UWOMJ. — 2006. — N 74 (2). — P. 36 — 39.
8.    McCrindle B. W. Kawasaki: A childhood disease with important consequences into adulthood // Circulation. — 2009. — N 120. — P. 6 — 8.
9.    Rowley A. H., Shulman S. T. Kawasaki syndrome // Clin. Microbiol. Rev. — 1998. — N 11 (3). — P. 405 — 414.
10.    To L., Krazit S. T., Kaye A. D. Perioperative consideration of Kawasaki disease // Ochsner J. — 2013. — N 13 (2). — P. 208 — 213.

Additional: P. 94-98.

Article received on September 22, 2015

Thromboangiitis obliterans (Buerger’s disease) is a systemic vasculitis that affects small-and medium-sized arteries and veins of distal parts of upper and lower extremities, usually occurring in male smokers younger than 45 years of age. The clinical picture presented symptoms of disorders of blood circulation of the limbs and migratory thrombophlebitis. In the absence of specific laboratory and instrumental criteria, the diagnosis was made by differential diagnostics with atherosclerotic obliterating lesions of arteries, diabetic angiopathy, hereditary and acquired thrombophilia, systemic connective tissue diseases. Pathomorphological study aims at identifying vascular changes characteristic of Buerger’s disease: hyperplasia of artery intima by capillary angiomatosis type; obstruction of blood clots; lack of calcification of tunica media; panphlebitis with intima hyperplasia. Buerger’s disease treatment involves the elimination of possible etiological factors — smoking, occupational exposures. Drug therapy is represented by antiischemic drugs: prostaglandin analogues (iloprost), type 3 phosphodiesterase inhibitors (cilostazol), calcium channel antagonists (amlodipine), methylxanthine derivatives (pentoxifylline), antiplatelet agents (acetylsalicylic acid), as well as anti-inflammatory agents. Standard reconstructive surgery on the arteries is not sufficiently effective due to diffuse inflammatory process, predominantly in distal localization of the affected vessels. The most effective methods of revascularization in Buerger’s disease are arterialization of venous blood flow in the foot, resection of the posterior tibial veins and transplantation of greater omentum in the shin.

Keywords: systemic vasculitis, thromboangiitis obliterans, Buerger’s disease, symptoms, diagnosis, pathomorphological study, treatment.

