Материалы доступны только для специалистов сферы здравоохранения. Авторизуйтесь или зарегистрируйтесь.
Сравнительная оценка различного выбора инициирующей антигипертензивной терапии в коррекции поражения органов-мишеней у больных гипертонической болезнью
Сравнительная оценка различного выбора инициирующей антигипертензивной терапии в коррекции поражения органов-мишеней у больных гипертонической болезнью
Материалы доступны только для специалистов сферы здравоохранения. Авторизуйтесь или зарегистрируйтесь.
Аннотация
Цель: оценка влияния комбинированной антигипертензивной терапии (АГТ) со старта на показатели поражения органов-мишеней у больных гипертонической болезнью (ГБ) независимо от исходного уровня артериального давления (АД).
Материалы и методы: обследовано 47 пациентов с ГБ, имеющих трехкомпонентное поражение органов-мишеней. Больные были разделены на 2 группы в зависимости от выбора АГТ. В 1-ю группу вошли 24 пациента, получавшие фиксированную комбинацию эпросартана мезилат и гидрохлоротиазид независимо от уровня АД и группы сердечно-сосудистого риска со старта. Во 2-й группе (23 пациента) АГТ назначали в зависимости от уровня АД: монотерапия эналаприлом и нефиксированная комбинация его с гидрохлоротиазидом. Длительность терапии составила 6 мес.
Основные результаты: достижение целевого уровня АД было равнозначным в обеих группах. Регресс поражения органов-мишеней был более выражен в 1-й группе, чем во 2-й, по массе миокарда и индексу массы миокарда левого желудочка (p=0,044, p=0,015), по скорости клубочковой фильтрации (p=0,003) и показателям, отражающим жесткость сосудистой стенки (p<0,001).
Заключение: степень коррекции поражения органов-мишеней при ГБ зависит не только от частоты достижения целевого уровня АД, но и от ее интенсивности, а также выбора АГТ и времени ее старта.
Ключевые слова: гипертоническая болезнь, комбинированная антигипертензивная терапия, регресс поражения органов-мишеней.
Subjects and methods. Forty-seven hypertensive patients who had three-component damage to target organs were examined. The patients were divided into two groups according to the choice of antihypertensive therapy. Group 1 comprised 24 patients who received a fixed-dose combination of eprosartan mesylate and hydrochlorothiazide regardless of the level of BP and the group of cardiovascular risk from the start. In Group 2 (n=23), antihypertensive therapy was initiated depending on the level of BP: monotherapy with enalapril and its non-fixed dose combination with hydrochlorothiazide. The duration of the therapy was 6 months.
Results. The attainment rate for BP goals was similar in both groups. Target organ damage regression in terms of myocardial weight (p=0,044), left ventricular mass index (p=0,015), glomerular filtration rate (p=0,003), and the parameters characterizing vascular wall stiffness (p<0,001), was more marked in Group 1 than that in Group 2.
Conclusion. The degree of correction of target organ damage in hypertensive disease depends not only on the attainment rate for BP goals, but also on the intensity and choice of antihypertensive therapy and the time of its start.
Key words: hypertensive disease, combination antihypertensive therapy, regression of target organ damage.
Материалы и методы: обследовано 47 пациентов с ГБ, имеющих трехкомпонентное поражение органов-мишеней. Больные были разделены на 2 группы в зависимости от выбора АГТ. В 1-ю группу вошли 24 пациента, получавшие фиксированную комбинацию эпросартана мезилат и гидрохлоротиазид независимо от уровня АД и группы сердечно-сосудистого риска со старта. Во 2-й группе (23 пациента) АГТ назначали в зависимости от уровня АД: монотерапия эналаприлом и нефиксированная комбинация его с гидрохлоротиазидом. Длительность терапии составила 6 мес.
Основные результаты: достижение целевого уровня АД было равнозначным в обеих группах. Регресс поражения органов-мишеней был более выражен в 1-й группе, чем во 2-й, по массе миокарда и индексу массы миокарда левого желудочка (p=0,044, p=0,015), по скорости клубочковой фильтрации (p=0,003) и показателям, отражающим жесткость сосудистой стенки (p<0,001).
Заключение: степень коррекции поражения органов-мишеней при ГБ зависит не только от частоты достижения целевого уровня АД, но и от ее интенсивности, а также выбора АГТ и времени ее старта.
Ключевые слова: гипертоническая болезнь, комбинированная антигипертензивная терапия, регресс поражения органов-мишеней.
