The aim — to analyze our own experience of bioresorbable coronary stents (BCS) use and to define the importance of optical coherence tomography (OCT) in clinical practice.
Materials and methods. The study included 67 consecutive patients (19 of them (86.3 %) males) who underwent implantation of 82 BCS. Of these, 22 patients had a series of primary and control OCT studies. According to the results of OCT, if necessary, a repeated angioplasty or additional stenting were performed. The age of patients was 56.3 ± 7.4 years. Most stenting and OCT procedures were performed in the defeat of the right interventricular branch (RIB) of left coronary artery (LCA) (50.0 %), right coronary artery (RCA) (38.4 %) and the bypass branch (BB) of LCA (11.5 %). OCT was performed in 5 patients with acute coronary syndrome (ACS), 3 of which had myocardial infarction with ST elevation, in 10 patients with chronic coronary occlusions, in 3 patients with restenosis in the metal stent with a further application of BCS by the method of «stent in stent» and in 4 patients — during the second coronary artery disease and its stable course.
Results and discussion. The most commonly suboptimal stent results, according to the intravascular imaging, were observed in patients with complex coronary artery disease. Optimization of the result, according to OCT after BCS implantation against the backdrop of an adequate angiographic pattern, was needed by one out of the 4 patients with stenting of RIB of LCA and by every third patient with stenting of PCA. The type C lesion needed the optimization of the implanted stent in 28.6 %. Most often BCS implantation result optimization was required after recanalisation of chronically occluded arteries in 7 out of 10 cases (70 %), and also in patients after performance of the «stent in the stent» procedure in all three cases. Stent optimization was performed using noncompliant balloons usually at high pressure (16 — 24 atm). No cases of acute BCS thrombosis, perioperative MI, or lethal outcomes were fixed.
Conclusions. The use of BCS in clinical practice is an effective and safe method of stenting in different clinical and angiographic situations. OCT is a highly informative method of visualisation of intravascular structures. According to OCT, optimization of results after BCS was required in 25 % of type A lesions and in 28.5 % of type C lesions. The best results were achieved in case of BCS with the use of intravascular imaging techniques.

Keywords: coronary stenting, bioresorbable stent, optical coherence tomography.

List of references:  
1.    Brugaletta S., Radu M. D., Garcia-Garcia et H. M. al. Circumferential evaluation of the neointima by optical coherence tomography after ABSORB bioresorbable vascular scaffold implantation: can the scaffold cap the plaque? // Atherosclerosis. — 2012. — 22. — P. 106 — 112.
2.    Brugaletta S., Heo J. H., Garcia-Garcia et H. M. al. Endothelial-dependent vasomotion in a coronary segment treated by ABSORB everolimus-eluting bioresorbable vascular scaffold system is related to plaque composition at the time of bioresorption of the polymer: indirect finding of vascular reparative therapy? // Eur. Heart J. — 2012. — 33. — P. 1325 — 1333.
3.    Brugaletta S., Gori T., Low et A. F. al. Absorb bioresorbable vascular scaffold versus everolimus-eluting metallic stent in ST-segment elevation myocardial infarction: 1-year results of a propensity score matching comparison: the BVS-EXAMINATION Study (Bioresorbable Vascular Scaffold-A Clinical Evaluation of Everolimus Eluting Coronary Stents in the Treatment of Patients With ST-segment Elevation Myocardial Infarction) // JACC Cardiovasc. Interv. — 2015. — 8. — P. 189 — 197.
4.    Brown A. J., McCormick L. M., Braganza et D. M. al. Expansion and malapposition characteristics after bioresorbable vascular scaffold implantation // Catheter Cardiovasc. Interv. — 2014. — 84. — P. 37 — 45.
5.    Dudek D., Rzeszutko Ł., Zasada W. et al. Bioresorbable vascular scaffolds in patients with acute coronary syndromes: the POLAR ACS study // Pol. Arch. Med. Wewn. — 2014. — 124. — P. 669 — 677.
6.    Everaert B., Felix C., Koolen J. et al. Appropriate use of bioresorbable vascular scaffolds in percutaneous coronary interventions: a recommendation from experienced users: a position statement on the use of bioresorbable vascular scaffolds in the Netherlands // Neth. Heart J. — 2015. — 23. — P. 161 — 165.
7.    Fernández-Rodríguez D., Brugaletta S., Otsuki S. et al. Acute bioresorbable vascular scaffold thrombosis in ST-segment elevation myocardial infarction: to stent or not to stent? // EuroIntervention. — 2014. — 10. — P. 600.
8.    Ishibashi Y., Onuma Y., Muramatsu T. et al., ABSORB EXTEND Investigators. Lessons learned from acute and late scaffold failures in the ABSORB EXTEND trial // EuroIntervention. — 2014. — 10. — P. 449 — 457.
9.    Kajiya T., Liang M., Sharma et R. K. al. Everolimus-eluting bioresorbable vascular scaffold (BVS) implantation in patients with ST-segment elevation myocardial infarction (STEMI) // EuroIntervention. — 2013. — 9. — P. 501 — 504.
10.    Kirtane A. J., Stone How G. W. to minimize stent thrombosis // Circulation. — 2011. — 124. — P. 1283 — 1287.
11.    Kočka V., Malý M., Toušek P. et al. Bioresorbable vascular scaffolds in acute ST-segment elevation myocardial infarction: a prospective multicentre study ‘Prague 19’ // Eur. Heart J. — 2014. — 35. — P. 787 — 794.
12.    Puricel S., Arroyo D., Corpataux N. et al. Comparison of everolimus and biolimus-eluting coronary stents with everolimus-eluting bioresorbable vascular scaffolds // J. Am. Coll. Cardiol. — 2015. — 65. — P. 791 — 801.
13.    Rzeszutko Ł., Siudak Z., Włodarczak A. et al. Use of bioresorbable vascular scaffolds in patients with stable angina and acute coronary syndromes. Polish National Registry // Kardiol. Pol. — 2014. — 72. — P. 1394 — 1399.
14.    Scalone G., Brugaletta S., Gómez-Monterrosas O. et al. ST-segment elevation myocardial infarction — ideal scenario for bioresorbable vascular scaffold implantation? // Circ. J. — 2015. — 79. — P. 263 — 270.
15.    Serruys P. W., Garcia-Garcia H. M., Onuma Y. From metallic cages to transient bioresorbable scaffolds: change in paradigm of coronary revascularization in the upcoming decade? // Eur. Heart J. — 2012. — 33. — P. 16 — 25b.
16.    Serruys P. W., Chevalier B., Dudek D. et al. A bioresorbable everolimus-eluting scaffold versus a metallic everolimus-eluting stent for ischaemic heart disease caused by de-novo native coronary artery lesions (ABSORB II): an interim 1-year analysis of clinical and procedural secondary outcomes from a randomised controlled trial // Lancet. — 2015. — 385. — P. 43 — 54.
17.    Tamburino C., Latib A., van Geuns et R. J. al. Contemporary practice and technical aspects in coronary intervention with bioresorbable scaffolds: a European perspective // EuroIntervention. — 2015. — 11. — P. 45 — 52.
18.    Wiebe J., Nef H. M., Hamm Current C. W. status of bioresorbable scaffolds in the treatment of coronary artery disease // J. Am. Coll. Cardiol. — 2014. — 64. — P. 2541 — 2551.

Additional: P. 30-37.

The aim — to examine the features of blood flow in the visceral branches of the abdominal aorta and to determine the relationship between these parameters and the clinical features of gastroesophageal reflux disease (GERD) in patients with concomitant coronary artery disease (CAD).
Materials and methods. A comparative evaluation was conducted of dopplerographic parameters of blood flow in the superior mesenteric artery (SMA) and the celiac trunk (CT) in patients with various forms of endoscopic GERD and concomitant coronary artery disease and patients with isolated GERD. The severity of clinical symptoms of GERD was evaluated according to the results of modified GERD Screener. Endoscopic GERD stage was determined by Savary-Miller classification in Carisson et al. modification (1996).
Results and discussion. A significant decrease of blood flow velocity parameters in the CT and SMA in patients with GERD and coronary artery disease was established. Higher values of resistance indexes of these vessels were also found. More expressed disturbances of blood flow in the CT and SMA were observed in patients with erosive lesions of the esophagus. Significant correlations and connections of the investigated ultrasonic parameters with the patients’ age, body mass index, the severity of clinical manifestations of GERD and CAD in patients with co-morbidities were established.
Conclusions. The reduction of velocity parameters of blood flow and the increase in rigidity of the visceral branches of the abdominal aorta (CT and SMA), the pool of which supplies the lower third part of the esophagus, give grounds to assert that chronic ischemia of this area of the digestive tract occurs in patients with the comorbidity of GERD and CAD, and is linked with clinical symptoms of both diseases.

Keywords: gastroesophageal reflux disease, coronary artery disease, сomorbidity, clinical symptoms, abdominal aortic visceral branches blood flow.

