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Динамика обратного ремоделирования сердца и сосудов у больных гипертонической болезнью в зависимости от выбора и тактики назначения антигипертензивной терапии со старта
Динамика обратного ремоделирования сердца и сосудов у больных гипертонической болезнью в зависимости от выбора и тактики назначения антигипертензивной терапии со старта
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Аннотация
Цель работы – оценка динамики регресса гипертрофии левого желудочка и сосудистого ремоделирования у больных гипертонической болезнью в зависимости от выбора и тактики антигипертензивной терапии со старта.
Материал и методы. Обследованы 67 нелеченых больных гипертонической болезнью трудоспособного возраста, имеющих поражение сердца и сосудов без ассоциированных клинических состояний. Больные были разделены на 2 группы в зависимости от выбора и тактики антигипертензивной терапии. Первая группа (34 пациента) получала фиксированную комбинацию эпросартана мезилата и гидрохлортиазида со старта независимо от уровня артериального давления. Во 2-й группе (33 пациента) антигипертензивная терапия назначалась в зависимости от исходной степени повышения артериального давления: монотерапия эналаприлом и нефиксированная комбинация его с гидрохлортиазидом. Длительность терапии составила 6 мес.
Результаты. Достижение целевого уровня артериального давления было равнозначным в 2 группах через 4 нед и 6 мес лечения. Регресс гипертрофии левого желудочка, по данным индекса массы миокарда левого желудочка, был более выражен в 1-й группе, чем во 2-й (p=0,025). Обратное ремоделирование артериальной стенки было более выражено на фоне приема фиксированной комбинации со старта эпросартана мезилата и гидрохлортиазида, чем при монотерапии эналаприлом или в свободной комбинации с гидрохлортиазидом по данным динамики показателей объемной сфигмоплетизмографии, но не толщины комплекса интима–медиа сонных артерий (p<0,05).
Выводы. Степень коррекции сердечно-сосудистого ремоделирования у нелеченых больных гипертонической болезнью зависит от тактики, выбора и интенсивности антигипертензивной терапии со старта и не связана с частотой и скоростью достижения целевого уровня АД.
Ключевые слова: гипертоническая болезнь, выбор антигипертензивной терапии со старта, регресс сердечно-сосудистого ремоделирования.
Materials and methods. 67 non-treated patients of working age with arterial hypertension, who had heart and arteries damage without associated clinical conditions. Patients were divided into 2 groups depending on choice and management of baseline antihypertensive therapy.
The first group consisted of 34 patients who received the fixed combination of eprosartan mesylate 600 mg and hydrochlorthyazide 12,5 mg from baseline regardless of blood pressure level. The second group (n=34) received either enalapril as monotherapy or its different combinations with hydrochlorthyazide depending on blood pressure level. The therapy lasted 6 months.
Results: target blood pressure was reached equivalently in both groups after 4 weeks and after 6 months. Left ventricle hypertrophy regression according to left ventricle myocardial mass index was reliably more expressed in the first group than in the second one (p=0,025). Regression of arterial wall remodeling according to artery stiffness but not intima–media thickness was more evident during therapy with fixed-combined eprosartan mesylate and hydrochlorthyazide than with enalapril as monotherapy or its different combinations with hydrochlorthyazide (p<0,05).
Conclusion: in untreated patients with arterial hypertension correction rate of cardio-vascular remodeling depends on choice, management and intensity of baseline antihypertensive therapy and does not correlate with rapidity and frequency of target blood pressure achievement.
Key words: arterial hypertension, choice of baseline antihypertensive therapy, cardio-vascular remodeling regression.
Материал и методы. Обследованы 67 нелеченых больных гипертонической болезнью трудоспособного возраста, имеющих поражение сердца и сосудов без ассоциированных клинических состояний. Больные были разделены на 2 группы в зависимости от выбора и тактики антигипертензивной терапии. Первая группа (34 пациента) получала фиксированную комбинацию эпросартана мезилата и гидрохлортиазида со старта независимо от уровня артериального давления. Во 2-й группе (33 пациента) антигипертензивная терапия назначалась в зависимости от исходной степени повышения артериального давления: монотерапия эналаприлом и нефиксированная комбинация его с гидрохлортиазидом. Длительность терапии составила 6 мес.
Результаты. Достижение целевого уровня артериального давления было равнозначным в 2 группах через 4 нед и 6 мес лечения. Регресс гипертрофии левого желудочка, по данным индекса массы миокарда левого желудочка, был более выражен в 1-й группе, чем во 2-й (p=0,025). Обратное ремоделирование артериальной стенки было более выражено на фоне приема фиксированной комбинации со старта эпросартана мезилата и гидрохлортиазида, чем при монотерапии эналаприлом или в свободной комбинации с гидрохлортиазидом по данным динамики показателей объемной сфигмоплетизмографии, но не толщины комплекса интима–медиа сонных артерий (p<0,05).
