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Органопротективный эффект фиксированной комбинированной антигипертензивной терапии эпросартаном и гидрохлоротиазидом при субклиническом и клиническом поражении органов-мишеней у пациентов с гипертонической болезнью
Органопротективный эффект фиксированной комбинированной антигипертензивной терапии эпросартаном и гидрохлоротиазидом при субклиническом и клиническом поражении органов-мишеней у пациентов с гипертонической болезнью
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Аннотация
Цель исследования – оценка влияния фиксированной комбинированной антигипертензивной терапии эпросартаном и гидрохлоротиазидом со старта на клинические и субклинические показатели поражения органов-мишеней у пациентов с гипертонической болезнью (ГБ) независимо от исходного уровня артериального давления (АД) и сердечно-сосудистого риска.
Материалы и методы. Исследование представляет два параллельных субисследования. В первом субисследовании при скрининге 3536 рабочих промышленного предприятия выявлены 13,0% (395 человек) больных ГБ. Среди них зарегистрированы 12,7% (50 человек) нелеченых больных ГБ, имеющих трехкомпонентное поражение органов-мишеней: гипертрофию левого желудочка, гипертоническую нефропатию, поражение периферических артерий. Во втором субисследовании среди той же когорты были зарегистрированы 15,2% (60 человек) нелеченых больных ГБ I стадии без клинических признаков органных изменений. 1-я группа в обоих субисследованиях получала фиксированную комбинацию эпросартана мезилат в дозе 600 мг и гидрохлоротиазида в дозе 12,5 мг 1 раз в сутки независимо от исходного уровня АД в дебюте исследования. 2-й группе назначалась монотерапия эналаприлом и/или в комбинации с гидрохлоротиазидом в зависимости от степени повышения АД и группы сердечно-сосудистого риска.
Результаты. Комбинированная фиксированная антигипертензивная терапия (эпросартан + гидрохлоротиазид) со старта независимо от исходного уровня АД и сердечно-сосудистого риска в сравнении с монотерапией эналаприлом и/или его свободной комбинацией с гидрохлоротиазидом, назначаемой с учетом уровня АД и сердечно-сосудистого риска, обеспечила более выраженный регресс как клинического, так и субклинического поражения органов-мишеней на фоне 6-месячной терапии по данным динамики массы миокарда левого желудочка (ММЛЖ), индекса ММЛЖ и тканевого ингибитора матриксных металлопротеиназ 1-го типа, микроальбуминурии и скорости клубочковой фильтрации, толщины комплекса интима–медиа при выполнении допплерографического ультразвукового исследования сонных артерий и показателей скорости пульсовой волны в разных сегментах по результатам объемной сфигмоплетизмографии.
Выводы. Назначение фиксированной комбинации эпросартана и гидрохлоротиазида нелеченым больным ГБ трудоспособного возраста со старта независимо от исходного уровня АД и сердечно-сосудистого риска обеспечивает регресс поражения органов-мишеней и профилактику их развития при отсутствии органных изменений.
Ключевые слова: гипертоническая болезнь, поражение органов-мишеней, фиксированная комбинация эпросартана мезилата и гидрохлоротиазида.
Subjects and methods. The study consisted of two parallel substudies. Substudy 1 that screened 3536 workers from industrial enterprises identified 395 (13%) hypertensive patients. Among them, there were 50 (12,7%) untreated patients with HD who had three-component target organ damages: left ventricular hypertrophy, hypertensive nephropathy, peripheral artery lesion. Sixty (15,2%) untreated patients with Stage 1 HD without clinical signs of organ changes were recorded among the same cohort in Substudy 2. In both substudies, Group 1 received a fixed-dose combination of eprosartan mesylate 600 mg once daily and hydrochlorothiazide 12,5 once daily regardless of baseline BP at the onset of the study. Group 2 had monotherapy with enalapril and/or its combination with hydrochlorothiazide depending on the degree of BP elevation and the group of a cardiovascular risk.