List of references:  
1.    «Алгоритм раннього виявлення гастроезофагеальної рефлюксної хвороби»: Свідоцтво № 26148 / Фадєєнко Г. Д., Кушнір І. Е., Чернова В. М. та співавт. — Заявка № 26255. — заявлено 03.07.2008, зареєстровано 17.10.2008.
2.    Алексеева О. П., Долбин И. В., Пикулев Сочетанное Д. В. течение ишемической болезни сердца и гастроэзофагеальной рефлюксной болезни // Научн. мед. журн. — 2006. — № 7. — С. 7 — 12.
3.    Кабанец Н. С., Моногарова Н. Е., Колкина и В. Я. др. Сосудистые заболевания пищевода [Электронный ресурс] // Новости медицины и фармации. Гастроэнтерология. — Рeжим доступа: http://www.mif-ua.com.
4.    Лазебник Диагностика Л. Б. и лечение ГЭРБ у пожилых // Эксперимент. и клин. гастроэнтерол. — 2004. — № 5. — С. 16 — 20.
5.    Ливзан М. А., Денисова Особенности О. А. курации больных пожилого и старческого возраста с гастроэзофагеальной рефлюксной болезнью // Лечащий врач. — 2015. — № 8. — С. 36 — 38.
6.    Машарова А. А., Бордин Особенности Д. С. гастроэзофагеальной рефлюксной болезни у пожилых // Эксперимент. и клин. гастроэнтерол. — 2007. — № 4. — С. 1 — 4.
7.    Опарин А. Г., Опарин А. А., Лобунец О. А., Шаповалова Механизмы О. Е. формирования сопутствующей железодефицитной анемии при ГЭРБ у студентов // Світ медицини та біології. — 2010. — № 2. — С. 141 — 142.
8.    Butler N. National Guidelines at a glance: GO // SA Pharmaceutical J. — 2009. — N 10. — P. 32 — 36.
9.    Dent J., Jones R., Kahrilas P., Talley N. Management of gastro-oesophageal reflux disease in general practice // BMJ. — 2001. — N 322. — P. 344 — 347.
10.    Kahrilas P., Shaheen N., Vaezi M. et al. American Gastroenterological Association Medical Position Statement on the management of gastroesophageal reflux disease // Gastroenterology. — 2008. — 135 (4). — P. 1383 — 1391.
11.    Schneider Gastro H. R.-oesophageal reflux disease: The Montreal definition and classification // SA Fam. Pract. — 2007. — 49 (1). — P. 19 — 26.

Additional:

The aim — to identify changes in home blood pressure (BP) in comparison with changes in office BP and assess the variability of home blood pressure under the influence of stepped algorithmic antihypertensive therapy based on a fixed combination of perindopril and amlodipine in patients with uncomplicated hypertension in clinical practice.
Materials and methods. The survey data of 209 patients — an open prospective study participants with uncomplicated essential hypertension, mean age 58.0 ± 0.4 years, BP ≥ 160/100 mm Hg in patients not previously treated, or ≥ 140/90 mm Hg in those who previously received antihypertensive therapy. All patients took a fixed combination of perindopril and amlodipine, and later (in 7 days, 1, 2, 3, 6 months), in the case of failure to reach the target office blood pressure, if necessary,  — indapamide, spironolactone, moxonidine or doxazosin. Office and home blood pressure was measured using oscillometric automatic instruments with a universal or individually fitted cuff. Home blood pressure was measured before breakfast and before bedtime (three dimensions) for 7 days prior to each visit to the doctor. Variability of home systolic (SBP) and diastolic (DBP) blood pressure was evaluated by the standard deviation (SD), coefficient of variation (CV) of the average value and the criterion variation independent of mean (VIM) for SBP.
Results and discussion. After 6 months of treatment office SBP decreased from 164.5 ± 14.9 to 130.1 ± 10.3 mm Hg, DBP  — from (95 ± 10.8) to 78.5 ± 6.7 mm Hg, home SBP  — from 147.1 ± 17.3 to 131.8 ± 11.7 mm Hg, DBP  — from 85.3 ± 10.2 to 78.3 ± 7.0 mm Hg, respectively, (all p < 0.0001). The proportion of patients with a target level of office blood pressure in 6 months was 83.7 %, with recommended level of home blood pressure (< 135/85 mm Hg)  — 66.5 % (p < 0.01), with simultaneous control of the office and home BP  — 61.2 %. The magnitude of changes in office SBP after 6 months exceeded the dynamics of home SBP by 18.4 % (p < 0.04), diastolic blood pressure  — by 19.4 % (p < 0.05). Probable strong positive correlations (all p < 0.0001) were established between the office and home SBP and DBP at the initial stage of the study and after 6 months of treatment. After 6 months, SD of home SBP and DBP decreased from 8.5 ± 4.2 to 5.6 ± 3.3 mm Hg (p < 0.0001) and from 5.5 ± 2.4 to 4.2 ± 1.8 mm Hg (p < 0.001), CV  — from 5.9 ± 0.3 to 4.3 ± 0.3 % (p < 0.001) and from 6.5 ± 0.3 to 5.4 ± 0.2 % (p < 0.01), respectively, VIM SAT  —  from 9.3 ± 4.2 to 6.0 ± 4.1 (p < 0.001).
Conclusions. Changes in home blood pressure in patients with uncomplicated hypertension under the influence of algorithmic antihypertensive therapy based on a fixed combination of perindopril and amlodipine were by 18.4 % lower than changes in the office BP, in the presence of a close direct correlation between them. Application for 6 months of algorithmic antihypertensive therapy based on a fixed combination of perindopril and amlodipine in patients with uncomplicated hypertension can not only achieve simultaneous control of the office and home blood pressure in 61.2 % of cases, but also reduce the variability of home blood pressure.

Keywords: аrterial hypertension, office blood pressure, home blood pressure, home blood pressure variability, antihypertensive therapy.