List of references:  
1.    Багрій М. М. Облітеруючий тромбангіїт (хвороба Бюргера): захворюваність та пошук етіологічних стимулів // Укр. мед. часопис. — 2006. — № 2. — С. 76 — 79.
2.    Багрій М. М., Сливка В. І. Варіанти клінічного перебігу облітеруючого тромбангіїту (хвороби Бюргера) // Серце і судини. — 2006. — № 1. — C. 112 — 117.
3.    Багрій М. М., Сливка В. І. Облітеруючий тромбангіїт (хвороба Бюргера): патоморфологічні зміни у судинах ампутованих нижніх кінцівок // Патологія. — 2007. — № 2. — C. 76 — 80.
4.    Вачёв А. Н., Михайлов М. С., Новожилов А. В., Черновалов Д. А. Хирургические аспекты трансплантации большого сальника на нижнюю конечность у больных облитерирующим тромбангиитом // Хирургия. Журн. им. Н. И. Пирогова. — 2011. — № 12. — C. 19 — 22.
5.    Затевахин И. И., Юдин Р. Ю., Комраков В. Е. Облитерирующий тромбангиит. — М., 2002. — 317 с.
6.    Зербино Д. Д. Васкулиты и ангиопатии. — К.: Здоровье, 1977. — 100 с.
7.    Зербино Д. Д. Патологоанатомическая характеристика системных васкулитов // Второй съезд патологоанатомов УССР. — Черновцы, 1976. — С. 7 — 9.
8.    Национальные рекомендации по ведению пациентов с заболеваниями артерий нижних конечностей // Ангиол. и сосуд. хирург. — 2013. — № 2. — 67 с.
9.    Національний підручник з ревматології / За ред. В. М. Коваленка, Н. М. Шуби. — К.: Моріон, 2013. — 672 с.
10.    Покровский А. В., Дан В. Н., Чупин А. В. Артериализация венозного кровотока стопы в спасении конечности от ампутации у больных облитерирующим тромбангиитом с окклюзией артерий голени и стопы при критической ишемии // Ангиол. и сосуд. хирург. — 2000. — № 1. — С. 86 — 89.
11.    Buerger L. Thrombo-angiitis obliterans: a study of the vascular lesions leading topresenile spontaneous gangrene // Am. J. Med. Sci. — 1908. — Vol. 136. — P. 567 — 580.
12.    De Haro J., Bleda S., Acin F. Initial evidence in thromboangiitis obliterans (Buerger’s disease) treatment with bosentan // EMJ Cardiol. — 2013. — Vol. 1. — P. 96 — 100.
13.    Fazeli B. Buerger’s disease as an indicator of socioeconomic development in different societies, a crosssectional descriptive study in the North-East of Iran // Arch. Med. Sci. — 2010. — Vol. 6. — P. 343 — 347.
14.    Ferry Fred F. Ferri’s clinical advisor 5 books in 1. — Philadelphia: Elsevier Mosby, 2015. — P. 1158.e2 — 1158.e4.
15.    Guideline for management of vasculitis syndrome JCS 2008 // Circ. J. — 2011. — Vol. 75. — P. 474 — 503.
16.    Heno P., Fourcade L., N’Guyen D. H. Buerger’s disease and coronary disease // Arch. Mal. Coeur. Vaiss. — 2000. — Vol. 93 (10). — P. 1239 — 1242.
17.    Hoffman G. S., Weyand C. M., Langford C. A., Goronzy J. J. Inflammatory diseases of blood vessels.— 2nd edition. — Blackwell Publishing Ltd., 2012. — 567 p.
18.    Igari K., Inoue Y., Iwai T. The epidemiologic and clinical findings of patients with Buerger disease // Ann. Vasc. Surg. — 2016. — Vol. 30. — P. 263 — 269.
19.    Jennette J. C., Falk R. J., Bacon P. A. et al. 2012 Revised International Chapel Hill Consensus Conference Nomenclature of Vasculitides // Arthritis. Rheum. — 2013. — Vol. 65. — P. 1 — 11.
20.    Maturana I. L., Rodriguez J., González C. et al. Chronic ulcers in thromboangiitis obliterans (Buerger’s disease): updating epidemiology, physiopathology, and bosentan — a novel strategy of therapy // Hindawi Publishing Corporation, 2013. — Ulcers Volume. — 6 p.
21.    Mills J. L. Buerger ’s disease in the 21st century: diagnosis, clinical features, and therapy // Sem. Vasc. Surg. — 2003. — Vol. 16. — P. 179 — 189.
22.    Papa M., Rabi I., Adar R. A point scoring system for the clinical diagnosis of Buerger’s disease // Eur. J. Vasc. Endovasc. Surg. — 1996. — Vol. 11. — P. 335 — 339.
23.    Salimi J., Tavakkoli H., Salimzadeh A. et al. Clinical characteristics of Buerger’s disease in Iran // J. Coll. Phys. Surg. Pakistan. — 2008. — Vol. 18 (8). — P. 502 — 505.
24.    Sasaki S., Sakuma M., Kunihara T., Yasuda K. Distribution of arterial involvement in thromboangiitis obliterans (Buerger’s disease): results of a study conducted by the intractable vasculitis syndromes research group in Japan // Surgery Today. — 2000. — Vol. 30. — P. 600 — 605.
25.    Shionoya S. Diagnostic criteria of Buerger’s disease // Int. J. Cardiol. — 1998. — Vol. 66. — P. 243 — 245.
26.    Von Winiwarter F. Über eine eigenthümliche form von endarteritis und endophlebitis mit gangrän des fusses // Arch. Klin. Chir. — 1879. — Vol. 23. — P. 202 — 206.

Additional: P. 99-106.

