Цель – провести сравнительный анализ особенностей профиля артериального давления (АД) у пациентов среднего возраста (45–65 лет) с гипертонической болезнью (ГБ) II стадии 1–2-й степени без сопутствующих сердечно-сосудистых заболеваний в зависимости от статуса курения; оценить влияние на данные показатели фиксированной комбинации амлодипин/лизиноприл (ФК А/Л). Материалы и методы. На I этапе обследованы 60 нелеченых пациентов (31 мужчина, 29 женщин, средний возраст 53,6±0,8 года) с ГБ II стадии 1–2-й степени, которые были подразделены на 2 группы в зависимости от статуса курения. Группу курящих пациентов с ГБ составили 11 мужчин и 11 женщин, средний возраст 53,4±1,2 года; группу некурящих – 20 мужчин и 18 женщин, средний возраст 53,7±1,0 года. Всем обследуемым проводили суточное мониторирование АД – СМАД (монитор МДП-НС-02с, ДМС) и рутинное измерение АД по методу Короткова, а также трансторакальную эхокардиографию. На II этапе была сформирована подгруппа из 30 нелеченых пациентов: 16 мужчин, средний возраст 52,7±1,11 года, курильщики – 40% (12 человек). Пациенты получали ФК А/Л (препарат Экватор®) в стартовой дозе 5/10 мг с титрацией через каждые 14 дней до достижения целевого АД ниже 140/90 мм рт. ст. и последующим продолжением терапии в подобранном сочетании доз в течение 12 нед, после чего повторяли СМАД. Результаты. В группах курящих и некурящих пациентов с ГБ не было выявлено достоверных различий в уровне АД по данным офисного измерения и СМАД. На II этапе исследования все 30 (100%) пациентов, получавших ФК А/Л, достигли целевых показателей офисного АД. В подгруппах курящих и некурящих пациентов с ГБ на фоне терапии ФК А/Л произошло достоверное снижение офисного систолического АД – САД (p<0,001 в обеих группах), диастолического АД – ДАД (p<0,001 в обеих группах), пульсового АД – ПАД (p<0,05 и р<0,001, соответственно). Достоверных различий в динамике показателей офисного АД между подгруппами обнаружено не было. В конце периода наблюдения в подгруппах курящих и некурящих пациентов отмечено достоверное снижение САД в течение суток (p<0,001 в обеих группах), ДАД в течение суток (p<0,001 в обеих группах), ПАД в течение суток (р<0,01 и p<0,001 соответственно). В группах курящих и некурящих пациентов с ГБ в дневное время достоверно снизились САД и ДАД (p<0,001 для обоих показателей в каждой группе) и ПАД (p<0,01 и p<0,001 соответственно). В группах курящих и некурящих пациентов с ГБ также отмечено достоверное снижение в ночное время САД (p<0,001 в обеих группах), ДАД (p<0,01 и p<0,001 соответственно) и ПАД (p<0,01 в обеих группах). Достоверных различий в динамике показателей САД, ДАД и ПАД по данным СМАД между группами выявлено не было. На фоне терапии ФК А/Л в группах курящих и некурящих пациентов с ГБ произошло достоверное снижение вариабельности САД в дневное время (p<0,01 и p<0,05 соответственно), вариабельности ДАД в ночные часы (p<0,001 и p<0,05 соответственно). В группе курящих пациентов с ГБ произошло также достоверное снижение вариабельности ДАД в дневное время (p<0,05). Выводы. У нелеченых пациентов с ГБ II стадии 1–2-й степени в возрасте 45–65 лет курение не оказывает влияния на параметры суточного профиля АД. У данной категории больных ГБ ФК А/Л обладает эффективными антигипертензивными свойствами независимо от статуса курения.