List of references:  
1.    Амосова К. М., Руденко Ю. В., Рокита та О. І. ін. 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.    Хвороби системи кровообігу як медико-соціальна і суспільно-політична проблема: аналітично-статистичний посібник / під ред. Коваленко В. М., Корнацького В. М. — К., 2014. — 116 с.
3.    Agarwal R., Bills J. E., Hecht W T. J.., Light Role R. P. of Home Blood Pressure Monitoring in Overcoming Therapeutic Inertia and Improving Hypertension Control. A Systematic Review and Meta-Analysis // Hypertension. — 2011. — 57. — P. 29 — 38.
4.    Asayama K., Ohkubo T., Metoki H. et al. Cardiovascular outcomes in the first trial of antihypertensive therapy guided by self-measured home blood pressure // Hypertens. Res. — 2012. — 35. — P. 1102 — 1110.
5.    Bobrie G., Delonca J., Moulin C. et al. A home blood pressure monitoring study comparing the antihypertensive efficacy of two angiotensin II receptor antagonist fixed combinations // Am. J. Hypertens. — 2005. — 18. — P. 1482 — 1488.
6.    Cuckson A. C., Reinders A., Shabeeh H., Shennan Validation A. H. of the Microlife BP 3BTO-A oscillometric blood pressure monitoring device according to a modified British Hypertension Society protocol // Blood Press. Monit. — 2002. — Vol. 7. — P. 319 — 324.
7.    Eguchi K., Matsui Y., Shibasaki S. et al. Changes in self-monitored pulse pressure correlate with improvements in B-type natriuretic Peptide and urinary albumin in treated hypertensive patients // Am. J. Hypertens. — 2007. — 20. — P. 1268 — 1275.
8.    Ewald S., vor dem Esche J., Uen S. et al. Relationship between the frequency of blood pressure self-measurement and blood pressure reduction with antihypertensive therapy: results of the OLMETEL (OLMEsartan TELemonitoring blood pressure) study // Clin. Drug Investig. — 2006. — 26. — P. 439 — 446.
9.    Feldman R. D., Zou G. Y., Vandervoort et M. K. al. A simplified approach to the treatment of uncomplicated hypertension: a cluster randomized, controlled trial // Hypertension. — 2009. — Vol. 53. — P. 646 — 653.
10.    Franklin S. S., O’Brien E., Thijs L. et al. Masked hypertension: A  phenomenon of measurement // Hypertension. — 2015. — 65. — P. 16 — 20.
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.    Glynn L. G., Murphy A. W., Smith et S. M. al. Interventions used to improve control of blood pressure in patients with hypertension // Cochrane Database of Syst. Rev. — 2010, Issue 3. Art. No.: CD005182. DOI: 10.1002/14651858.CD005182.pub4
13.    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. — 32. — P. 218 — 225.
14.    Hashimoto J., Hirayama H., Hanasawa T. et al. Efficacy of combination antihypertensive therapy with low-dose indapamide: assessment by blood pressure self-monitoring at home // Clin. Exp. Hypertens. — 2005. — 27. — P. 331 — 341.
15.    Ishikawa J., Carroll D. J., Kuruvilla S. et al. Changes in home versus clinic blood pressure with antihypertensive treatments. A meta-analysis // Hypertension. — 2008. — 52. — P. 856 — 864.
16.    Kamoi K., Ikarashi T. The bedtime administration of doxazosin controls morning hypertension and albuminuria in patients with type-2 diabetes: evaluation using home-based blood pressure measurements // Clin. Exp. Hypertens. — 2005. — 27. — P. 369 — 376.
17.    Karotsis A. K., Symeonidis A., Mastorantonakis S. E., Stergiou Additional G. S. antihypertensive effect of drugs in hypertensive subjects uncontrolled on diltiazem monotherapy: a randomized controlled trial using office and home blood pressure monitoring // Clin. Exp. Hypertens. — 2006. — 28. — P. 655 — 662.
18.    Kikuya M., Ohkubo T., Metoki H. et al. Day-by-day variability of blood pressure and heart rate at home as a novel predictor of prognosis: the Ohasama Study // Hypertension. — 2008. — 52. — P. 1045 — 1050.
19.    Mancia G., De Backer G., Dominiczak A. et al. 2007 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. — 2007. — Vol. 25. — P. 1105 — 1187.
20.    Mancia G., Ombonib S., Chazova I. et al. Effects of the lercanidipine-enalapril combination vs. the corresponding monotherapies on home blood pressure in hypertension: evidence from a large database // J. Hypertens. — 2016. — Vol. 34 (1). — P. 139 — 148.
21.    Marui F., Bombig M., Francisco et Y. A. al. Assessment of resistant hypertension with home blood pressure monitoring // Arq. Bras. Cardiol. — 2010. — 95 (4). — P. 536 — 540.
22.    Matsui Y., Ishikawa J., Eguchi K. et al. Maximum value of home blood pressure: a novel indicator of target organ damage in hypertension // Hypertension. — 2011. — 57. — P. 1087 — 1093.
23.    Matsui Y., O’Rourke M. F., Hoshide S. et al. Combined effect of angiotensin II receptor blocker and either a calcium channel blocker or diuretic on day-by-day variability of home blood pressure: the Japan Combined Treatment With Olmesartan and a Calcium-Channel Blocker Versus Olmesartan and Diuretics Randomized Efficacy Study // Hypertension. — 2012. — 59. — P. 1132 — 1138.
24.    Mozaffarian D., Benjamin E. J., Go et A. S. al. Heart Disease and Stroke Statistics — 2016 Update A Report From the American Heart Association // Circulation. — 2016. — 133. — P. e38—e360.
25.    Nakamoto H., Nishida E., Ryuzaki M. et al. Effect of telmisartan and amlodipine on home blood pressure by monitoring newly developed telemedicine system: monitoring test by using telemedicine. Telmisartan’s effect on home blood pressure (teltelbosu) // Clin. Exp. Hypertens. — 2008. — 30. — P. 57 — 67.
26.    Niiranen T. J., Kantola I. M., Vesalainen R. et al. A comparison of home measurement and ambulatory monitoring of blood pressure in the adjustment of antihypertensive treatment // Am. J. Hypertens. — 2006. — 19. — P. 468 — 474.
27.    Niiranen T. J., Maki J., Puukka P. et al. Office, home, and ambulatory blood pressures as predictors of cardiovascular risk // Hypertension. — 2014. — 19. — P. 03292.
28.    Paratia G., Stergiou European G. S. Society of Hypertension guidelines for blood pressure monitoring at home: a summary report of the Second International Consensus Conference on Home Blood Pressure Monitoring // J. Hypertens. — 2008. — 26. — P. 1505 — 1530.
29.    Qamar N., Bray E. P., Glynn et L. G. al. Self-monitoring for improving control of blood pressure in patients with hypertension // Cochrane Database of Syst. Rev. — 2013, Issue 1. Art. No.: CD010311. DOI: 10.1002/14651858.CD010311.
30.    Rothwell P. M., Howard S. C., Dolan E. et al. Prognostic significance of visit-to-visit variability, maximum systolic blood pressure and episodic hypertension // Lancet. — 2010. — 375. — P. 895 — 905.
31.    Sato A., Watanabe S., Okubo S. et al. The therapeutic importance of home blood pressure assessment and combination antihypertensive therapy for achieving target blood pressure control: Ibaraki hypertension assessment trial // Hypertens. Res. — 2010. — 33. — P. 1264 — 1271.
32.    Stergiou G. S., Asayama K., Thijs L. et al. Prognosis of White-Coat and Masked Hypertension International Database of Home Blood Pressure in Relation to Cardiovascular Outcome // Hypertension. — 2014. — 63. — P. 675 — 682.
33.    Stergiou G. S., Bliziotis Home I. A. Blood Pressure Monitoring in the Diagnosis and Treatment of Hypertension: A Systematic Review // Am. J. Hypertens. — 2011. — 24 (2). — P. 123 — 134.
34.    Tai C., Sun Y., Dai N. et al. Prognostic Significance of Visit-to-Visit Systolic Blood Pressure Variability: A Meta-Analysis of 77,299 Patients // J. Clin. Hypertens (Greenwich). — 2015. — 17. — P. 107 — 115.
35.    Ushigome E., Fukui M., Hamaguchi M. et al. The coefficient variation of home blood pressure is a novel factor associated with macroalbuminuria in type 2 diabetes mellitus // Hypertens. Res. — 2011. — 34. — P. 1271 — 1275.
36.    Verberk W. J., Kroon A. A., Lenders et J. W. al. Self-measurement of blood pressure at home reduces the need for antihypertensive drugs: a randomized, controlled trial // Hypertension. — 2007. — 50. — P. 1019 — 1025.
37.    Ward A. M., Takahashi O., Stevens R., Heneghan C. Home measurement of blood pressure and cardiovascular disease: systematic review and meta-analysis of prospective studies // J. Hypertens. — 2012. — 30. — P. 449 — 456.
38.    Yamagishi T. Efficacy of azelnidipine on home blood pressure and pulse rate in patients with essential hypertension: comparison with amlodipine // Hypertens. Res. — 2006. — 29. — P. 767 — 773.

Additional:

The aim — to study the clinical-anamnestic parameters and genotypes of polymorphic marker for endothelial NO-synthase (eNOs) Т(–786)С gene, which are associated with the presence and clinical features and manifestations of ischemic heart disease (IHD) in patients with peripheral arterial disease (PAD).
Materials and methods. The study involved 100 patients with PAD of lower extremities (mean age 60.7 ± 0.9 years) with IIA—IV stages of limb chronic ischemia. Besides clinical tests, we determined glomerular filtration rate (GFR), ankle-brachial index, selective coronary angiography, Doppler ultrasound of the lower extremities and carotid arteries (CA) with estimation of intima-media thickness (IMT), echocardiography, Holter monitoring. The study of allelic polymorphism of eNOs gene promoter was performed by polymerase chain reaction.
Results and discussion. Patients were divided into two groups: I — 63 (63 %) patients without IHD, II — 37 (37 %) patients with IHD. Patients of II group had significantly lower average age of PAD manifestation (p = 0.001), higher IMT (р = 0.003), higher frequency of CA atherosclerosis (р = 0.0002), significantly lower GFR (р = 0.004) and probability of renal disfunction (72 % (p = 0.0043)) than patients of I group. We revealed independent direct association with the presence of myocardial infarction in anamnesis (β = 0.37 ± 0.08; B = 0.73 ± 0.17; p = 0.00003), C allele (β = 0.28 ± 0.09; B = 0.24 ± 0.07; p = 0.002), CA atherosclerosis (β = 0.15 ± 0.08; B = 0.24 ± 0.13; p = 0.05) and inverse association with patients’ age (β = 0.21 ± 0.08; B = 0.02 ± 0.01; p = 0.01).
Conclusions. The examination of patients with PAD revealed that the clinical manifestations of IHD were found in 37 %; presence of concomitant IHD is associated with CA atherosclerosis (OR 80 %, p = 0.0005), a more severe stage of lower limb ischemia (OR 64 %, p = 0.03) and significantly more frequent reduction of GFR (p = 0.0043). The presence of C allele of eNOs gene promoter Т(–786)С polymorphism in genotype of patients with PAD, according to regression analysis, makes 11.6 % probability of presence of IHD (p = 0.002).

Keywords: peripheral arterial disease of lower extremities, ischemic heart disease, polymorphism of endothelial NO-synthase gene.