Results. Starting fixed-dose combination antihypertensive therapy (eprosartan + hydrochlorothiazide) irrespective of baseline BP and cardiovascular risk versus monotherapy with enalapril and/or its free combination with hydrochlorothiazide, which was used in terms of BP level and cardiovascular risk ensured a more significant regression of both clinical and subclinical target organ damages during 6-month therapy according to the changes in left ventricular mass (LVM), LVM index, and tissue inhibitor of type 1 matrix metalloproteinases, microalbuminuria and glomerular filtration rate, intima-media complex thickness during carotid Doppler ultrasound study, and pulse wave velocity in different segments, as evidenced by volumetric sphygmoplethysmography.
Conclusions. The use of a fixed-dose combination of eprosartan and hydrochlorothiazide in untreated patients of able-bodied age regardless of baseline BP and cardiovascular risk ensures the regression of target organ damages and the prevention of their development in the absence of organ changes.
Key words: hypertensive disease, target organ damage, fixed-dose combination of eprosartan mesylate and hydrochlorothiazide.
Материалы и методы. Исследование представляет два параллельных субисследования. В первом субисследовании при скрининге 3536 рабочих промышленного предприятия выявлены 13,0% (395 человек) больных ГБ. Среди них зарегистрированы 12,7% (50 человек) нелеченых больных ГБ, имеющих трехкомпонентное поражение органов-мишеней: гипертрофию левого желудочка, гипертоническую нефропатию, поражение периферических артерий. Во втором субисследовании среди той же когорты были зарегистрированы 15,2% (60 человек) нелеченых больных ГБ I стадии без клинических признаков органных изменений. 1-я группа в обоих субисследованиях получала фиксированную комбинацию эпросартана мезилат в дозе 600 мг и гидрохлоротиазида в дозе 12,5 мг 1 раз в сутки независимо от исходного уровня АД в дебюте исследования. 2-й группе назначалась монотерапия эналаприлом и/или в комбинации с гидрохлоротиазидом в зависимости от степени повышения АД и группы сердечно-сосудистого риска.
Результаты. Комбинированная фиксированная антигипертензивная терапия (эпросартан + гидрохлоротиазид) со старта независимо от исходного уровня АД и сердечно-сосудистого риска в сравнении с монотерапией эналаприлом и/или его свободной комбинацией с гидрохлоротиазидом, назначаемой с учетом уровня АД и сердечно-сосудистого риска, обеспечила более выраженный регресс как клинического, так и субклинического поражения органов-мишеней на фоне 6-месячной терапии по данным динамики массы миокарда левого желудочка (ММЛЖ), индекса ММЛЖ и тканевого ингибитора матриксных металлопротеиназ 1-го типа, микроальбуминурии и скорости клубочковой фильтрации, толщины комплекса интима–медиа при выполнении допплерографического ультразвукового исследования сонных артерий и показателей скорости пульсовой волны в разных сегментах по результатам объемной сфигмоплетизмографии.
Выводы. Назначение фиксированной комбинации эпросартана и гидрохлоротиазида нелеченым больным ГБ трудоспособного возраста со старта независимо от исходного уровня АД и сердечно-сосудистого риска обеспечивает регресс поражения органов-мишеней и профилактику их развития при отсутствии органных изменений.
Ключевые слова: гипертоническая болезнь, поражение органов-мишеней, фиксированная комбинация эпросартана мезилата и гидрохлоротиазида.
________________________________________________
Subjects and methods. The study consisted of two parallel substudies. Substudy 1 that screened 3536 workers from industrial enterprises identified 395 (13%) hypertensive patients. Among them, there were 50 (12,7%) untreated patients with HD who had three-component target organ damages: left ventricular hypertrophy, hypertensive nephropathy, peripheral artery lesion. Sixty (15,2%) untreated patients with Stage 1 HD without clinical signs of organ changes were recorded among the same cohort in Substudy 2. In both substudies, Group 1 received a fixed-dose combination of eprosartan mesylate 600 mg once daily and hydrochlorothiazide 12,5 once daily regardless of baseline BP at the onset of the study. Group 2 had monotherapy with enalapril and/or its combination with hydrochlorothiazide depending on the degree of BP elevation and the group of a cardiovascular risk.