Article received on February 23, 2016

Cardiovascular diseases and osteoporosis come first in the structure of deaths of residents of Ukraine. There is a hypothesis that calcification of blood vessels, which is a risk factor for cardiovascular disasters, increases due to the calcium exit out of the depot — the bone tissue — and its accumulation in the blood vessels, but the mechanisms of this process are not clear. According to many studies, the risk of osteoporotic fractures in patients with echogenic plaques in the carotid arteries is higher than in patients with normal vessels. At present, two types of vascular calcification are distinguished — that of intima (as focal calcification of atherosclerotic plaque) and that of media (as part of arteriolosclerosis development caused, for example, by secondary hyperparathyroidism in chronic kidney disease). It remains unknown which type of calcification is accelerated by the decrease in bone mineral density. Also, doctors have a problem of choice of drugs that would affect both pathogenic mechanisms, significantly improving the results of treatment. There are no answers to questions about the connection between the development of atherosclerosis, aterocaltsynosis and osteoporosis in men. In the current medical literature there is not enough information on the structural and functional state of bone tissue in patients with stenosing atherosclerosis of the coronary vessels that have suffered cardiovascular disasters (heart attacks, strokes), and the likelihood of bone fractures in them according to FRAX calculator. These issues require further study.

Keywords: osteoporosis, atherosclerosis, сalcification, arteriolosclerosis.