List of references:  
1.    Барбараш О. Л., Зыков М. В., Кашталап и В. В. др. Распространенность и клиническая значимость мультифокального атеросклероза у пациентов с ишемической болезнью сердца // Кар­диол. — 2011. — Т. 51 (8). — С. 66 — 71.
2.    Бобров В. О., Жарінов О. Й., Куць та В. О. ін. Амбулаторне моніторування ЕКГ. Сучасні технології, діагностичні можливості, показання: медичний посібник. Київська медична академія післядипломної освіти. — К., 2014. — 68 с.
3.    Кочетов А. Г., Лянг О. В., Масенко и В. П. др. Методы статистической обработки медицинских данных: Методические рекомендации для ординаторов и аспирантов медицинских учебных заведений, научных работников. — М.: РКНПК, 2012. — 42 с.
4.    Рекомендации Европейского общества кардиологов по диагностике и лечению заболеваний периферических артерій // Рацио­н. фармакотер. в кардиол. — 2012. — Прил. 4. — 73 с.
5.    Соколов Ю. Н., Соколов М. Ю., Терентьев Коронарная В. Г. болезнь и интервенционная кардиология. — К.: Морион, 2011. — 767 с.
6.    Целуйко В. Й., Яковлева Клінічна Л. М. характеристика і порівняльна оцінка атеросклеротичного ураження різних судинних басейнів у хворих на хронічну ішемічну хворобу серця залежно від поліморфізму Т (–786)С промотора гена ендотеліальної NO-синтази // Серце і судини. — 2013. — № 4. — C. 95 — 102.
7.    Alberts M. J., Bhatt D. L., Mas et J. L. al. Three-year follow-up and event rates in the international REduction of atherothrombosis for continued health registry // Eur. Heart J. — 2009. — Vol. 30 (19). — P. 2318 — 2326.
8.    Forstermann U., Sessa Nitric W. C. oxide synthases: regulation and function // Eur. Heart J. — 2012. — Vol. 33. — P. 829 — 837.
9.    Gutierrez E., Flammer A. J., Lerman at L. O. al. Endothelial dysfunction over the course of coronary artery disease // Eur. Heart J. — 2013. — Vol. 34. — P. 3175 — 3181.
10.    Jiangping S., Zhe Z., Wei W.et al. Assessment of coronary artery stenosis by coronary angiography // Circulation. — 2013. — N 6. — Р. 262 — 268.
11.    Kathiresan S., Srivastava D. Genetics of human cardiovascular disease // Cell. — 2012. — Vol. 148, Iss. 6. — P. 1242 — 1257.
12.    Lang R. M., Badano L. P., 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. — Vol. 16. — P. 233 — 271.
13.    Levey A. S., 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. — 2000. — N 11. — P. 155.
14.    Lieb W., Vasan Genetics R. S. of coronary artery disease // Circulation. — 2013. — Vol. 128 (10). — P. 1131 — 1138.
15.    Management of patients with peripheral artery disease (Compilation of 2005 and 2011 ACCF/AHA Guideline Recommendations). A Report of the American college of cardiology foundation. American heart association // J. Am. Coll. Cardiol. — 2013. — Vol. 61, N 14. — P. 1555 — 1570.
16.    Nigam Calculated P. K. low density lipoprotein-cholesterol: Friedewald’s formula versus other modified formulas // Int. J. Life Sci. Med. Res. — 2014. — Vol. 4, Iss. 2. — P. 25 — 31.
17.    Rai H., Parveen F., Kumar S. et al. Association of endothelial nitric oxide synthase gene polymorphisms with coronary artery disease: an updated meta-analysis and systematic review // PLoS One. — 2014. — Vol. 9, Iss.11. — Р. e113363.
18.    Rossi G. P., Cesari M., Zanchetta M. et al. The T-786C endo¬thelial nitric oxide synthase genotype is a novel risk factor for coro¬nary artery disease in Caucasian patients of the GENICA study // J. Am. Coll. Cardiology. — 2003. — Vol. 41 (6). — P. 930 — 937.
19.    Sticchi E., Sofi F., Romagnuolo I. et al. eNOS and ACE genes influence peripheral arterial disease predisposition in smokers // Journal of vascular surgery. — 2010. — Vol. 52, N 1. — P. 97 — 102.
20.    Thygesen K., Alpert J. S., Jaffe et A. S. al. Third universal definition of myocardial infarction // Circulation. — 2012. — Vol. 126. — P. 2020 — 2035.
21.    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. — Vol. 63, Iss. 12.
22.    Tsujimura T., Ishihara T., Iida O. Syntax score is an independent predictor of 4-years mortality in patients with peripheral artery disease // J. Am. Coll. Cardiol. — 2015. — Vol. 65, Iss.10S.
23.    Yang J., Lu Ch., Yuejin Y., Dayi H.. Subclinical Peripheral Artery Disease as a Predictor for Mortality in Patients With Coronary Heart Disease // J. Am. Coll. Cardiol. — 2014. — Vol. 63, Iss. 12.

Additional:

The aim — to evaluate the nature of lipidosis in patients with coronary artery disease (CAD) based on the presence of type 2 diabetes mellitus (T2DM) and the character of coronary artery (CA) lesions.
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 without concomitant T2DM. All patients underwent coronary angiography to verify the diagnosis of CAD. The levels of total cholesterol, high density lipoproteins, low density lipoproteins, very low density lipoproteins, triglycerides (TG) were also assessed.
Results and discussion. Characteristics of CA lesions in patients with CAD based on the presence of T2DM were analyzed. It was found that patients with type 2 diabetes significantly more often suffered from diffuse coronary arteries vessels (60 % vs 13.1 %; р < 0.0001). Patients of the 2nd group compared with patients of the 1st group had single-vessel and two vessel CA lesions significantly more often: in 26 (42.6 %) vs 16 (22.9 %) and in 20 (32.8 %) vs 11 (15.7 %) patients, respectively (p = 0.016; p = 0.03). At the same time, three vessel defeat was registered significantly more often in the 1st group than in the 2nd group: in 31 (44.3 %) vs 10 (16.4 %) patients, respectively, (p = 0.0008), confirming a negative impact of type 2 diabetes on the atherosclerotic process in such patients. The average number of affected vessels per person in the 1st group was higher than that in the 2nd group: 2.7 ± 1.3 vs 1.9 ± 1.1, respectively, (p = 0.0004). Moreover, the 1st group patients had significantly higher average number of plaques per person than the 2nd group patients (4.1 ± 2.8 vs 2.2 ± 1.4; p = 0.00001). The average number of affected segments per one patient was also significantly bigger in the 1st group than in the 2nd group (3.5 ± 2.1 vs 2.2 ± 1.3; p = 0.0001). In the 1st group, mean values of TG levels were significantly higher than in the 2nd group (1.9 ± 0.8 vs 1.6 ± 0.6 mmol/l; p = 0.02), the prevalence of combined dyslipidemia was also higher (14.3 % vs 4.9 %; p = 0.02).
Conclusions. CAD patients with concomitant type 2 DM compared with those without diabetes had significantly more frequent multivessel diffuse lesion of coronary bed and showed a greater average number of stenoses of CA per patient, the average number of affected segments of CA per patient, the average number of hemodynamically significant stenoses of CA per patient. When analyzing lipid abnormalities in patients with coronary artery disease and concomitant type 2 diabetes, we found significantly higher levels of TG and a greater prevalence of combined dyslipidemia than in patients without concomitant diabetes mellitus type 2, which probably causes specific features of lesions of coronary bed in patients with type 2 diabetes and must be taken into consideration in primary prevention in this group.

Keywords: coronary atherosclerosis, coronary artery disease, type 2 diabetes mellitus, hypertriglyceridemia, dyslipidemia.

List of references:  
1.    Дисліпідемії: діагностика, профілактика та лікування // Методичні рекомендації Асоціації кардіологів України / За ред. Мітченко О. І., Лутай М. І.. — К., 2011. — 25 с.
2.    Москаленко В. Ф., Гульчій О. П., Голубчиков та М. В. ін. / За ред. Москаленка В. Ф.. — К.: Книга плюс, 2009. — 184 с.
3.    Рекомендации по диабету, предиабету и сердечно-сосудистым заболеваниям. EASD/ESC // Рос. кардиол. журн. — 2014. — № 3 (107). — С. 6 — 70.
4.    Стабільна ішемічна хвороба серця: адаптована клінічна настанова, заснована на доказах. — К., 2016. — 177 с.
5.    Уніфікований клінічний протокол первинної та вторинної (спеціалізованої) медичної допомоги: Стабільна ішемічна хвороба серця / Hаказ МОЗ України від 02.03.2016 № 152. — 61 с.
6.    Уніфікований клінічний протокол первинної та вторинної (спеціалізованої) медичної допомоги: цукровий діабет 2 типу (наказ МОЗ № 1118 від 21.12.2012 р.). — 115 с.
7.    Шкробанець І. Д., Леонець С. І., Бідучак Епідеміологічні А. С. особливості хвороб системи кровообігу в Україні й Чернівецькій області // Буковин. мед. вісн. — 2013. — Т. 17, № 3 (67). — Ч. 2. — С. 100 — 103.
8.    Goldfine A. B., Phua E. J., Abrahamson Glycemic M. J. management in patients with coronary artery disease and prediabetes or type 2 diabetes mellitus // Circulation. –2014. — Vol. 129. — P. 2567 — 2573.
9.    Huang Y., Cai X., Chen P. et al. Associations of prediabetes with all-cause and cardiovascular mortality: A meta-analysis // Annals of Medicine. — 2014. — Vol. 46. — P. 684 — 692.
10.    Naito R., Kasai T. Coronary artery disease in type 2 diabetes mellitus: Recent treatment strategies and future perspectives // World J. Cardiol. — 2015. — Mar 26. — 7 (3). — Р. 119 — 124.
11.    Standards of medical care in diabetes — 2016. American Diabetes Association // Diabetes Care. — 2016. — Vol. 39 (suppl. 1). —
S.1 — S.109.

Additional: P. 63-71.

Article received on May 13, 2016

The aim — to study the biochemical parameters in platelet-rich plasma (PRP) and platelet-free plasma (PFP) in people of various ages.
Materials and methods. The blood of 44 conditionally healthy people that do not fall under the exclusion criteria (vascular disorders, chronic pathology of gastrointestinal tract, cancer) was examined. Age groups were allocated: 20 — 29, 40 — 49, 50 — 59 and 60 — 69 years. We investigated the activity of glyceraldehyde-3-phosphate dehydrogenase (GAPDH, EC 1.2.1.12); fructose-1.6-bisphosphate aldolase — (aldolase, EC 4.1.2.13); glutathione peroxidase (GPO, EC 1.11.1.9); superoxide dismutase (SOD, EC 1.15.1.1); adenosine deaminase (ADA, EC 3.5.4.4). Enzyme activity in PRP was expressed in platelet concentration, reduced to 108 platelets per 1 ml of plasma.
Results and discussion. Aldolase activity and GAPDH in PRP was 2 — 3 times higher than in PFP and significantly increased with age: in group of 60 — 69 years it was twofold higher than in the group of 20 — 29 years. PRP showed a significant decrease in GAPDH activity in older age groups. GPO activity in the group of 20 — 29 years was significantly higher than in the older age groups (40 to 69 years). The activity of SOD in PRP was significantly higher in the groups of 50 — 59 and 60 — 69 years. ADA activity in PRP increased with age, maximum activity was observed in the group of 60 — 69 years. ADA activity in platelet-free plasma was not significantly changed with age. The results indicate the presence of age-related changes that contribute to an increase in the activity of platelet’s part of coagulation system.
Conclusions. The restructuring of metabolic activity of platelets in advanced age was registered. Age-related changes in platelet-free plasma and platelet rich plasma are different, which should be considered when examining patients with vascular disease.

Keywords: platelet rich plasma, age-related changes, platelets, metabolism.