Objective. To conduct a comparative analysis of blood pressure (BP) profile characteristics in middle-aged (45–65 years) patients with stage 1–2 hypertension not associated with comorbid cardiovascular disease depending on smoking status; to estimate the influence of fixed combination of amlodipine and lisinopril (FC A/L) use on these characteristics. Materials and methods. At the first stage of the study 60 untreated patients (31 men, 29 women, mean age 53.6±0.8 years) with stage 1–2 hypertension were divided in two groups according to smoking status. The smoking group included 11 men and 11 women with mean age 53.4±1.2 years, non-smoking group – 20 men and 18 women with mean age 53.7±1.0 years. Ambulatory blood pressure monitoring (ABPM) (monitor MDP-НС-02с, DMS) and BP measurement based on Korotkov sound technique as well as transthoracic echocardiography were performed in all patients. At the second stage a subgroup of 30 untreated patients (16 men, mean age 52.7±1.11 years, 40% smokers [12 patients]) was formed. Patients received FC A/L (Ekvator®) with starting dose 5 mg/10 mg titrated every 14 days until target BP lower than 140/90 mm Hg was reached. The therapy was continued for 12 weeks, after that ABPM was performed again. Results. In smokers and non-smokers with hypertension no significant differences in BP levels in office BP measurement and ABPM were observed. At the second stage all 30 patients receiving FC A/L reached target office BP levels. In subgroups of smokers and non-smokers with hypertension significant office systolic BP (p<0.001 in both groups), diastolic BP (p<0.001 in both groups), and pulse BP (p<0.05 and р<0.001, respectively) reduction was observed on FC A/L treatment. There were no significant differences in office BP dynamics between subgroups. At the end of follow-up a significant decrease of systolic BP within 24 hours (p<0.001 in both groups), diastolic BP within 24 hours (p<0.001 in both groups), and pulse BP within 24 hours (р<0.01 and p<0.001, respectively) was observed. A significant decrease of day systolic and diastolic BP (p<0.001 for both parameters in both groups) and also pulse BP (p<0.01 and p<0.001, respectively) was observed in both groups of patients. A significant decrease of night systolic BP (p<0.001 in both groups), diastolic BP (p<0.01 and p<0.001, respectively), and pulse BP (p<0.01 in both groups) was observed in smokers and non-smokers. There were no significant differences between the groups in systolic, diastolic, and pulse BP dynamics according to ABPM. There was a significant reduction in systolic day BP variability (p<0.01 and p<0.05, respectively) and diastolic night BP variability (p<0.001 и p<0.05, respectively) in smokers and non-smokers on FC A/L therapy. In hypertensive smokers a significant reduction of diastolic day BP variability was also observed (p<0.05). Conclusions. Smoking does not influence a 24 hours BP profile in patients aged 45–65 years with stage 1-2 hypertension. The FC A/L use in these patients has antihypertensive effect regardless of smoking status.
1. Nakamura K, Barzi F, Lam TH et al.; Asia Pacific Cohort Studies Collaboration. Cigarette smoking, systolic blood pressure, and cardiovascular diseases in the Asia-Pacific region. Stroke 2008; 39 (6): 1694–702. DOI: 10.1161/STROKEAHA.107.496752.
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8. Dahlöf B, Sever PS, Poulter NR et al.; ASCOT Investigators. Prevention of cardiovascular events with an antihypertensive regimen of amlodipine adding perindopril as required versus atenolol adding bendroflumethiazide as required, in the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT-BPLA): a multicentre randomized controlled trial. Lancet 2005; 366: 895–906.
9. Jamerson K, Weber MA, Bakris GL et al.; ACCOMPLISH Trial Investigators. Benazepril plus Amlodipine or hydrochlorothiazide for Hypertension in High-Risk Patients. N Engl J Med 2008; 359 (23): 2417–28.
10. World Health Organization. Obesity: preventing and managing the global epidemic. Report of a WHO consultation. World Health Organ Tech Rep Ser 2000; 894: 1–253.
11. Levey AS, Stevens LA, Schmid CH et al.; CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration). A new equation to estimate glomerular filtration rate. Ann Intern Med 2009; 150: 604–612.
12. O'Brien E, Parati G, Stergiou G et al.; European Society of Hypertension Working Group on Blood Pressure Monitoring. European Society of Hypertension position paper on ambulatory blood pressure monitoring. J Hypertens 2013; 31 (9): 1731–68.
13. Parati G, Stergiou G, O'Brien E et al.; European Society of Hypertension Working Group on Blood Pressure Monitoring and Cardiovascular Variability. European Society of Hypertension practice guidelines for ambulatory blood pressure monitoring. J Hypertens 2014; 32 (7): 1359–66.
14. Lang RM, Badano LP, 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. J Am Soc Echocardiogr 2015; 28 (1): 1-39.e14.
15. Csiszar A, Podlutsky A, Wolin MS et al. Oxidative stress and accelerated vascular aging: implications for cigarette smoking. Front Biosci (Landmark Ed) 2009; 14: 3128–44.