List of references:  
1.    Аникин С. Г., Боневоленская Л. И. Остеопороз и кардиоваскулярные заболевания // Научно-практическая ревматология. — 2006. — № 5. — С. 39 — 45.
2.    Байдак М. М. Состояние минеральной плотности костной ткани у женщин репродуктивного возраста при нейрообменном синдроме // Акушерство и гинекология. — 1996. — № 2. — С. 33 — 36.
3.    Бутенко Г. М. Остеопороз и иммунная система // Остеопороз: эпидемиология, клиника, диагностика, профилактика и лечение / Под ред. Н. А. Коржа, В. В. Поворознюка, Н. В. Дедух, И. А. Зупанца. — Харьков: Золотые страницы, 2002. — С. 55 — 59.
4.    Ильяш М. Г. Сучасний стан та тенденції інвалідності внаслідок серцево-судинних захворювань населення України працездатного віку // Укр. кардіол. журн. — 2006. — Спец. вип. — С. 65 — 67.
5.    Лузин В. И., Иванова Л. Н., Нишкумай О. И., Горошко С. А. Особенности прочности костей у белых крыс старческого возраста, получавших диету с повышенным содержанием холестерина // Проблеми остеології. — 2003. — Т. 7, № 3 — 4. — С. 23 — 25.
6.    Лякишев А. А. Кальциноз коронарных артерий, факторы риска ишемической болезни сердца, С-реактивный белок и атеросклеротические сердечно–сосудистые осложнения // Кардиол. — 2005. — № 45. — С. 34 — 40.
7.    Методичні рекомендації Асоціації кардіологів України: Дисліпідемії: діагностика, профілактика та лікування / За ред. проф. Мітченко О. І., Лутай М. І. — К., 2011. — С. 12 — 48.
8.    Остеопороз: эпидемиология, клиника, диагностика, профилактика и лечение / Под ред. Н. А. Коржа, В. В. Поворознюка, Н. В. Дедух, И. А. Зупанца. — Харьков: Золотые страницы, 2002. — 648 с.
9.    Поворознюк В. В., Григор’єва В. В. Менопауза та остеопороз. — К., 2005. — 356 с.
10.    Поворознюк В. В., Григорьева Н. В. Менопауза и костно-мышечная система. — К.: Эспресс, 2004. — 512 с.
11.    Руководство по кардиологии / Под ред. Н. В. Коваленко. — К.: Морион, 2008. — С. 635 — 706.
12.    Серцево-судинні захворювання. Рекомендації з діагностики, профілактики та лікування / За ред. В. М. Коваленка, М. І. Лутая. — К.: Моріон, 2011. — С. 13 — 15.
13.    Соломенчук Т. М., Скибчик В. А. Атерогенна дисліпідемія чи ксенобіотики: що насамперед визначає кардіоваскулярний ризик в осіб віком до 50 років? // Укр. мед. часопис. — 2006. — № 3. — С. 84 — 89.
14.    Сорока Н. Ф., Зібалова Т. С. Роль активации цитокинов в развитии и прогрессировании хронической сердечной недостаточности // Медицинские новости. — 2003. — № 1. — С. 12 — 15.
15.    Ярема Н. І. Вплив лізиноприлу на мінеральну щільність кісток і вегетативну регуляцію у жінок з есенціальною гіпертензією у період постменопаузи // Укр. кардіол. журн. — 2006. — № 2. — С. 86 — 89.
16.    Abedin M., Omland T., Ueland T. et al. Relation of osteoprotegerin to coronary calcium and aortic plaque (from the Dallas Heart Study) // Am. J. Cardiol. — 2007. — Vol. 99. — P. 513 — 518.
17.    Abedin M., Tintut Y., Demer L. L. Vascular calcification: mechanisms and clinical ramifications // Arterioscler. Thromb. Vasc. Biol. — 2004. — Vol. 24. — P. 1161 — 1170.
18.    Arko B., Prezelj J., Kocijancic A. et al. Association of the osteoprotegerin gene polymorphism with bone mineral density in postmenopausal women // Maturitas. — 2005. — Vol. 51. — P. 270 — 279.
19.    Armstrong Z. B., Boughner D. R., Drangova M., Rogers K. A. Angiotensin II type 1 receptor blocker inhibits arterial calcification in a preclinical model // Cardiovasc. Res. — 2011. — Vol. 90. — P. 165 — 170.
20.    Bagger Y. Z., Rasmussen H. B., Alexandersen P. et al. Link between cardiovascular disease and osteoporosis in postmenopausal women: serum lipids or atherosclerosis per se? // Osteoporosis Int. — 2007. — Vol. 18. — P. 505 — 512.
21.    Bagger Y. Z., Tanko L. B. Radiographic measure of aorta calcification is a sitespecific predictor of bone loss and fracture risk at the hip // J. Intern. Med. — 2006. — Vol. 259. — P. 598 — 605.
22.    Baldini V., Mastropasqua M., Francucci C. M., D’Erasmo E. Cardiovascular disease and osteoporosis // J. Endocrinol. Invest. — 2005. — Vol. 28, suppl. 10. — Р. 69 — 72.
23.    Bennett B. J., Scatena M., Kirk E. A. et al. Osteoprotegerin inactivation accelerates advanced atherosclerotic lesion progression and calcification in older ApoE-/- mice // Arterioscler. Thromb. Vasc. Biol. — 2006. — Vol. 26. — P. 2117 — 2124.