List of references:  
1.    Борзенко Б. Г., Бакурова Е. М., Миронова и К. А. др. Патогенетические особенности метаболизма клеток крови при различном течении язвенной болезни у человека // Таврич. мед.-биол. вестн. — 2012. — Т. 15, № 3. — Ч. 2 (59). — С. 47 — 50.
2.    Демина О. В., Ходонов А. А., Швец В. И., Варфоломеев Агрегация С. Д. тромбоцитов человека: молекулярно-кинетические механизмы и пути регуляции // Биологические мембраны. — 2002. — Т. 19, № 2. — С. 115 — 152.
3.    Ермолаева Е. Н., Кривохижина Л. В., Кантюков С. А., Сурина-марышева Свободнорадикальное Е. Ф. окисление в интактных и активированных тромбоцитах // Фундаментальные исследования. — 2014. — № 7 — 1. — С. 61 — 65.
4.    Кочетов Практическое Г. А. руководство по энзимологии: Учеб. пособие для студентов биологических специальностей университетов. — [2-е изд.]. — М.: Высш. школа, 1980. — 272 с.
5.    Макаревич О. П., Голиков Активность П. П. супероксиддисмутазы крови в острый период различных заболеваний // Лаб. дело. — 1983. — № 6. — С. 24 — 27.
6.    Савченко А. А., Черняева М. С., Петрова и М. М. др. Метаболический статус тромбоцитов у больных острым инфарктом миокарда с подъемом сегмента ST в сочетании с тревожно-депрессивными расстройствами // Фундаментальные исследования. — 2015. — № 1 — 3. — С. 583 — 591.
7.    Супрун Э. В., Ищенко А. М., Симбирцев и А. С. др. Влияние рецепторного антагониста интерлейкина-1 на соотношение показателей тиол-дисульфидной системы, окислительной модификации белков и энергетического метаболизма в клетках головного мозга крыс на фоне экспериментальной гипергликемии и церебральной ишемии // Цитокины и воспаление. — 2014. — № 2.
8.    Carol A. Dangelmaiera, Holm Holmsena. Glyoxylate lowers metabolic ATP in human platelets without altering adenylate energy charge or aggregation // Platelets. — 2014. — Vol. 25, Iss. 1. — Р. 36 — 44.
9.    Chianeh Y. R., Ahuja J., Prasad A. Evaluation of Oxidative Protein Damage in Patients with Hypercholesterolemia // NJIRM. — 2013. — Vol. 4 (4). — P. 64 — 68.
10.    Graven K., McDonald R., Farber H. Hypoxic regulation of endothelial glyceraldehyde-3-phosphate dehydrogenase // Am. J. Physiol. Cell Physiol. — 1998. — Vol. 274. — P. 347 — 355.
11.    Moin Simple V. M. and specific method of measurement of glutathione peroxidase activity in the erythrocytes // Lab. Manuals. — 1986. — N 12. — P. 724 — 727.
12.    Rinalducci S., Marrocco C., Zolla L. Thiol-based regulation of glyceraldehyde-3-phosphate dehydrogenase in blood bank-stored red blood cells: a strategy to counteract oxidative stress // Transfusion. — 2015. — Vol. 55, Iss. 3. —  P. 499 — 506.
13.    Stafford N. P., Pink A. E., White et A. E. al. Mechanisms Involved in Adenosine Triphosphate-Induced Platelet Aggregation in Whole Blood // Arterioscler. Thromb. Vasc. Biol. — 2003. — Vol. 23. — P. 1928 — 1933.

Additional: P. 72-75.

Article received on May 19, 2016

The aim — to improve the criteria for recognition of ventricular premature beats (VPB) substrate location in the sinuses of Valsalva (SV) by retrospective ECG analysis after radiofrequency ablation.
Materials and methods. The work is based on retrospective analysis of results of treatment of 24 consecutive patients who underwent radiofrequency ablation (RFA) of ventricular premature beats with SV. The criterion for inclusion into the study was the presence of frequent symptomatic VPBs with SV, refractory to medical treatment. Evaluation of cardiac rhythm was performed using Holter-ECG before surgery, 3 and 6 months thereafter. Electrophysiological mapping and ablation of VPB were performed according to standard protocols of electrophysiological study. Obtained during electrophysiological study data of the anatomical location of the ventricular premature beats substrate was compared with morphological characteristics of QRS extrasystolic complexes, obtained by 12-leads ECG.
Results and discussion. The cumulative success of surgery was 100 %. The amount of VPB in the daily rhythm decreased from 28.3 ± 17.1 % to 0.8 ± 2.1 %, that is by 97.17 % (p < 0.01). The analysis revealed that in 15 (62.5 %) patients, the source of VPB was the left SV, in 9 (37.5 %) patients it was the right SV. Retrospective analysis of ECG characteristics of VPB from left and right SV revealed the following patterns: VPB from the left SV is characterized by a pronounced R-wave amplitude in abduction II (2.4 ± 0.4 mV compared to 1.8 ± 0.4 mV; p < 0.01), a pronounced R-wave amplitude in abduction III (2.3 ± 0.4 mV compared with 1.6 ± 0.5 mV; p < 0.01), the presence of S-wave in abduction I (100 % compared with 22 %; p < 0.001), a more pronounced ratio of R III/II amplitude wave (1.1 ± 0.2 compared to 0.9 ± 0.2; p < 0.01), a larger amplitude of the S wave in aVL abduction (1.1 ± 0.5 mV compared to 0.1 ± 0.3 mV; p < 0.001), an increased ratio of the length of the R wave to QRS (1.1 ± 0.2 mV compared with 0.1 ± 0.3 mV; p < 0.01).
Conclusions. RFA is an effective method of treatment of VPBs from SV which can reduce the relative weight of the VPBs in the diurnal rhythm by 97.17 %. Location of VPBs focus in the area of the aortic root is potentially dangerous for the RFA, given the anatomical proximity of the mouth of the coronary arteries and the conduction system. Strict adherence to the intervention protocol permits avoiding the violations of perfusion of the coronary arteries and atrioventricular block. Careful analysis of the ECG in the preoperative period suggests VPBs substrate localization in SV. The presence of the S wave in abduction I is more common for the left SV than for the right. The ratio of the wave amplitude R III/II > 0.9 is a sign of arrhythmia substrate in the left SV. A greater amplitude of the S wave in lead aVL is more common for the left CV than for the right.

Keywords: radiofrequency ablation, ventricular premature beats, sinuses of Valsalva.

List of references:  
1.    Anderson Clinical R. H. anatomy of the aortic root // Heart. — 2000. — Vol. 84. — P. 670 — 673.
2.    Ban J. E., Park H. C., Park et J. S. al. Electrocardiographic and electrophysiological characteristics of premature ventricular complexes associated with left ventricular dysfunction in patients without structural heart disease // Europace. — 2013. — Vol. 15. — P. 735 — 741.
3.    Bogun F., Crawford T., Reich S. et al. Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: comparison with a control group with out intervention // Heart Rhythm. — 2007. — Vol. 4. — P. 863 — 867.
4.    Gaita F., Giustetto C., DiDonna P. et al. Long-term follow-up of right ventricular monomorphic extrasystoles // J. Am. Coll. Cardiol. — 2001. — Vol. 38. — P. 364 — 370.
5.    Hasdemir C., Ulucan C., Yavuzgil O. et al. Tachycardia-induced cardiomyopathy in patients with idiopathic ventricular arrhythmias: the incidence, clinical and electrophysiologic characteristics, and the predictors // J. Cardiovasc. Electrophysiol. — 2011. — Vol. 22. — P. 663 — 668.
6.    Kennedy H. L., Whitlock J. A., Sprague et M. K. al. Long-term follow-up of asymptomatic healthy subjects with frequent and complex ventricular ectopy // N. Engl. J. Med. — 1985. — 312. — P. 193 — 197.
7.    Kostis J. B., McCrone K., Moreyra et A. E. al. Premature ventricular complexes in the absence of identifiable heart disease // Circulation. — 1981. — 63. — P. 1351 — 1356.
8.    Krittayaphong R., Bhuripanyo K., Punlee K. et al. Effect of atenolol on symptomatic ventricular arrhythmia without structural heart disease: a randomized placebo-controlled study / // Am. Heart J. — 2002. — Vol. 144 (6). — P. e10.
9.    McAlpine Heart W. A. and Coronary Arteries. — New York: Springer-Verlag, 1975. — 209 p.
10.    Messineo Ventricular F. C. ectopic activity: prevalence and risk // Am. J. Cardiol. — 1989. — 64. — P. 53 — 56.
11.    Ouyang F., Fotuhi P., Ho et S. Y. al. Repetitive monomorphic ventricular tachycardia originating from the aortic sinus cusp: electrocardiographic characterization for guiding catheter ablation // J. Am. Coll. Cardiol. — 2002. — Vol. 39. — P. 500 — 508.
12.    Ouyang F., Ma J., Ho et S. Y. al. Focal atrial tachycardia originating from the non-coronary aortic sinus: electrophysiological characteristics and catheter ablation // J. Am. Coll. Cardiol. — 2006. — Vol. 48. — P. 122 — 131.
13.    Pons M., Beck L., Leclercq F. et al. Chronic left main coronary artery occlusion: a complication of radio frequency ablation of idiopathic left ventricular tachycardia // Pacing Clin. Electrophysiol. — 1997. — Vol. 20. — P. 1874 — 1876.
14.    Preservation of the anterior fat pad paradoxically decreases the incidence of postoperative atrial fibrillation // Coll. Cardiol. — 2004. — Vol. 43. — P. 994 — 1000.
15.    Sekiguchi Y., Aonuma K., Yamauchi Y. et al. Chronic hemodynamic effects after radiofrequency catheter ablation of frequent monomorphic ventricular premature beats // J. Cardiovasc. Electrophysiol. — 2005. — Vol. 16. — P. 1057 — 1063.
16.    Sheldon S. H., Gard J. J., Asirvatham Premature S. J. ventricular contractions and non-sustained ventricular tachycardia: association with sudden cardiac death, risk stratification, and managements strategies // Ind. Pacing Electrophysiol. J. — 2010. — 10. — P. 357 — 371.
17.    Stec S., Sikorska A., Zaborska B. et al. Benign symptomatic premature ventricular complexes: short- and long-term efficacy of antiarrhythmic drugs and radiofrequency ablation // Kardiol. Pol. — 2012. — Vol. 70. — P. 351 — 358.