16. Barua RS, Ambrose JA, Srivastava S et al. Reactive oxygen species are involved in smoking-induced dysfunction of nitric oxide biosynthesis and upregulation of endothelial nitric oxide synthase: an in vitro demonstration in human coronary artery endothelial cells. Circulation 2003; 107 (18): 2342–7.
17. Czernin J, Waldherr C. Cigarette smoking and coronary blood flow. Prog Cardiovasc Dis 2003; 45 (5): 395–404.
18. Ungvari Z, Csiszar A, Edwards JG et al. Increased superoxide production in coronary arteries in hyperhomocysteinemia: role of tumor necrosis factor-alpha, NAD(P)H oxidase, and inducible nitric oxide synthase. Arterioscler Thromb Vasc Biol 2003; 23 (3): 418–24.
19. Raveendran M, Wang J, Senthil D et al. Endogenous nitric oxide activation protects against cigarette smoking induced apoptosis in endothelial cells. FEBS Lett 2005; 579 (3): 733–40.
20. Orosz Z, Csiszar A, Labinskyy N et al. Cigarette smoke-induced proinflammatory alterations in the endothelial phenotype: role of NAD(P)H oxidase activation. Am J Physiol Heart Circ Physiol 2007; 292 (1): H130–H139.
21. Knight-Lozano CA, Young CG, Burow DL et al. Cigarette smoke exposure and hypercholesterolemia increase mitochondrial damage in cardiovascular tissues. Circulation 2002; 105 (7): 849–54.
22. Harrison D, Griendling KK, Landmesser U et al. Role of oxidative stress in atherosclerosis. Am J Cardiol 2003; 91 (3A): 7A–11A.
23. Jaimes EA, DeMaster EG, Tian RX, Raij L. Stable compounds of cigarette smoke induce endothelial superoxide anion production via NADPH oxidase activation. Arterioscler Thromb Vasc Biol 2004; 24 (6): 1031–6.
24. Pacher P, Beckman JS, Liaudet L. Nitric oxide and peroxynitrite in health and disease. Physiol Rev 2007; 87 (1): 315–424.
25. József L, Khreiss T, El Kebir D, Filep JG. Activation of TLR-9 induces IL-8 secretion through peroxynitrite signaling in human neutrophils. J Immunol 2006; 176 (2): 1195–202.
26. Loft S, Vistisen K, Ewertz M et al. Oxidative DNA damage estimated by 8-hydroxydeoxyguanosine excretion in humans: influence of smoking, gender and body mass index. Carcinogenesis 1992; 13 (12): 2241–7.
27. Chen HW, Chien ML, Chaung YH et al. Extracts from cigarette smoke induce DNA damage and cell adhesion molecule expression through different pathways. Chem Biol Interact 2004; 150 (3): 233–41.
28. Ames BN. Endogenous oxidative DNA damage, aging, and cancer. Free Radic Res Commun 1989; 7 (3–6): 121–8.
29. Bátkai S, Rajesh M, Mukhopadhyay P et al. Decreased age-related cardiac dysfunction, myocardial nitrative stress, inflammatory gene expression, and apoptosis in mice lacking fatty acid amide hydrolase. Am J Physiol Heart Circ Physiol 2007; 293 (2): H909–H918.
30. Kamp DW, Srinivasan M, Weitzman SA. Cigarette smoke and asbestos activate poly-ADP-ribose polymerase in alveolar epithelial cells. J Investig Med 2001; 49 (1): 68–76.
31. Hassa PO, Covic M, Hasan S et al. The enzymatic and DNA binding activity of PARP-1 are not required for NF-kappa B coactivator function. J Biol Chem 2001; 276 (49): 45588–97.
32. Harman D. Aging: a theory based on free radical and radiation chemistry. J Gerontol 1956; 11 (3): 298–300.
33. Labinskyy N, Csiszar A, Veress G et al. Vascular dysfunction in aging: potential effects of resveratrol, an anti-inflammatory phytoestrogen. Curr Med Chem 2006; 13 (9): 989–96.
34. Csiszar A, Ungvari Z, Koller A et al. Aging-induced proinflammatory shift in cytokine expression profile in coronary arteries. FASEB J 2003; 17 (9): 1183–5.
35. Mahmud A, Feely J. Effect of smoking on arterial stiffness and pulse pressure amplification. Hypertension 2003; 41 (1): 183–7.
36. Liang YL, Shiel LM, Teede H et al. Effects of Blood Pressure, Smoking, and Their Interaction on Carotid Artery Structure and Function. Hypertension 2001; 37 (1): 6–11.