Выводы. Степень коррекции сердечно-сосудистого ремоделирования у нелеченых больных гипертонической болезнью зависит от тактики, выбора и интенсивности антигипертензивной терапии со старта и не связана с частотой и скоростью достижения целевого уровня АД.
Ключевые слова: гипертоническая болезнь, выбор антигипертензивной терапии со старта, регресс сердечно-сосудистого ремоделирования.
________________________________________________
Materials and methods. 67 non-treated patients of working age with arterial hypertension, who had heart and arteries damage without associated clinical conditions. Patients were divided into 2 groups depending on choice and management of baseline antihypertensive therapy.
The first group consisted of 34 patients who received the fixed combination of eprosartan mesylate 600 mg and hydrochlorthyazide 12,5 mg from baseline regardless of blood pressure level. The second group (n=34) received either enalapril as monotherapy or its different combinations with hydrochlorthyazide depending on blood pressure level. The therapy lasted 6 months.
Results: target blood pressure was reached equivalently in both groups after 4 weeks and after 6 months. Left ventricle hypertrophy regression according to left ventricle myocardial mass index was reliably more expressed in the first group than in the second one (p=0,025). Regression of arterial wall remodeling according to artery stiffness but not intima–media thickness was more evident during therapy with fixed-combined eprosartan mesylate and hydrochlorthyazide than with enalapril as monotherapy or its different combinations with hydrochlorthyazide (p<0,05).
Conclusion: in untreated patients with arterial hypertension correction rate of cardio-vascular remodeling depends on choice, management and intensity of baseline antihypertensive therapy and does not correlate with rapidity and frequency of target blood pressure achievement.
Key words: arterial hypertension, choice of baseline antihypertensive therapy, cardio-vascular remodeling regression.
Полный текст
Список литературы
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12. 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.
13. 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.
14. 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.
15. Miller AB, Reichek N, St. John Sutton M et al. Importance of blood pressure control in left ventricular mass regression. J Am Soc Hypertens 2010; 4 (6): 302–10.
16. 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.
17. 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.
18. Asmar R, Garcia-Puig J, Gosse P et al. Ambulatory blood pressure in hypertensive patients with left ventricular hypertrophy: efficacy of first-line combination perindopril/indapamide therapy. Vasc Health Risk Manag 2007; 3 (4): 371–80.
19. Neutel JM, Smith DH, Weber MA. Effect of antihypertensive monotherapy and combination therapy on arterial distensibility and left ventricular mass. Am J Hypertens 2004; 17 (1): 37–42.
20. Andreadis EA, Sfakianakis ME, Tsourous GI et al. Differential impact of angiotensin receptor blockers and calcium channel blockers on arterial stiffness. Int Angiol 2010; 29 (3): 266–72.
21. Chrysant SG. Using fixed-dose combination therapies to achieve blood pressure goals. Clin Drug Investig 2008; 28 (11): 713–34.
22. Smith DH Fixed-dose combination antihypertensives and reduction in target organ damage: are they all the same? Am J Cardiovasc Drugs 2007; 7 (6): 413–22.
23. Mourad JJ, Le Jeune S, Pirollo A et al. Combinations of inhibitors of the renin-angiotensin system with calcium channel blockers for the treatment of hypertension: focus on perindopril/amlodipine. Curr Med Res Opin 2010; 26 (9): 2263–76.
24. Fagard RH, Celis H, Thijs L, Wouters S. Regression of left ventricular mass by antihypertensive treatment: a meta-analysis of randomized comparative studies. Hypertension 2009; 54 (5): 1084–91.
25. 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.
26. Schiffrin EL. Vascular changes in hypertension in response to drug treatment: effects of angiotensin receptor blockers. Can J Cardiol 2002; 18 (Suppl. A): 15A–18A.
27. 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.
28. Amerena J, Pappas S, Ouellet JP et al. ABPM comparison of the anti-hypertensive profiles of telmisartan and enalapril in patients with mild-to-moderate essential hypertension. J Int Med Res 2002; 30 (6): 543–52.
29. Park CG, Lee JY. The significance of the j-curve in hypertension and coronary artery diseases. Korean Circ J 2011; 41 (7): 349–53.
30. Chrysant SG. Current status of aggressive blood pressure control. World J Cardiol 2011; 3 (3): 65–71.
31. 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.
32. Vase H, Lauridsen TG, Graffe CC, Pedersen EB. The effect of eprosartan on reflex sympathetic activation in sodium restricted patients with essential hypertension. J Am Soc Hypertens 2011; 5 (5): 385–94.
2. Rolande DM, Fantini JP, Cardinalli NA et al. Prognostic determinants of patients with chronic systolic heart failure secondary to systemic arterial hypertension. Arq Bras Cardiol 2011. pii: S0066-782X2011005000123.
3. Oganov RG, Pogosova GN, Koltunov IE et al. Hypertensives in Russia are interested in a healthier lifestyle: results of the RELIF multicenter study. Eur J Cardiovasc Prev Rehabil 2011; 18 (2): 224–32.