Additional: P. 76-81.

Article received on May 26, 2016

The aim — to make a comparative analysis of the efficacy and safety of traditional medical solutions and original compositions for use in tumescent anesthesia (TA) in the surgical treatment of patients with the use of mini-invasive technologies.
Materials and methods. During 182 (83.5 %) interventions in 157 (83.1 %) patients, Klein solution was used for TA. Original drug composition based on articaine was used for tumescent anesthesia in 36 (16.5 %) cases in 32 (16.9 %) patients.
Results and discussion. The volume of anesthetic injection per patient during a single intervention averaged (366 ± 92) ml (p < 0.05) in the case of using Klein solution and (540 ± 167) mL (p < 0.001) in the case of the proposed drug composition.
Conclusions. The use of improved drug composition for TA allows not to limit the scope of endovascular laser ablation performed during one intervention on one or two legs.

Keywords: tumescent anesthetic, lidocaine, articaine.

List of references:  
1.    Османов Р. Р., Рябинская О. С., Кабаков Б. А., Кузьменко К О. В. вопросу о растворах для тумесцентной анестезии // Хірургія України. — 2016. — № 1 (57).
2.    Пат. 100842 Україна, МПК А61Р23/02. Лікарська композиція для тумесцентної анестезії / Бойко В. В., Османов Р. Р., Рябінська О. С., Кабаков Б. О.; заявник та патентовласник ДУ «Інститут загальної та невідкладної хірургії ім. Зайцева В. Т. НАМНУ». — № u201502033; заявл. 06.03.2015; опубл. 10.08.2015, Бюл. № 15).
3.    Butterwick K. J., Goldman Safety M. P. of lidocaine during tumescent anesthesia for liposuction // Liposuction Principles and Practice Springer. — 2016. — Ch. 12.
4.    Fatemi A. Tumescent local anesthesia with articaine // Liposuction Principles and Practice Springer. — 2016. — Ch. 13.
5.    Izraitel’ N. A., Chashinskaia T. I., Dal’nova et T. S. al. Neutrophil damage index (NDI test) and leukocytosis response in the diagnosis of scleroma // Zh. Mikrobiol. Epidemiol. Immunobiol. — 1977. — Jul; (7). — P. 120 — 123.

Additional: P. 82-86.

Article received on May 23, 2016

The aim — to investigate the influence of treatment with alpha-lipoic acid (ALA) on the dynamics of echocardiographic parameters in patients with type 2 diabetes mellitus (DM) who have had non-Q-myocardial infarction (MI).
Materials and methods. The study involved 39 patients with type 2 DM who have had non-Q-MI. ALA was added in a daily dose of 600mg to the basic treatment of patients for 4 months. Echocardiography with the assessment of morphological and functional state of the myocardium was performed by the standard method before treatment and after its completion.
Results and discussion. When using ALA in patients with type 2 DM who have had non-Q-MI, a significant decrease was identified in the maximum speed of the late peak of diastolic filling (Vа) — from 0.50 ± 0.01 to 0.46 ± 0.01 m/s on the mitral (p < 0.05) and from 0.48 ± 0.01 to 0.43 ± 0.01 m/s on the tricuspid valves (p < 0.01), in deceleration time of early diastolic filling of the right ventricle —from 166.58 ± 3.09 to 158.27 ± 2.72 ms (p < 0.05). A significant increase was registered in the ratio of velocities of early and late peaks of diastolic filling (Vе/Vа) of the ventricles (p < 0.05): for left ventricle — from 0.89 ± 0.03 to 0.97 ± 0.02 and for right ventricle — from 0.79 ± 0.02 to 0.86 ± 0.02. A decrease in diastolic filling of the left ventricle  (p < 0.1) and isovolumic relaxation time of left ventricle (p < 0.1) were also recorded. The study of systolic blood flow from the output portion of the right ventricle showed a significant decrease in PA pressure — from 21.95 ± 1.02 to 18.85 ± 0.79 mm Hg (p < 0.05) in patients receiving ALA.
Conclusions. The use of ALA for 4 months in patients with type 2 DM who have had non-Q-MI, improves both left and right ventricular diastolic function and causes a decrease in the average pressure in РA.

Keywords: type 2 diabetes mellitus, non-Q-myocardial infarction, alpha-lipoic acid, echocardiography.

List of references:  
1.    Мохорт Альфа Т. В.-липоевая кислота: полифакторное влияние и обоснование возможностей использования при сахарном диабете // Мед. новости. — 2011. — № 3. — С. 67 — 71.
2.    Шиллер Н. Б., Осипов Клиническая М. А. эхокардиография. — М.: Практика, 2005. — 344 с.
3.    Boudina S., Abel Diabetic E. D. cardiomyopathy, causes and effects // Rev. Endocr. Metab. Disord. — 2010. — P. 11 — 31.
4.    Chun-jun Li., Lin Lv., Hui Li. et al. Cardiac fibrosis and dysfunction in experimental diabetic cardiomyopathy are ameliorated by alpha-lipoic acid // Cardiovasc. Diabetol. — 2012. — 11. — P. 73.
5.    Constantinescu A., Pick U., Handelman GJ. et al. Reduction and transport of lipoic acid by human erythrocytes // Biochemical pharmacology. — 1995. — N 50 (2). — Р. 253 — 261.
6.    Haidara M. A., Yassin H. Z., Rateb M. et al. Role of oxidative stress in development of cardiovascular complications in diabetes mellitus // Curr. Vasc. Pharmacol. — 2006. — N 4. — Р. 215 — 227.
7.    Haramaki N., Han D., Handelman et G. J. al. Cytosolic and mitochondrial systems for NADH- and NADPH-dependent reduction of alpha-lipoic acid // Free Radical Biol. Med. — 1997. — N 22 (3). — Р. 535 — 542.
8.    Harding S. V., Rideout T. C., Jones Evidence P. J. for using alpha-lipoic acid in reducing lipoprotein and inflammatory related atherosclerotic risk // J. Diet Suppl. — 2012. — N 9 (2). — Р. 116 — 127.
9.    Heinisch B. B., 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. — N 40 (2). — Р. 148 — 154.
10.    Jones W., Li X., Qu et Z. C. al. Uptake, recycling, and antioxidant actions of alpha-lipoic acid in endothelial cells // Free Radical Biol. Med. — 2002. — N 33 (1). — Р. 83 — 93.
11.    Kain V., Kumar S., Sitasawad Azelnidipine S. L. prevents cardiac dysfunction in streptozotocin-diabetic rats by reducing intracellular calcium accumulation, oxidative stress and apoptosis // Cardiovasc. Diabetol. — 2011. — 10. — P. 97.
12.    Keech A. C., Colquhoun D., Best J. et al. Secondary prevention of cardiovascular events with long-term pravastatin in patients with diabetes or impaired fasting glucose: result from the LIPID trail // Diabetes Care. — 2003. — N 26. — Р. 2713 — 2721.
13.    Kunt T., Forst T., Wilhelm A. Alpha-lipoic acid reduces expression of vascular cell adhesion molecule-1 and endothelial adhesion of human monocytes after stimulation with advanced glycation end products // Clin. Sci. (Lond). — 1999. — N 96 (1). — Р. 75 — 82.
14.    Malmberg K., Ryden L., Wedel H. et al. Intense metabolic control by means of insulin in patients with diabetes mellitus and acute myocardial infarction (DIGAMI 2): effects on mortality and morbidity // Eur. Heart J. — 2005. — N 26. — Р. 650 — 661.
15.    Otto The C. M. Practice of Clinical Echocardiography. — 4th ed. — Washington: Elsevier, 2012. — 942 p.
16.    Packer L., Witt E. H., Tritschler Alpha H. J.-lipoic acid as a biological antioxidant // Free Radical Biol. Med. — 1995. — N 19 (2). — Р. 227 — 250.
17.    Petrov V. V., Fagard R. H., Lijnen Stimulation P. J. of collagen production by transforming growth factor-beta1 during differentiation of cardiac fibroblasts to myofibroblasts // Hypertension. — 2002. — N 39. — Р. 258 — 263.
18.    Publications of the World Health Organization. Use of Glycated Haemoglobin (HbA1c) in the Diagnosis of Diabetes Mellitus. Abbreviated Report of a WHO Consultation. — Geneva: WHO Press, 2011. — 25 р.
19.    Somaratne J. B., Whalley G. A., Poppe et K. K. al. Screening for left ventricular hypertrophy in patients with type 2 diabetes mellitus in the community // Cardiovasc. Diabetol. — 2011. — 10. — P. 29.
20.    Zhang L., Zou J., Chai E. et al. Alpha-lipoic acid attenuates cardiac hypertrophy via downregulation of PARP-2 and subsequent activation of SIRT-1 // Eur. J. Pharmacol. — 2014. — Vol. 744. — Р. 203 — 210.
21.    Zou J., Gan X., Zhou H. et al. Alpha-lipoic acid attenuates cardiac hypertrophy via inhibition of C/EBPβ activation // Mol. Cell. Endocrinol. — 2015. — Vol. 399. — Р. 321 — 329.
22.    Zou P., Wu L. L., Wu D. et al. High glucose increases periostin expression and the related signal pathway in adult rat cardiac fibroblasts // Acta Physiologica Sinica. — 2010. — N 62 (3). — Р. 247 — 254.
23.    Zuanetti G., Latini R., Maggioni et A. P. al. Influence of diabetes on mortality in acute myocardial infarction: data from the GISSI-2 study // J. Am. Coll. Cardiol. — 1993. — N 22. — Р. 1788 — 1794.