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1. Nakamura K, Barzi F, Lam TH et al.; Asia Pacific Cohort Studies Collaboration. Cigarette smoking, systolic blood pressure, and cardiovascular diseases in the Asia-Pacific region. Stroke 2008; 39 (6): 1694–702. DOI: 10.1161/STROKEAHA.107.496752.
2. Balanova Iu.A., Kontsevaia A.V., Shal'nova S.A. i dr. Rasprostranennost' povedencheskikh faktorov riska serdechno-sosudistykh zabolevanii v rossiiskoi populiatsii po rezul'tatam issledovaniia ESSE-RF. Profilakticheskaia meditsina. 2014; 5: 42–52. [in Russian]
3. Kompleksnoe nabliudenie uslovii zhizni naseleniia. Federal'naia sluzhba gosudarstvennoi statistiki. URL: http://www.gks.ru/free_doc/new_site/KOUZ/survey0/index.html. [in Russian]
4. Sud'ba kuril'shchikov v Rossii. Press-vypusk №2643. Institut VTsIOM. URL: https://wciom.ru/index.php?id=236&uid=114927. [in Russian]
5. Minzdrav reshil otuchit' rossiian ot kureniia zapretom na prodazhu sigaret. Izvestiia. URL: http://izvestia.ru/news/656193 [in Russian]
6. Chazova I.E., Ratova L.G., Boitsov S.A., Nebieridze D.V. Diagnostika i lechenie arterial'noi gipertenzii (Rekomendatsii Rossiiskogo meditsinskogo obshchestva po arterial'noi gipertonii i Vserossiiskogo nauchnogo obshchestva kardiologov). Systemic Hypertension. 2010; 7 (3): 5–26. [in Russian]
7. Mancia G, Fagard R, Narkiewicz K et al. 2013 ESH/ESC 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 2013; 31: 1281–357.
8. Dahlöf B, Sever PS, Poulter NR et al.; ASCOT Investigators. Prevention of cardiovascular events with an antihypertensive regimen of amlodipine adding perindopril as required versus atenolol adding bendroflumethiazide as required, in the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT-BPLA): a multicentre randomized controlled trial. Lancet 2005; 366: 895–906.
9. Jamerson K, Weber MA, Bakris GL et al.; ACCOMPLISH Trial Investigators. Benazepril plus Amlodipine or hydrochlorothiazide for Hypertension in High-Risk Patients. N Engl J Med 2008; 359 (23): 2417–28.
10. World Health Organization. Obesity: preventing and managing the global epidemic. Report of a WHO consultation. World Health Organ Tech Rep Ser 2000; 894: 1–253.
11. Levey AS, Stevens LA, Schmid CH et al.; CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration). A new equation to estimate glomerular filtration rate. Ann Intern Med 2009; 150: 604–612.
12. O'Brien E, Parati G, Stergiou G et al.; European Society of Hypertension Working Group on Blood Pressure Monitoring. European Society of Hypertension position paper on ambulatory blood pressure monitoring. J Hypertens 2013; 31 (9): 1731–68.
13. Parati G, Stergiou G, O'Brien E et al.; European Society of Hypertension Working Group on Blood Pressure Monitoring and Cardiovascular Variability. European Society of Hypertension practice guidelines for ambulatory blood pressure monitoring. J Hypertens 2014; 32 (7): 1359–66.
14. Lang RM, Badano LP, 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. J Am Soc Echocardiogr 2015; 28 (1): 1-39.e14.
15. Csiszar A, Podlutsky A, Wolin MS et al. Oxidative stress and accelerated vascular aging: implications for cigarette smoking. Front Biosci (Landmark Ed) 2009; 14: 3128–44.
16. Barua RS, Ambrose JA, Srivastava S et al. Reactive oxygen species are involved in smoking-induced dysfunction of nitric oxide biosynthesis and upregulation of endothelial nitric oxide synthase: an in vitro demonstration in human coronary artery endothelial cells. Circulation 2003; 107 (18): 2342–7.
17. Czernin J, Waldherr C. Cigarette smoking and coronary blood flow. Prog Cardiovasc Dis 2003; 45 (5): 395–404.
18. Ungvari Z, Csiszar A, Edwards JG et al. Increased superoxide production in coronary arteries in hyperhomocysteinemia: role of tumor necrosis factor-alpha, NAD(P)H oxidase, and inducible nitric oxide synthase. Arterioscler Thromb Vasc Biol 2003; 23 (3): 418–24.