4. Yoon SS, Ostchega Y, Louis T. Recent trends in the prevalence of high blood pressure and its treatment and control 1999–2008. NCHS Data Brief 2010; (48): 1–8.
5. Prugger C, Keil U, Wellmann J et al. Blood pressure control and knowledge of target blood pressure in coronary patients across Europe: results from the EUROASPIRE III survey. J Hypertens 2011; 29 (8): 1641–8.
6. Egan BM, Zhao, Neal Axon R et al. US Trends in prevalence, awareness, treatment, and control of hypertension 1988–2008. JAMA 2010; 303: 2043–50.
7. Gil-Guillén V, Orozco-Beltrán D, Márquez-Contreras E et al. Is there a predictive profile for clinical inertia in hypertensive patients? An observational, cross-sectional, multicenter study. Drugs Aging 2011; 28 (12): 981–92.
8. Hoepfner C, Franco SC. Therapeutic inertia and control of high blood pressure in primary health care units. Arq Bras Cardiol 2010; 95 (2): 223–8.
9. Sur G, Sur M, Kudor-Szabadi L, Sur L. Difficulties in achieving arterial hypertension control. Maedica (Buchar) 2011; 6 (2): 114–9.
10. Israili ZH, Hernández-Hernández R, Valasco M. The future of antihypertensive treatment. Am J Ther 2007; 14 (2): 121–34.
11. 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. 7th report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure. Hypertension 2003; 42: 206–1252.
12. 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.
13. 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.
14. 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.
15. Miller AB, Reichek N, St. John Sutton M et al. Importance of blood pressure control in left ventricular mass regression. J Am Soc Hypertens 2010; 4 (6): 302–10.
16. 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.
17. 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.
18. Asmar R, Garcia-Puig J, Gosse P et al. Ambulatory blood pressure in hypertensive patients with left ventricular hypertrophy: efficacy of first-line combination perindopril/indapamide therapy. Vasc Health Risk Manag 2007; 3 (4): 371–80.
19. Neutel JM, Smith DH, Weber MA. Effect of antihypertensive monotherapy and combination therapy on arterial distensibility and left ventricular mass. Am J Hypertens 2004; 17 (1): 37–42.
20. Andreadis EA, Sfakianakis ME, Tsourous GI et al. Differential impact of angiotensin receptor blockers and calcium channel blockers on arterial stiffness. Int Angiol 2010; 29 (3): 266–72.
21. Chrysant SG. Using fixed-dose combination therapies to achieve blood pressure goals. Clin Drug Investig 2008; 28 (11): 713–34.
22. Smith DH Fixed-dose combination antihypertensives and reduction in target organ damage: are they all the same? Am J Cardiovasc Drugs 2007; 7 (6): 413–22.
23. Mourad JJ, Le Jeune S, Pirollo A et al. Combinations of inhibitors of the renin-angiotensin system with calcium channel blockers for the treatment of hypertension: focus on perindopril/amlodipine. Curr Med Res Opin 2010; 26 (9): 2263–76.
24. Fagard RH, Celis H, Thijs L, Wouters S. Regression of left ventricular mass by antihypertensive treatment: a meta-analysis of randomized comparative studies. Hypertension 2009; 54 (5): 1084–91.
25. 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.
26. Schiffrin EL. Vascular changes in hypertension in response to drug treatment: effects of angiotensin receptor blockers. Can J Cardiol 2002; 18 (Suppl. A): 15A–18A.
27. 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.
28. Amerena J, Pappas S, Ouellet JP et al. ABPM comparison of the anti-hypertensive profiles of telmisartan and enalapril in patients with mild-to-moderate essential hypertension. J Int Med Res 2002; 30 (6): 543–52.
29. Park CG, Lee JY. The significance of the j-curve in hypertension and coronary artery diseases. Korean Circ J 2011; 41 (7): 349–53.
30. Chrysant SG. Current status of aggressive blood pressure control. World J Cardiol 2011; 3 (3): 65–71.
31. 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.
32. Vase H, Lauridsen TG, Graffe CC, Pedersen EB. The effect of eprosartan on reflex sympathetic activation in sodium restricted patients with essential hypertension. J Am Soc Hypertens 2011; 5 (5): 385–94.
Авторы
Н.А.Ковалевская*1, Н.А.Козиолова1, А.В.Бушмакина1, И.М.Шатунова1,2
1 ГБОУ ВПО Пермская государственная медицинская академия им. акад. Е.А.Вагнера Минздрава РФ;
2 Поликлиника ОАО Газпром, Москва
*valenta72005@yandex.ru
*valenta72005@yandex.ru
1 ГБОУ ВПО Пермская государственная медицинская академия им. акад. Е.А.Вагнера Минздрава РФ;
2 Поликлиника ОАО Газпром, Москва
*valenta72005@yandex.ru
________________________________________________
*valenta72005@yandex.ru
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