Results. Starting fixed-dose combination antihypertensive therapy (eprosartan + hydrochlorothiazide) irrespective of baseline BP and cardiovascular risk versus monotherapy with enalapril and/or its free combination with hydrochlorothiazide, which was used in terms of BP level and cardiovascular risk ensured a more significant regression of both clinical and subclinical target organ damages during 6-month therapy according to the changes in left ventricular mass (LVM), LVM index, and tissue inhibitor of type 1 matrix metalloproteinases, microalbuminuria and glomerular filtration rate, intima-media complex thickness during carotid Doppler ultrasound study, and pulse wave velocity in different segments, as evidenced by volumetric sphygmoplethysmography.
Conclusions. The use of a fixed-dose combination of eprosartan and hydrochlorothiazide in untreated patients of able-bodied age regardless of baseline BP and cardiovascular risk ensures the regression of target organ damages and the prevention of their development in the absence of organ changes.
Key words: hypertensive disease, target organ damage, fixed-dose combination of eprosartan mesylate and hydrochlorothiazide.
Полный текст
Список литературы
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22. Düsing R. Optimizing blood pressure control through the use of fixed combinations. Vasc Health Risk Manag 2010; 25 (6): 321–5.
23. Slavachevsky I, Rachmani R, Levi Z et al. Effect of enalapril and nifedipine on orthostatic hypotension in older hypertensive patients. J Am Geriatr Soc 2000; 48 (7): 807–10.
24. Schrader J, Lüders S, Kulschewski A et al. Morbidity and Mortality After Stroke, Eprosartan Compared with Nitrendipine for Secondary Prevention: principal results of a prospective randomized controlled study (MOSES). Stroke 2005; 36 (6): 1218–26.
25. Lonn E, Shaikholeslami R, Yi Q et al. Effects of ramipril on left ventricular mass and function in cardiovascular patients with controlled blood pressure and with preserved left ventricular ejection fraction: a substudy of the Heart Outcomes Prevention Evaluation (HOPE) Trial. J Am Coll Cardiol 2004; 43: 2200–6.
26. Verdecchia P, Sleight P, Mancia G et al. Effects of telmisartan, ramipril, and their combination on left ventricular hypertrophy in individuals at high vascular risk in the Ongoing Telmisartan Alone and in Combination With Ramipril Global End Point Trial and the Telmisartan Randomized Assessment Study in ACE Intolerant Subjects With Cardiovascular Disease. Circulation 2009; 120: 1380–9.
27. Okin PM, Devereux RB, Jern S et al. Regression of electrocardiographic left ventricular hypertrophy by losartan versus atenolol: the Losartan Intervention for Endpoint reduction in Hypertension (LIFE) Study. Circulation 2003; 108: 684–90.
28. Milan A, Caserta MA, Avenatti E et al. Anti-hypertensive drugs and left ventricular hypertrophy: a clinical update. Intern Emerg Med 2010; 5 (6): 469–79.
29. Saglam M, Karakaya O, Esen AM et al. Contribution of plasma matrix metalloproteinases to development of left ventricular hypertrophy and diastolic dysfunction in hypertensive subjects. Tohoku J Exp Med 2006; 208 (2): 117–22.
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31. Spiers JP, Kelso EJ, Siah WF et al. Alterations in vascular matrix metalloproteinase due to ageing and chronic hypertension: effects of endothelin receptor blockade. J Hypertens 2005; 23 (9): 1717–24.