24.    Bolland M. J., Avenell A., Baron J. A. et al. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis // BMJ. — 2010. — Vol. 341. — P. 3691.
25.    Brownbill R. A., Illich J. Z. Lipid profile and bone paradox: higher serum lipids are assotiated with higher bone mineral density in postmenopausal women // J. Womens Health. — 2006. — Vol. 15. — P. 261 — 270.
26.    Bucay N., Sarosi I., Dunstan C. R. et al. Osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification // Genes Dev. — 1998. — Vol. 12. — P. 1260 — 1268.
27.    Camargo C. A. Vitamin D and Cardiovascular Disease // JACC. — 2011. — Vol. 58, N 14. — P. 1442 — 1444.
28.    Carbone L. D., Cross J. D., Raza S. H. et al. Fracture Risk in Men With Congestive Heart Failure // JACC. — 2008. — Vol. 52, N 2. — P. 135 — 138.
29.    Cecelja M., Jiang B., Bevan L. et al. Arterial Stiffening Relates to Arterial Calcification But Not to Noncalcified Atheroma in Women // JACC. — 2011. — Vol. 57, N 13. — P. 1480 — 1485.
30.    Demer L. L., Tintut Y. Vascular calcification: pathobiology of a multifaceted disease // Circulation. — 2008. — Vol. 117. — P. 2938 — 2948.
31.    Dupuy A. M., Carriere L., Scali J. et al. Lipid levels and cardivascular risk in elderly women: a general population study of the effects of hormonal treatment and lipid–lowering agents // Climacteric. — 2008. — Vol. 11. — Р. 74 — 83.
32.    Dweck M. R., Boon N. A., Newby D. E. Calcific Aortic Stenosis A Disease of the Valve and the Myocardium // JACC. — 2012. — Vol. 60. — P. 1854 — 1860.
33.    Grandi N. C., Breitling L. P., Brenner H. Vitamin D and cardiovascular disease: systematic review and meta-analysis of prospective studies // Prev. Med. — 2010. — Vol. 51. — P. 228 — 233.
34.    Hamerman D. Osteoporosis and atherosclerosis: biological linkages and the emergence of dual–purpose therapies // QJM. — 2005. — Vol. 98, N 7. — P. 467 — 484.
35.    Hofbauer L. C., Brueck C. C., Shanahan C. M. et al. Vascular calcification and osteoporosis – from clinical observation towards molecular understading // Osteoporosis Int. — 2007. — Vol. 18. — P. 251 — 259.
36.    Hofbauer L. C., Schoppet M. Osteoprotegerin: a link between osteoporosis and arterial calcification? // Lancet. — 2006. — Vol. 358. — P. 257 — 259.
37.    Isidori A. M., Giannetta E., Pozza C. et al. Androgens, cardiovascular disease and osteoporosis // J. Endocrinol. Invest. — 2005. — Vol. 28 (10). — P. 73 — 79.
38.    Jahnus R. Cross-cectional analysis of baseline date to identify the major determinants of carotid intima-media thickness in a Europen population the IMPROVE study // Eur. Heart J. — 2010. — Vol. 31. — P. 614 — 622.
39.    Jamada Y., Ando F., Niino N. et al. Association of polymorphism of paraoxonase 1 and 2 genes, alone or in combination, with bone mineral density in community-dwelling Japanese // J. Hum. Genet. — 2003. — Vol. 48. — P. 469 — 475.
40.    Johnson R. C., Leopold J. A., Loscalzo J. Vascular calcification: pathobiological mechanisms and clinical implications // Circ. Res. — 2006. — Vol. 99. — P. 1044 — 1059.
41.    Jorgensen L., Joakimsen O., Mathiesen E. B. et al. Carotid plague echogenicity and risk of nonvertebral fractures in women: a longitudinal population-based study // Calcif. Tissue. Int. — 2006. — Vol. 79 (4). — P. 207 — 213.
42.    Kalra S. S., Shanahan C. M. Vascular calcification and hypertension:cause and effect // Ann. Med. — 2012. — Vol. 44, suppl. 1. — P. S85 — 92.
43.    Kelly-Arnold A., Maldonado N., Laudier D. et al. Revised microcalcification hypothesis for fibrous cap rupture in human coronary arteries // Proc. Natl. Acad. Sci. U S A. — 2013. — Vol. 110. — P. 10741 — 10746.
44.    Kestenbaum B., Katz R., de Boer I. et al. Vitamin D, parathyroid hormone, and cardiovascular events among older adults // J. Am. Coll. Cardiol. — 2011. — Vol. 58. — P. 1433 — 1441.
45.    Lee J. H., O`Keefe J. H., Belletal. Vitamin D Deficiency. An Important, Common, and Easily Treatable Cardiovascular Risk Factor? // JACC. — 2008. — 52 (24). — P. 1949 — 1955.
46.    Li J. J., Zhu C. G., Yu B. et al. The role of inflamation in coronary artery calcification // Ageing Res. — 2007. — Vol. 6 (4). — P. 263 — 270.
