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Влияние антигипертензивной и СИПАП-терапии на маркеры воспалительного ответа и эндотелиальной функции у пациентов с синдромом обструктивного апноэ сна тяжелой степени в сочетании с артериальной гипертонией
Влияние антигипертензивной и СИПАП-терапии на маркеры воспалительного ответа и эндотелиальной функции у пациентов с синдромом обструктивного апноэ сна тяжелой степени в сочетании с артериальной гипертонией
Елфимова Е.М., Рвачева А.В., Трипотень М.И. и др. Влияние антигипертензивной и СИПАП-терапии на маркеры воспалительного ответа и эндотелиальной функции у пациентов с синдромом обструктивного апноэ сна тяжелой степени в сочетании с артериальной гипертонией. Системные гипертензии. 2017; 14 (1): 37–40.
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Аннотация
Цель исследования – оценить влияние антигипертензивной (АГТ) и СИПАП-терапии на маркеры воспалительного ответа и эндотелиальной функции у пациентов с синдромом обструктивного апноэ сна (СОАС) тяжелой степени в сочетании с артериальной гипертонией (АГ).
Материал и методы. В исследование были включены 43 пациента мужского пола с СОАС тяжелой степени (индекс апноэ/гипопноэ 52,4 [46,1; 58,6] соб./ч) и АГ (систолическое артериальное давление – АД 144,0 [142,0; 156,0] мм рт. ст., диастолическое АД 90,9 [88,3; 93,5] мм рт. ст.). Пациентам проводился ступенчатый подбор АГТ ингибитором ангиотензинпревращающего фермента, антагонистом кальция, тиазидоподобным диуретиком до достижения целевых значений АД по методу Короткова. Пациенты, достигшие целевого уровня АД (АД≤140/90 мм рт. ст), были рандомизированы в группу продолжения приема АГТ (1-я группа, n=23) и группу, в которой к АГТ подбиралась эффективная СИПАП-терапия (2-я группа, n=22). Исходно, при достижении целевых цифр АД на фоне АГТ (2-й визит) и через 3 мес терапии (АГТ или АГТ+СИПАП) – 3-й визит, проводились иммунофенотипирование лимфоцитов периферической крови, определение панели цитокинов (интерлейкин – ИЛ-1b, ИЛ-6, фактор некроза опухоли a, ИЛ-2Ra, sCD40L) и молекул адгезии (ICAM-1, VCAM-1) в сыворотке крови, оценка уровня тромбоксана В2, 6-кетопростациклина (6-кето-PGF1a) и эндотелина-1. Пациентам осуществлялась оценка потокзависимой вазодилатации плечевой артерии в ходе пробы с реактивной гиперемией по D.Celermajer.
Результаты. На фоне комбинированной АГТ целевого уровня клинического АД достигли 95% пациентов. На фоне достижения целевых цифр АД у пациентов с АГ в сочетании с СОАС тяжелой степени было выявлено достоверное снижение уровня ИЛ-1b -0,16 [-0,5; 0], р=0,000 и количества CD50+ клеток (лимфоцитов, несущих молекулу межклеточной адгезии – ICAM-3): с 2158,5 [1884,7; 2432,3] до 1949,6 [1740,9; 2158,3], р=0,050. Достоверных изменений в вазомоторной функции эндотелия на фоне АГТ зафиксировано не было. На фоне комбинации АГТ и СИПАП-терапии выявлено достоверное снижение уровня фибриногена (-0,3 [-0,4; -0,1], р=0,002) и гомоцистеина: D -2,03 [-3,8; -0,2], p=0,03.
Заключение. Комбинация АГТ и СИПАП-терапии у пациентов с СОАС тяжелой степени и АГ позволяет не только достичь целевых значений АД, но и приводит к снижению маркеров активности воспалительного процесса и уменьшению проявлений эндотелиальной дисфункции.
Ключевые слова: СИПАП, артериальная гипертония, антигипертензивная терапия, синдром обструктивного апноэ сна, маркеры воспаления, эндотелиальная дисфункция.
