Цель: изучить поражение органов-мишеней у пациентов с метаболическим синдромом (МС) и артериальной гипертонией (АГ) 1-й степени. Материалы и методы. В исследование включены 20 здоровых добровольцев (группа контроля) и 60 пациентов с МС, АГ 1-й степени и тем или иным нарушением липидного обмена. Всем больным проводились измерение офисного артериального давления, суточное мониторирование артериального давления, определение показателей углеводного обмена, уровня вазоактивных медиаторов, ультразвуковая допплерография сонных артерий, эхокардиография. Результаты. У значительной части пациентов с МС и АГ 1-й степени определялись нарушения углеводного обмена, уровень вазоконстрикторов был достоверно выше по сравнению с группой контроля. У 30% больных выявлялось атеросклеротическое поражение сонных артерий и у 40% – гипертрофия миокарда левого желудочка. Заключение: полученные результаты свидетельствуют о высокой распространенности поражения органов-мишеней у пациентов с МС и АГ 1-й степени.
Ключевые слова: метаболический синдром, эндотелиальная дисфункция, поражение органов-мишеней.
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Aims: to study the target organ damage in patients with metabolic syndrome (MS) and arterial hypertension (AH) 1 degree. Design and methods. We included 20 healthy volunteers and 60 patients with MS, AH 1 degree and dyslipidemia. Office blood pressure, 24-hour ambulatory blood pressure monitoring, measurements of the endothelial vasoactive mediators, carotid ultrasonography and echocardiography had performed at baseline. Results. The majority of patients with MS and AH 1 degree had metabolic abnormalities; the levels of vasoactive mediators were higher in comparison with control group; 30% of patients had signs of atherosclerotic process in carotid arteries; 40% of patients had left ventricular hypertrophy. Conclusion: the results showed high prevalence of target organ damage in patients with MS and AH 1 degree.
Key words: metabolic syndrome, endothelial vasoactive mediators, target organ damage.
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________________________________________________
1. Diagnostika i lechenie arterial'noi gipertonii. Klinicheskie rekomendatsii. Kardiol. vestn. 2015. X (1): 3–30. [in Russian]
2. Ferrara LA, Guida L, Ferrara F et al. Cardiac structure and function and arterial circulation in hypertensive patients with and without metabolic syndrome. J Hum Hypertens 2007а; 21 (9): 729–35.
3. Viazzi F, Leoncini G, Parodi D et al. Impact of Target Organ Damage Assessment in the Evaluation of Global Risk in Patients with Essential Hypertension. J Am Soc Nephrol 2005; 16: S89–S91.
4. Sharipova G.Kh. Osobennosti porazheniia organov-mishenei u bol'nykh arterial'noi gipertoniei v zavisimosti ot nalichiia i otsutstviia metabolicheskogo sindroma. Dis. … d-ra med. nauk. M., 2009. [in Russian]
5. Cuspidi C, Meani S, Valerio C et al. Age and target organ damage in essential hypertension: role of the metabolic syndrome. Am J Hypertens 2007; 20 (3): 296–303.
6. Rekomendatsii ekspertov VNOK po diagnostike i lecheniiu MS (2-i peresmotr). Kardiovask. terapiia i profilaktika (Pril. 2). 2009; 7 (6). [in Russian]
7. Boytsov S.A., Balanova Yu.A., Shal'nova S.A. et al. Arterial'naia gipertoniia sredi lits 25–64 let: rasprostranennost', osvedomlennost', lechenie i kontrol'. Po materialam issledovaniia ESSE. Kardiovask. terapiia i profilaktika. 2014; 13 (4): 4–14. [in Russian]
8. Stoks JI, Kannel WB, Wolf PA. Blood pressure as a risk factor for cardiovascular disease. The Framingham study – 30 years of follow-up. Hypertension 1989; 13 (Suppl. 1): 1–13.
9. Mendizábal Y, Llorens S, Nava E. Hypertension in metabolic syndrome: vascular pathophysiology. Int J Hypertens 2013; 2013: 230868. DOI: 10.1155/2013/230868. Epub 2013 Mar 20.
10. Morise T, Takeuchi Y, Kawano M et al. Increased plasma levels of immunoreactive endothelin and von Willebrand factor in NIDDM patients. Diabetes Care 1995; 18 (1): 87–9.
11. Da Silva AA, Kuo JJ, Tallam LS, Hall JE. Role of endothelin-1 in blood pressure regulation in a rat model of visceral obesity and hypertension. Hypertension 2004; 43 (2): 383–7.