Additional: P. 89-95.

Article received on April 24, 2016

Vascular injury remains relevant and complex area of vascular surgery both in the clinic and organizational aspect. The success of treatment is largely determined by how timely the qualified medical assistance is rendered. Treatment of patients with damaged major vessels should be performed in specialized institutions. Surgical strategy depends on the extent and severity of ischemia. However, even the relief operations lead to unsatisfactory results of treatment due to the late detection of damage, organizational, tactical and technical errors.

Keywords: stages of medical evacuation, injury to blood vessels, bypass surgery, prosthetics.

List of references:  
1.    Абушев Хирургическая Н. С. тактика при огнестрельных повреждениях магистральных артерий конечностей // Грудная и сердечно-сосудистая хир. — 1996. — № 6. — С. 117.
2.    Бельков Ю. А., Желтовский Ю. В., Расулов Хирургия Р. И. посттравматических осложнений магистральных сосудов конечностей // Грудная и сосудистая хир. — 1996. — № 6. — С. 118.
3.    Брюсов Современные П. Г. принципы лечения огнестрельных ранений магистральных сосудов // Ангиол. и сосуд. хир. — 1997. — № 3. — С. 119 — 120.
4.    Вишневский А. А., Шрайбер Военно М. И.-полевая хирургия: руководство для врачей. — М.: Медицина, 1975. — С. 12 — 14, 51 — 66.
5.    Гаибов А. Д., Урунбаев Д. У., Дадажанова Особенности Ф. А. хирургической тактики при сочетанных костно-сосудистых огнестрельных ранениях // Ангиол. и сосуд. хир. — 1999. — № 2. — С. 57 — 61.
6.    Губка А. В., Никоненко А. С., Перцов Хирургическая В. И. тактика при травме сосудов // Ангиол. и сосуд. хир. — 1997. — № 3. — С. 132 — 133.
7.    Гуманеко Е. К., Самохвалов Военно И. М.-полевая хирургия локальных войн и вооруженных конфликтов: руководство для врачей. — М.: ИГ «Гэотар-Медиа», 2011. — С. 135 — 139, 472 — 478.
8.    Гуманенко Современные Е. К. принципы лечения огнестрельных ранений // Современная огнестрельная травма: материалы Всероссийской научной конференции. — 22.05.98, Санкт-Петербург. — СПб, 1998. — С. 10 — 11.
9.    Гур’єв С. О., Кукуруз Я. С., Яловенко В. А., Волна Аналіз І. М. досвіду лікування вогнепальних поранень кінцівок // Актуальні теми. — 2014. — С. 25 — 32.
10.    Дуданов И. П., Ижиков Повреждения Ю. А. сосудов конечностей // Вестн. хир. — 2000. — № 4. — С. 112 — 117.
11.    Капустин Р. Ф., Гомбалевский Огнестрельные Д. В. ранения конечностей: методические рекомендации. — Минск, 2004. — С. 1 — 34.
12.    Корнилов Повреждения В. А. магистральных сосудов: клиника, диагностика и лечение: Автореф. дис. ...д-ра мед. наук. — Л., 1978. — 23 с.
13.    Кувшинский Актуальные Д. Д. проблемы этапного лечения современной боевой травмы // ВМЖ. — 1974. — № 3. — С. 8 — 13.
14.    Кузьмина Руководство А. И. по травматологии МС ГО. — М.: Медицина, 1978. — С. 27 — 29, 153.
15.    Лисицына К. М., Шапошникова Военно Ю. Г.-полевая хирургия: руководство для врачей. — М.: Медицина, 1982. — С. 48 — 52.
16.    Лыткин М. И., Зубарев Огнестрельная П. Н. травма // Вестн. хир. — 1995. — Т. 154, № 1. — С. 67 — 71.
17.    Нечаев Хирургические Э. А. аспекты уроков войны в Афганистане // Воен. мед. журнал. — 1991. — № 8. — С. 7 — 12.
18.    Обельчак И. С., Бокерия Л. А., Войновский А. Е., Акимов Мультиспиральная А. В. компьютерная томография в диагностике огнестрельных повреждений магистральных сосудов // Радиология-практика. — 2012. — № 5.
19.    Роговський Вказівки В. М. по військово-польовій хірургії МО України. — К., 2014.
20.    Указания по военно-ролевой хирургии. Утверждены Начальником Главного военно-медицинского управления МО РФ. — М., 2013.
21.    Усманов Б. С., Махмудов Н. И., Исмаилов Ж. Т., Дадабаев Тактика Х. Р. лечения больных с повреждениями магистральных сосудов нижних конечностей // Вестн. экстренной медицины. — 2009. — № 3. — С. 49 — 51.
22.    Харузина Опыт О. В. ведения пациентов с ранениями магистральных сосудов шеи, верхних и нижних конечностей в многопрофильном стационаре. — Пермь, 2013.
23.    Шалимов А. А., Дрюк Хирургия Н. Ф. аорты и магистральных артерий. — К.: Здоровье, 1979. — 208 с.
24.    Aronson J. Limb-lenghtening, skeletal reconstruction, and bone transport with the llizarov method // J. Bone Joint Surg. — 1997. — Vol. 79-A, N 8. — Р. 1243 — 1258.
25.    Balkenor A. H., Lord The J. W. sevored prima-artery in the War wounded: A nonsture metod of bridging arterial defects // Surgery. — 1942. — Vol. 12. — P. 488 — 508.
26.    Berk Arteriography M. E. in peripheral trauma // Clin. Med. — 1963. — Vol. 14. — P. 235 — 239.
27.    Burnett et H. F. al. Periferal arterial injuries. A reastesment // Ann. Surg. — 1976. — Vol. 183, N 3. — Р. 701 — 709.
28.    Campbell W. B., Wolfe The J. N. role of non-invasive tests in arterial disease // Brit. J. Syrg. — 1987. — Vol. 74, N 2.
29.    De Bakey M. E., Simeone Battle F. A. injuries of the arteries in world war II: An analysis of 2471 cases // Ann. Surg. — 1946. — Vol. 123, N 4. — Р. 534 — 579.
30.    Denck N. Control angiographies after reconstructive vascular surgery // J. Cardiov. Surg. (Torino). — 1975
31.    Dimond F. C., Rich M N. M.-16 rifle in Vietnam // J. Trauma. — 1967. — Vol. 7, N 5. — Р. 619 — 625.
32.    Fisher Acute G. W. arterial injuries treated by the United states army medical service in Vietnam 1965 — 1966 // J. Trauma. — 1967. — Vol. 7, N 6. — Р. 844 — 855.
33.    Fry Is W. J. arteriography necessary in the management of vascular trauma of extremities // Surgery. — 1978. — Vol. 84, N 4. — Р. 557 — 562.
34.    Gill S. S., Egglleston F., Sing Arterial C. E. injuries the extremities // J. Trauma. — 1976. — Vol. 16, N 10. — Р. 766 — 785.
35.    Hughes Arterial C. W. repair during the Korean War // Ann. Surg. — 1958. — Vol. 147. — P. 555 — 561.
36.    Kelly G., Eismann B. Managemant of small arterial injuries: Clinical and experimental studies // J. Trauma. — 1976. — Vol. 16, N 9. — Р. 681 — 685.
37.    Kelly S. B., Snyder W., Weiglt Arterial J. A. injuries below the knee. Fifty-one patients with 82 injuries // J. Trauma. — 1983. — Vol. 23, N 4. — Р. 285 — 292.
38.    Lavenson G. S., Rich N. M., Baugh Value J. N. of ultrasonic flow detector in the management of peripheral vascular disease // Amer. J. Surg. — 1970. — Vol. 12, N 4. — Р. 522 — 526.
39.    Levitsky S. Vascular trauma in Vietnam battle causcaltion // Ann. Surg. — 1968. — Vol. 168, N 2. — Р. 831 — 836.
40.    Learmont J. Injuries of blood vessels // History of the second war Surgery. — London, 1953. — P. 538 — 544.
41.    Love L., Braun T. Arteriography of peripheral vascular trauma // Am. J. Roengenol. — 1968. — Vol. 192, N 2. — Р. 431 — 440.
42.    Makins Injuries G. N. to the blood vessels: History of the great War Medical services // Surgery of the war. — London, 1992. — Vol. 2. — P. 170 — 206.
43.    Norris B. L., Kellam Soft J. F.-tissue injuries associated with hith-energgi extremity trauma: principles of management // J. Am. Acad. Jrthop. Surg. — 1997. — Vol. 5, N 1. — P. 37 — 46.
44.    Rich N. M., Spencer Vascular F. C. trauma. Philadelphia etc. — Saunders Co., 1978. — 610 p.
45.    Saleh M., Yang L., Sims M. Limb reconstruction after hith-energgi trauma // Br. Med. bull. — 1999. — Vol. 55, N 4. — P. 870 — 884.