________________________________________________
Subjects and methods. Forty-seven hypertensive patients who had three-component damage to target organs were examined. The patients were divided into two groups according to the choice of antihypertensive therapy. Group 1 comprised 24 patients who received a fixed-dose combination of eprosartan mesylate and hydrochlorothiazide regardless of the level of BP and the group of cardiovascular risk from the start. In Group 2 (n=23), antihypertensive therapy was initiated depending on the level of BP: monotherapy with enalapril and its non-fixed dose combination with hydrochlorothiazide. The duration of the therapy was 6 months.
Results. The attainment rate for BP goals was similar in both groups. Target organ damage regression in terms of myocardial weight (p=0,044), left ventricular mass index (p=0,015), glomerular filtration rate (p=0,003), and the parameters characterizing vascular wall stiffness (p<0,001), was more marked in Group 1 than that in Group 2.
Conclusion. The degree of correction of target organ damage in hypertensive disease depends not only on the attainment rate for BP goals, but also on the intensity and choice of antihypertensive therapy and the time of its start.
Key words: hypertensive disease, combination antihypertensive therapy, regression of target organ damage.
Полный текст
Список литературы
1. 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.
2. Lantelme P. Blood pressure control: time for action. Arch Cardiovasc Dis 2009; 102 (6–7): 465–67.
3. 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.
4. Erdine S. Compliance with the treatment of hypertension: the potential of combination therapy. J Clin Hypertens (Greenwich) 2010; 12 (1): 40–6.
5. 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.
6. 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.
7. 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.
8. 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.
9. 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.
10. 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.
11. 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.
12. 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.
13. Düsing R. Optimizing blood pressure control through the use of fixed combinations.Vasc Health Risk Manag 2010; 25 (6): 321–5.
14. 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: 2200–06.
15. 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.
16. 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.
17. 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.
18. Martin DE, DeCherney GS, Ilson BE et al. Eprosartan, an angiotensin II receptor antagonist, does not affect the pharmacodynamics of glyburide in patients with type II diabetes mellitus. J Clin Pharmacol 1997; 37 (2): 155–9.
19. Ilson BE, Boike SC, Martin DE, et al. A dose-response study to assess the renal hemodynamic, vascular, and hormonal effects of eprosartan, an angiotensin II AT1-receptor antagonist, in sodium-replete healthy men. Clin Pharmacol Ther 1998; 63 (4): 471–81.
20. Labiós M, Martínez M, Gabriel F et al. Effects of eprosartan on mitochondrial membrane potential and H2O2 levels in leucocytes in hypertension. J Hum Hypertens 2008; 22 (7): 493–500.
21. Ram CV. Angiotensin blockade with eprosartan: vascular and functional implications. Curr Med Res Opin 2007; 23 (5): 5–11.
2. Lantelme P. Blood pressure control: time for action. Arch Cardiovasc Dis 2009; 102 (6–7): 465–67.
3. 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.
4. Erdine S. Compliance with the treatment of hypertension: the potential of combination therapy. J Clin Hypertens (Greenwich) 2010; 12 (1): 40–6.
5. 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.
6. 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.
7. 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.
8. 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.
9. 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.
10. 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.
11. 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.
12. 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.
13. Düsing R. Optimizing blood pressure control through the use of fixed combinations.Vasc Health Risk Manag 2010; 25 (6): 321–5.
14. 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: 2200–06.
15. 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.
16. 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.
17. 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.
18. Martin DE, DeCherney GS, Ilson BE et al. Eprosartan, an angiotensin II receptor antagonist, does not affect the pharmacodynamics of glyburide in patients with type II diabetes mellitus. J Clin Pharmacol 1997; 37 (2): 155–9.
19. Ilson BE, Boike SC, Martin DE, et al. A dose-response study to assess the renal hemodynamic, vascular, and hormonal effects of eprosartan, an angiotensin II AT1-receptor antagonist, in sodium-replete healthy men. Clin Pharmacol Ther 1998; 63 (4): 471–81.
20. Labiós M, Martínez M, Gabriel F et al. Effects of eprosartan on mitochondrial membrane potential and H2O2 levels in leucocytes in hypertension. J Hum Hypertens 2008; 22 (7): 493–500.
21. Ram CV. Angiotensin blockade with eprosartan: vascular and functional implications. Curr Med Res Opin 2007; 23 (5): 5–11.
Авторы
Н.А.Козиолова*, Н.А.Ковалевская, А.В.Бушмакина, Н.Ю.Петрова
Пермская государственная медицинская академия имени академика Е.А.Вагнера
*nakoziolova@mail.ru
Academician E.A.Vagner Perm State Medical Academy, Perm
*nakoziolova@mail.ru
Пермская государственная медицинская академия имени академика Е.А.Вагнера
*nakoziolova@mail.ru
________________________________________________
Academician E.A.Vagner Perm State Medical Academy, Perm
*nakoziolova@mail.ru
Цель портала OmniDoctor – предоставление профессиональной информации врачам, провизорам и фармацевтам.