47.    Lorenz M. W., Markus H. S., Bots M. L. et al. Prediction of clinical cardiovascular events with carotid intima-media thickness: a systematic review and meta-analysis // Circulation. — 2007. — Vol. 115. — P. 459 — 467.
48.    Luegmayr E., Glantschnig H., Wesolowski G. A. et al. Osteoclast formation, survival and morphology are highly dependent on exogenous cholesterol/ lipoproteins // Cell. Death and Differentiation. — 2004. — Vol. 11. — P. 108 — 118.
49.    Madhavan M. V., Tarigopula M., Mintz G. S. et al. Coronary Artery Calcification Pathogenesis and Prognostic Implications // JACC. — 2014. — Vol. 63, N 17. — P. 1701 — 1711.
50.    Mauriège P., Roussel M., Garnier S. et al. Impact of a walking program on the metabolic risk profile of obese postmenopausal women // Maturitas. — 2009. — Vol. 63, suppl. 1. — P. S27.
51.    Meier C. R., Schlienger R. G., Kraenzlin M. E. et al. HmG-CoA reductase inhibitiors and risk of fractures // JAMA. — 2009. — Vol. 283 (24). — P. 3205 — 3210.
52.    Nishino M., Malloy M. J., Russell J. et al. Lack of Association of Lipoprotein (a) Levels With Coronary Calcium Deposits in Asymptomatic Postmenopausal Women // JACC. — 2000. — Vol. 35, N 2. — P. 1 — 7.
53.    Official Positions of the ISCD/IOF on the Interpretation and Use of FRAX in Clinical Practice [Электронный ресурс]. — Режим доступа: http://www.iscd.org/official-positions/2010-official-positions-iscd-iof-frax.
54.    Okwuosa T. M., Greenland P., Ning H. et al. Distribution of Coronary Artery Calcium Scores by Framingham 10-Year Risk Strata in the MESA (Multi-Ethnic Study of Atherosclerosis) // JACC. — 2011. — Vol. 57, N 18. — P. 1838 — 1844.
55.    Olcay A., Akin C., Sachin S. et al. Do bisphosphonates slow the progression of Aortic Stenosis? // JACC. — 2012. — Vol. 59, N 16. — P. 1452 — 1459.
56.    Parhami F., Jackson S. M., Tintut Y. et al. Atherоgenic diet and minimally oxidized low density lipoprotein inhibit osteogenic and promote adipogenic differentiation of marrow stromal cells // J. Bone Miner. Res. — 2009. — Vol. 14. — P. 2067 — 2078.
57.    Parhami F., Mody N., Gharavi N. et al. Role of the cholesterol biosynthetic pathway in osteoblastic differentiation of mirrow stromal cells // J. Bone Miner. Res. — 2002. — Vol. 17 (11). — P. 1997 — 2003.
58.    Parhami F., Tintut Y., Beamer W. G. et al. Atherogenic high-fat diet reduces bone mineralization in mice // J. Bone Miner. Res. — 2001. — Vol. 16. — P. 182 — 188.
59.    Schoppet M., Sattler A. Increased Osteoprotegerin serum levels in men with coronary artery disease // J. Clin. Endocrinol. Metab. — 2003. — Vol. 88, N 3. — P. 1024 — 1028.
60.    Schoulz E., Afrai K. Aortic calcification and the risk of osteoporosis and fractures // J. Clin. Endocrinol. Metab. — 2004. — Vol. 89 (9). — P. 4246 — 4253.
61.    Solomon D. H., Avorn J., Canning C. F., Wang P. S. Lipid levels and bone mineral density // Am. J. Med. — 2005. — Vol. 118 (12). — P. 1414 — 1416.
62.    Ueland T., Jemtland R., Godang K. et al. Prognostic Value of Osteoprotegerin in Heart Failure After Acute Myocardial Infarction // JACC. — 2004. — Vol. 44, N 10. — P. 1 — 6.
63.    Van Setten J., Isgum I., Smolonska J. et al. Genome-wide association study of coronary and aortic calcification implicates risk loci for coronary artery disease and myocardial infarction // Atherosclerosis. — 2013. — Vol. 228. — P. 400 — 405.
64.    Vander Recke P., Hansen M. A. The association between low bone mass at the menopause and cardiovascular mortality // Am. J. Med. — 1999. — Vol. 106. — P. 273 — 278.
65.    Venuraju S. M., Yerramasu A., Corder R. et al. Osteoprotegerin as a Predictor of Coronary Artery Disease and Cardiovascular Mortality and Morbidity // JACC. — 2010. — Vol. 55, N 19. — P. 2049 — 2058.
66.    Witte K. A., Clark A. L., Cleland J. G. F. Chronic Heart Failure and Micronutrients // JACC. — 2001. — Vol. 37, N 7. — P. 1 — 10.
67.    Xiaojuan B., Xin Z., Dongke L. et al. The changes of bone mineral density and atherosclerosis indexes with aging and estrogen levels in healthy women // JACC. — 2014. — Vol. 64, suppl. C. — P. 100.
68.    Yamada S., Inaba M., Goto H. et al. Associations between physical activity, peripheral atherosclerosis and bone status in healthy Japanese women // Atherosclerosis. — 2006. — Vol. 188. — P. 196 — 202.

Additional: P. 107-112.

Article received on February 22, 2016