12. Graziani F, Biasucci LM, Cialdella P et al. Thromboxane production in morbidly obese subjects. Am J Cardiol 2011; 107 (11): 1656–61.
13. Van Harmelen V, Eriksson A, Åström G et al. Vascular peptide endothelin-1 links fat accumulation with alterations of visceral adipocyte lipolysis. Diabetes 2008; 57 (2): 378–86.
14. Tessari P, Cecchet D, Artusi C et al. Roles of insulin, age, and asymmetric dimethylarginine, on nitric oxide synthesis in vivo. Diabetes 2013; 62 (10): e24–e24.
15. Caimi G, Hopps E, Montana M et al. Evaluation of nitric oxide metabolites in a group of subjects with metabolic syndrome. Diabetes Metab Syndr 2012; 6 (3): 132–5.
16. Kurshakov A.A. Insulinorezistentnost' i oksid azota na rannei stadii metabolicheskogo sindroma. Vestn. Sankt-Peterburgskoi meditsinskoi akademii im. I.I.Mechnikova. 2009; 2/1 (31): 125–9. [in Russian]
17. Blinova N.V., Masenko V.P., Chazova I.E. Effects of amlodipine and atorvastatin on endothelial vasoactive mediators in patients with metabolic syndrome. Systemic Hypertension. 2015; 12 (1): 37–43. [in Russian]
18. Greenland P, Alpert JS, Beller GA et al. 2010 ACCF/AHA guideline for assessment of cardiovascular risk in asymptomatic adults: a report of the American college of cardiology foundation/American heart association task force on practice guidelines. J Am Coll Cardiol 2010; 56 (25): 50–103.
19. Muromtseva G.A., Kontsevaya A.V., Konstantinov V.V. et al. Rasprostranennost' faktorov riska neinfektsionnykh zabolevanii v Rossiiskoi populiatsii v 2012–2013 gg. Rezul'taty issledovaniia ESSE-RF. Kardiovask. terapiia i profilaktika. 2014; 13 (6): 4–11. [in Russian]
20. Pasternak RC, Abrams J, Greenland P et al. 34th Bethesda Conference: Task force # 1-Identification of coronary heart disease risk: is there a detection gap? J Am Coll Cardiol 2003; 41: 1863–74.
21. Zanchetti A, Crepaldi G, Bond MG et al. Different effects of antihypertensive regimens based on fosinopril or hydrochlorothiazide with or without lipid lowering by pravastatin on progression of asymptomatic carotid atherosclerosis: principal results of PHYLLIS – a randomized double-blind trial. Stroke 2004; 35: 2807–12.
22. Hank Juo S, Lin H, Rundek T et al. Genetic and Environmental Contributions to Carotid Intima-Media thickness and obesity phenotypes in the Northern Manhattan Family Study. Stroke 2004; 35: 2243–7.
23. Kawamoto R, Tomita H, Ohtsuka N et al. Metabolic syndrome, diabetes and subclinical atherosclerosis as assessed by carotid intima-media thickness. J Atheroscler Thromb 2007; 14 (2): 78–85.
24. Fontbonne A, Eschwège E, Cambien F et al. Hypertriglyceridaemia as a risk factor of coronary heart disease mortality in subjects with impaired glucose tolerance or diabetes. Results from the 11-year follow-up of the Paris Prospective Study. Diabetologia 1989; 32 (5): 300–4.
25. Ferrara LA, Cardoni O, Mancini M et al. Metabolic syndrome and left ventricular hypertrophy in a general population. Results from the GUBBIO Study. J Hum Hypertens 2007; 21 (10): 795–801.
26. Cuspidi C, Sala C, Lonati L et al. Metabolic syndrome, left ventricular hupertrophy and carotid atherosclerosis in hypertension: a gender-based study. Blood Press 2013; 22 (3): 138–43.
Институт клинической кардиологии им. А.Л.Мясникова ФГБУ Российский кардиологический научно-производственный комплекс Минздрава России. 121552, Россия, Москва, ул. 3-я Черепковская, д. 15а
*nat-cardio1@yandex.ru
A.L.Myasnikov Institute of Clinical Cardiology, Russian Cardiological Scientific-Industrial Complex of the Ministry of Health of the Russian Federation. 121552, Russian Federation, Moscow, ul. 3-ia Cherepkovskaia, d. 15a
*nat-cardio1@yandex.ru