19. Raveendran M, Wang J, Senthil D et al. Endogenous nitric oxide activation protects against cigarette smoking induced apoptosis in endothelial cells. FEBS Lett 2005; 579 (3): 733–40.
20. Orosz Z, Csiszar A, Labinskyy N et al. Cigarette smoke-induced proinflammatory alterations in the endothelial phenotype: role of NAD(P)H oxidase activation. Am J Physiol Heart Circ Physiol 2007; 292 (1): H130–H139.
21. Knight-Lozano CA, Young CG, Burow DL et al. Cigarette smoke exposure and hypercholesterolemia increase mitochondrial damage in cardiovascular tissues. Circulation 2002; 105 (7): 849–54.
22. Harrison D, Griendling KK, Landmesser U et al. Role of oxidative stress in atherosclerosis. Am J Cardiol 2003; 91 (3A): 7A–11A.
23. Jaimes EA, DeMaster EG, Tian RX, Raij L. Stable compounds of cigarette smoke induce endothelial superoxide anion production via NADPH oxidase activation. Arterioscler Thromb Vasc Biol 2004; 24 (6): 1031–6.
24. Pacher P, Beckman JS, Liaudet L. Nitric oxide and peroxynitrite in health and disease. Physiol Rev 2007; 87 (1): 315–424.
25. József L, Khreiss T, El Kebir D, Filep JG. Activation of TLR-9 induces IL-8 secretion through peroxynitrite signaling in human neutrophils. J Immunol 2006; 176 (2): 1195–202.
26. Loft S, Vistisen K, Ewertz M et al. Oxidative DNA damage estimated by 8-hydroxydeoxyguanosine excretion in humans: influence of smoking, gender and body mass index. Carcinogenesis 1992; 13 (12): 2241–7.
27. Chen HW, Chien ML, Chaung YH et al. Extracts from cigarette smoke induce DNA damage and cell adhesion molecule expression through different pathways. Chem Biol Interact 2004; 150 (3): 233–41.
28. Ames BN. Endogenous oxidative DNA damage, aging, and cancer. Free Radic Res Commun 1989; 7 (3–6): 121–8.
29. Bátkai S, Rajesh M, Mukhopadhyay P et al. Decreased age-related cardiac dysfunction, myocardial nitrative stress, inflammatory gene expression, and apoptosis in mice lacking fatty acid amide hydrolase. Am J Physiol Heart Circ Physiol 2007; 293 (2): H909–H918.
30. Kamp DW, Srinivasan M, Weitzman SA. Cigarette smoke and asbestos activate poly-ADP-ribose polymerase in alveolar epithelial cells. J Investig Med 2001; 49 (1): 68–76.
31. Hassa PO, Covic M, Hasan S et al. The enzymatic and DNA binding activity of PARP-1 are not required for NF-kappa B coactivator function. J Biol Chem 2001; 276 (49): 45588–97.
32. Harman D. Aging: a theory based on free radical and radiation chemistry. J Gerontol 1956; 11 (3): 298–300.
33. Labinskyy N, Csiszar A, Veress G et al. Vascular dysfunction in aging: potential effects of resveratrol, an anti-inflammatory phytoestrogen. Curr Med Chem 2006; 13 (9): 989–96.
34. Csiszar A, Ungvari Z, Koller A et al. Aging-induced proinflammatory shift in cytokine expression profile in coronary arteries. FASEB J 2003; 17 (9): 1183–5.
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Авторы
О.Д.Остроумова*1,2, А.И.Кочетков1
1 ФГБОУ ВО «Московский государственный медико-стоматологический университет им. А.И.Евдокимова» Минздрава России. 127473, Россия, Москва, ул. Делегатская, д. 20, стр. 1;
2 ФГАОУ ВО «Первый Московский государственный университет им. И.М.Сеченова» Минздрава России. 119991, Россия, Москва, ул. Трубецкая, д. 8, стр. 2
*ostroumova.olga@mail.ru
________________________________________________
O.D.Ostroumova*1,2, A.I.Kochetkov1
1 A.I.Evdokimov Moscow State University of Medicine and Dentistry of the Ministry of Health of the Russian Federation. 127473, Russian Federation, Moscow, ul. Delegatskaia, d. 20, str. 1;
2 I.M.Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation. 119991, Russian Federation, Moscow, ul. Trubetskaia, d. 8, str. 2. *ostroumova.olga@mail.ru