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2. Cotter J, Oliveira P, Cunha P, Polónia J. Different patterns of one-year evolution of microalbuminuria in hypertensive patients treated with different inhibitors of the renin-angiotensin system. Rev Port Cardiol 2008; 27 (11): 1395–404.
3. Brouwers FP, Asselbergs FW, Hillege HL et al. Long-term effects of fosinopril and pravastatin on cardiovascular events in subjects with microalbuminuria: Ten years of follow-up of Prevention of Renal and Vascular End-stage Disease Intervention Trial (PREVEND IT). Am Heart J 2011; 161 (6): 1171–8.
4. Ari E, Kaya Y, Demir H et al. Oxidative DNA damage correlates with carotid artery atherosclerosis in hemodialysis patients. Hemodial Int 2011; 15 (4): 453–9.
5. Dormán G, Cseh S, Hajdú I et al. Matrix metalloproteinase inhibitors: a critical appraisal of design principles and proposed therapeutic utility. Drugs 2010; 70 (8): 949–64.
6. Bauvois B. New facets of matrix metalloproteinases MMP-2 and MMP-9 as cell surface transducers: Outside-in signaling and relationship to tumor progression. Biochim Biophys Acta 2012; 1825 (1): 29–36.
7. Romi F, Helgeland G, Gilhus NE. Serum Levels of Matrix Metalloproteinases: Implications in Clinical Neurology. Eur Neurol 2012; 67 (2): 121–8.
8. Saglam F, Celik A, Tayfur D et al. Decrease in cell proliferation by an matrix metalloproteinase inhibitor, doxycycline, in a model of immune-complex nephritis. Nephrology (Carlton) 2010; 15 (5): 560–7.
9. Chung AW, Yang HH, Kim JM et al. Upregulation of matrix metalloproteinase-2 in the arterial vasculature contributes to stiffening and vasomotor dysfunction in patients with chronic kidney disease. Circulation 2009; 120 (9): 792–801.
10. Fang JH, Zhou HC, Zeng C et al. MicroRNA-29b suppresses tumor angiogenesis, invasion, and metastasis by regulating matrix metalloproteinase 2 expression. Hepatology 2011; 54 (5): 1729–40.
11. Lantelme P. Blood pressure control: time for action. Arch Cardiovasc Dis 2009; 102 (6–7): 465–7.
12. Bramlage P, Hasford J. Blood pressure reduction, persistence and costs in the evaluation of antihypertensive drug treatment – a review. Cardiovasc Diabetol 2009; 27: 8–18.
13. Erdine S. Compliance with the treatment of hypertension: the potential of combination therapy. J Clin Hypertens (Greenwich) 2010; 12 (1): 40–6.
14. Nicodème R, Albessard A, Amar J et al. Poor blood pressure control in general practice: in search of explanations. Arch Cardiovasc Dis 2009; 102 (6–7): 477–83.
15. Chobanian AV, Bakris GL, Black HR et al. Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003; 42: 1206–52.
16. Pool JL, Glazer R, Crikelair N et al. The role of baseline blood pressure in guiding treatment choice: a secondary analysis of the use of valsartan/hydrochlorothiazide as initial therapy in hypertensive adults in a randomized, double-blind, placebo-controlled trial. Clin Drug Investig 2009; 29 (12): 791–802.
17. Philipp T, Glazer RD, Wernsing M et al. Initial combination therapy with amlodipine/valsartan compared with monotherapy in the treatment of hypertension. J Am Soc Hypertens 2011.
18. Ueng KC, Lin LC, Voon WC et al. An eight-week, multicenter, randomized, double-blind study to evaluate the efficacy and tolerability of fixed-dose amlodipine/benazepril combination in comparison with amlodipine as first-line therapy in chinese patients with mild to moderate hypertension. Blood Press 2008; 1: 24–31.
19. Julius S, Kjeldsen SE, Weber M et al. Outcomes in hypertensive patients at high cardiovascular risk treated with regimens based on valsartan or amlodipine: the VALUE randomised trial. Lancet 2004; 19: 2022–31.