Additional: P. 96-103.

In recent years, the incidence of coronary artery disease (CAD) in women of child-bearing age hs increased. Over the last decade the incidence of myocardial infarction (MI) in pregnant women has increased significantly as also the age of first birth. That is why cardiologists should carry out the risk assessment of MI in the pregnant, determine contraindications for pregnancy in women with proven CAD, MI in the past, conduct management of MI in pregnancy, estimate the safety of cardiological drugs. According to modified by WHO classification of maternal cardiovascular risk, which integrates all known maternal cardiovascular risk factors including the underlying heart disease and any other co-morbidity, pregnant women after MI with mild left ventricular impairment have II — III risk level. Risk factors for IM in pregnant women are the same as in general population and include smoking, hypertension, diabetes mellitus, age > 35. In addition, pregnancy complications such as preeclampsia, thromobophilia and postpartum infection, severe postpartum haemorrhage contribute to the development of MI not only in the postpartum period but also increase the risk of stroke, IM, thromboembolic event within the next 5 — 15 years. Compared with the general population, the major cause of MI in pregnant women is spontaneous coronary artery dissection occurring in 16 — 63 % cases. Spontaneous coronary artery dissection is connected with hormons changes in pregnancy, especially hyperprogesteronemia resulting in decrease of collagen and mucopolysaccharide synthesis, vessel wall thinning. With a view to revascularization, preference is given to primary percutaneous coronary interventions, as thrombolytic therapy significantly increases the risk of hypoplacental bleeding. But there is a danger of increasing coronary artery dissection associated with coronaroventriculography. Aspirin and heparin are considered safe for pregnant women. New antiplatelet agents are advisable only when strictly needed (e.g. after stenting). Nitrates are safe and commonly used in the management of MI. However, administration of them should be adjusted to hemodynamic status to avoid hypotension and fetal hypoxia. For antianginal effect, beta-blockers, especially labetalol are recommended as relatively safe drugs. Statins are contraindicated during pregnancy. Bile acid sequestrants are prescribed for management of dyslipidemia.

Keywords: coronary artery disease, pregnancy, spontaneous coronary artery dissections, teratogenic drugs.

List of references:  
1.    Ватутин Н. Т., Тарадин Г. Г., Тараторина и А. А. др. Ишемическая болезнь сердца и беременность // Медико-социальные проблемы семьи. — 2013. — Т. 18, № 4. — С. 97—106.
2.    Ткачева Инфаркт O. Н. миокарда и беременность // Проблемы женского здоровья. — 2008. — Т. 3, № 3. — C. 25—30.
3.    «Proposed rules», Federal Register. — 2008. — Vol. 73. — Р. 30831 — 30868.
4.    Alfonso F. Spontaneous coronary artery dissection: new insights from the tip of the iceberg? // Circulation. — 2012.—126. — Р. 667 — 670.
5.    Anderson Aortic R. A. dissection in pregnancy: importance of pregnancy induced changes in the vessel wall and bicuspid aortic valve in pathogenesis // Brit. J. Obstet.Gynaecol. — 1994. — Vol. 101. — P. 1085—1118.
6.    Bondagji Ischaemic N. S. heart disease in pregnancy // J. Saudi Heart Assoc. — 2012. — Vol. 24. — P. 89—97.
7.    Bowater S. E., Thorne Management S. A. of pregnancy in women with acquired and congenital heart disease // Postgrad. Med. J. — 2010. — Vol. 86. — P. 100 — 105.
8.    Burchill L. J., Heleen L., Roos-Hesselink J. et al. Pregnancy risks in women with pre-existing coronary artery disease, or following acute coronary syndrome // Heart. — 2014. — 30. — P. 66 — 76.
9.    Chandrasekhar S., Cook C.R, Collard Cardiac C. D. surgery in the parturient // Anesth. Analg. — 2009. — Vol. 108. — P. 777 — 785.
10.    Collyer M., Bellenger N., Nachimuthu P. et al. Postpartum coronary artery dissection // J. Obstet. Gynaecol. — 2008. — Vol. 28. — Р. 451 — 453.
11.    Drenthen W., Boersma E., Balci A. et al. Predictors of pregnancy complications in women with congenital heart disease // Eur. Heart J. — 2010. — Vol. 31. — P. 2124 — 2132.
12.    Elkayam U., Jalnapurkar S., Barakkat. et al. Cardiovascular Management in Pregnancy. Pregnancy-Associated Acute Myocardial Infarction // Circulation. — 2014. — Vol. 129. — P. 1695 — 1702.
13.    Gibson P. S., Powrie R. Anticoagulants and pregnancy: when are they safe? // Clev. Clin. J. Med. — 2009. — Vol. 76. — P. 113 — 127.
14.    Idelle M., Weisman R., Zeballos J. Clinical exercise testing // Karger Medical and Scientific Publishers. — 2002. — Р. 329.
15.    James A. H., Jamison M. G., Biswas et M. S. al. Acute myocardial infarcttion in pregnancy: a United States population-based study // Circulation. — 2006. — Vol. 113. — P. 1564 — 1571.
16.    Janion-Sadowska A.,  Sadowski M., Kurzawski J. et al. Pregnancy after Acute Coronary Syndrome: A Proposal for Patients’ Management and a Literature Review // BioMed Res. Int. Vol. — 2013. — P. 1—7.
17.    Jastrow N., Meyer P., Khairy P. et al. Prediction of complications in pregnant women with cardiac diseases referred to a tertiary center // Int. J. Cardiol. — 2010.— Jul 24. — P. 112 — 118.
18.    Ladner H. E., Danielsen B., Gilbert Acute W. M. myocardial infarction in pregnancy and the puerperium: a population-based study // Obstet. Gynecol. — 2005. — Vol. 105. — P. 480 — 484.
19.    Mader E. C., Kasinski D. J., Wilson et W. R. al. Two vessel coronary artery dissection in the peripartum period, case report and literature review // Angiology. — 1994. — Vol. 45. — P. 809 — 816.
20.    Manalo-Estrella P., Barker Histopathologic A. E. findings in human aortic media associated with pregnancy // Arch. Pathol. — 1967. — Vol. 83. — P. 336 — 341.
21.    Mosca E., Benjamin J., Berra K. et al. Effectiveness-based guidelines for the prevention of cardiovascular disease in women: 2011 update: a guideline from the American Heart Association // J. Am. Coll. Cardiol. — 2011. — 57(12). — P. 1404 — 1423.
22.    Oakley C., Warnes C. Coronary artery disease. Heart disease in pregnancy // Blackwell Publishing. — 2007. — Ch. 15. — P. 204 — 217.
23.    Petersen K. M., Jimenez-Solem E., Andersen et J. T. al. B-blocker treatment during pregnancy and adverse pregnancy outcomes: a nationwide population-based cohort study // Br. Med. J. Open. — 2012. — Vol. 2.
24.    Regitz-Zagrosek V., Lundqvist C., Borghi C. et al. ESC Guidelines on the management of cardiovascular diseases during pregnancy // Eur. Heart J. — 2011. — Vol. 32. — P. 3147 — 3197.
25.    Roberts J. M., Catov Pregnancy J. M. is a screening test for later life cardiovascular disease: now what? research recommendations // Women’s Health Issues. — 2012. — Vol. 22. — 2. — P. e123–e128.
26.    Roos-Hesselink J. W., Duvekot J. J., Thorne Pregnancy S. A. in high risk cardiac conditions // Heart. — 2009. — Vol. 95. — P. 680 — 686. — doi: 10.1136/hrt.2008.148932.
27.    Roos-Hesselink J. W., Titia P. E., Thilén U. et al. Outcome of pregnancy in patients with structural or ischaemic heart disease: results of a registry of the European Society of Cardiology // EHJ. — 2011. — 32. — P. 3147 — 3197.
28.    Roth A., Elkayam U. Acute myocardial infarction associated with pregnancy // J. Am. Coll. Cardiol. — 2008. — Vol. 52. — P. 171 — 180.
29.    Steg G., James S., Atar D. et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation // Eur. Heart J. — 2012. — 33. — P. 2569 — 2619.
30.    Thorogood M., Seed M., De Mott K. Management of fertility in women with familial hypercholesterolaemia: summary of NICE guidlince // Int. J. Obst. Gynaecol. —  Vol. 116, Iss. 4. — P. 478 — 479.
31.    Tweet M. S., Hayes S. N., Pitta et S. R. al. Clinical features, management, and prognosis of spontaneous coronary artery dissection // Circulation. — 2012. — Vol. 126. — P. 579 — 588.
32.    Ventura S. J., Curtin S. C., Abma et J. C. al. Estimated pregnancy rates and rates of pregnancy outcomes for the United States, 1990 — 2008 // Nat. Vit. Stat. Rep. — 2012. — Vol. 60. — P. 1 — 7.
33.    Vliegen H. W., van Dijk A. P., Voor et A. A. al. Predictors of pregnancy complications in women with congenital heart disease // Eur. Heart J. — 2010. — 31. [17]. — P. 2124 — 2132.
34.    Yiannis S., Chatzizisis Y. S., Gianmoglon G. D., George D. Is left coronary system more susceptible to atherosclerosis than right? A pathophysiological insight // Int. J. Cardiol. — 2007. — Vol. 116. — P. 7 — 13.

Additional: P. 104-111.

Article received on April 21, 2016