20. Zidek W. Preventing end-organ damage in hypertension. What is the significance of the VALUE Study for general practice? MMW Fortschr Med 2004; 8: 27–8.
21. Dezii CM. A retrospective study of persistence with single-pill combination therapy vs concurrent two-pill therapy in patients with hypertension. Manag Care 2009; l: 2–6.
22. Düsing R. Optimizing blood pressure control through the use of fixed combinations. Vasc Health Risk Manag 2010; 25 (6): 321–5.
23. Slavachevsky I, Rachmani R, Levi Z et al. Effect of enalapril and nifedipine on orthostatic hypotension in older hypertensive patients. J Am Geriatr Soc 2000; 48 (7): 807–10.
24. Schrader J, Lüders S, Kulschewski A et al. Morbidity and Mortality After Stroke, Eprosartan Compared with Nitrendipine for Secondary Prevention: principal results of a prospective randomized controlled study (MOSES). Stroke 2005; 36 (6): 1218–26.
25. Lonn E, Shaikholeslami R, Yi Q et al. Effects of ramipril on left ventricular mass and function in cardiovascular patients with controlled blood pressure and with preserved left ventricular ejection fraction: a substudy of the Heart Outcomes Prevention Evaluation (HOPE) Trial. J Am Coll Cardiol 2004; 43: 2200–6.
26. Verdecchia P, Sleight P, Mancia G et al. Effects of telmisartan, ramipril, and their combination on left ventricular hypertrophy in individuals at high vascular risk in the Ongoing Telmisartan Alone and in Combination With Ramipril Global End Point Trial and the Telmisartan Randomized Assessment Study in ACE Intolerant Subjects With Cardiovascular Disease. Circulation 2009; 120: 1380–9.
27. Okin PM, Devereux RB, Jern S et al. Regression of electrocardiographic left ventricular hypertrophy by losartan versus atenolol: the Losartan Intervention for Endpoint reduction in Hypertension (LIFE) Study. Circulation 2003; 108: 684–90.
28. Milan A, Caserta MA, Avenatti E et al. Anti-hypertensive drugs and left ventricular hypertrophy: a clinical update. Intern Emerg Med 2010; 5 (6): 469–79.
29. Saglam M, Karakaya O, Esen AM et al. Contribution of plasma matrix metalloproteinases to development of left ventricular hypertrophy and diastolic dysfunction in hypertensive subjects. Tohoku J Exp Med 2006; 208 (2): 117–22.
30. Cornish TC, Bagnasco SM, Macgregor AM et al. Glomerular protein levels of matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 are lower in diabetic subjects. J Histochem Cytochem 2009; 57 (11): 995–1001.
31. Spiers JP, Kelso EJ, Siah WF et al. Alterations in vascular matrix metalloproteinase due to ageing and chronic hypertension: effects of endothelin receptor blockade. J Hypertens 2005; 23 (9): 1717–24.
32. Castro MM, Rizzi E, Prado CM et al. Imbalance between matrix metalloproteinases and tissue inhibitor of metalloproteinases in hypertensive vascular remodeling. Matrix Biol 2010; 29 (3): 194–201.
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Авторы
Н.А.Козиолова*1, А.В.Бушмакина1, Н.А.Ковалевская1, И.М.Шатунова1,2
1 ГБОУ ВПО Пермская государственная медицинская академия им. акад. Е.А.Вагнера Минздрава РФ
2 Поликлиника ОАО «Газпром», Москва
*nakoziolova@mail.ru
*nakoziolova@mail.ru
1 ГБОУ ВПО Пермская государственная медицинская академия им. акад. Е.А.Вагнера Минздрава РФ
2 Поликлиника ОАО «Газпром», Москва
*nakoziolova@mail.ru
________________________________________________
*nakoziolova@mail.ru
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