Materials and methods. The study included 43 male patients with severe OSA syndrome (Apnea–Hypopnea Index 52.4 [46.1; 58.6]) and AH (systolic blood pressure 144.0 [142.0; 156.0] mm Hg, diastolic blood pressure 90.9 [88.3; 93.5] mm Hg). Treatment with angiotensin-converting enzyme inhibitors, calcium antagonists, and thiazide-like diuretics was performed till target BP level measured with Korotkoff method was achieved. The patients who had reached target BP level (BP≤140/90 mm Hg) were randomized into two groups: group 1 included 23 patients who continued taking the AHT, group 2 included 22 patients who continued taking the AHT to which CPAP therapy was added. Peripheral blood lymphocyte immunophenotyping, cytokine panel test (IL-1β, IL-6, tumor necrosis factor a, IL-2Ra, sCD40L), adhesion molecule analysis (ICAM-1, VCAM-1), thromboxane B2, 6-keto-prostaglandin F1 alpha (6-keto-PGF1a), and endothelin-1 levels in blood serum were evaluated at admission, after target BP level achievement (2nd visit) and after 3 months of AHT or AHT+CPAP therapy (3rd visit). Flow-mediated dilation of brachial artery was assessed using reactive hyperemia test by D.Celermajer.
Results. Against the background of combined AHT the target BP level was achieved by 95% of patients. After target BP level achievement a significant decrease of IL-1β -0.16 [-0.5; 0], p=0.000 level and number of CD50+ cells (lymphocytes with inter-cellular adhesion molecule ICAM-3) from 2158.5 [1884.7; 2432.3] to 1949.6 [1740.9; 2158.3], p=0.050 were observed in patients with severe OSA associated with AH. There were no significant changes in vascular endothelial function observed in patients taking only AHT. Significant decrease of fibrinogen (-0.3 [-0.4; -0.1], p=0.002) and homocystein (-2.03 [-3.8; -0.2], p=0.03) levels was observed in patients taking both AHT and CPAP therapy.
Conclusion. The combination of AHT and CPAP therapy in patients with severe OSA and AH not only allows reaching the target BP level but also leads to inflammatory and endothelial dysfunction markers levels decrease.
Key words: CPAP, arterial hypertension, antihypertensive therapy, obstructive sleep apnea syndrome, inflammatory markers, endothelial dysfunction.
Материал и методы. В исследование были включены 43 пациента мужского пола с СОАС тяжелой степени (индекс апноэ/гипопноэ 52,4 [46,1; 58,6] соб./ч) и АГ (систолическое артериальное давление – АД 144,0 [142,0; 156,0] мм рт. ст., диастолическое АД 90,9 [88,3; 93,5] мм рт. ст.). Пациентам проводился ступенчатый подбор АГТ ингибитором ангиотензинпревращающего фермента, антагонистом кальция, тиазидоподобным диуретиком до достижения целевых значений АД по методу Короткова. Пациенты, достигшие целевого уровня АД (АД≤140/90 мм рт. ст), были рандомизированы в группу продолжения приема АГТ (1-я группа, n=23) и группу, в которой к АГТ подбиралась эффективная СИПАП-терапия (2-я группа, n=22). Исходно, при достижении целевых цифр АД на фоне АГТ (2-й визит) и через 3 мес терапии (АГТ или АГТ+СИПАП) – 3-й визит, проводились иммунофенотипирование лимфоцитов периферической крови, определение панели цитокинов (интерлейкин – ИЛ-1b, ИЛ-6, фактор некроза опухоли a, ИЛ-2Ra, sCD40L) и молекул адгезии (ICAM-1, VCAM-1) в сыворотке крови, оценка уровня тромбоксана В2, 6-кетопростациклина (6-кето-PGF1a) и эндотелина-1. Пациентам осуществлялась оценка потокзависимой вазодилатации плечевой артерии в ходе пробы с реактивной гиперемией по D.Celermajer.
Результаты. На фоне комбинированной АГТ целевого уровня клинического АД достигли 95% пациентов. На фоне достижения целевых цифр АД у пациентов с АГ в сочетании с СОАС тяжелой степени было выявлено достоверное снижение уровня ИЛ-1b -0,16 [-0,5; 0], р=0,000 и количества CD50+ клеток (лимфоцитов, несущих молекулу межклеточной адгезии – ICAM-3): с 2158,5 [1884,7; 2432,3] до 1949,6 [1740,9; 2158,3], р=0,050. Достоверных изменений в вазомоторной функции эндотелия на фоне АГТ зафиксировано не было. На фоне комбинации АГТ и СИПАП-терапии выявлено достоверное снижение уровня фибриногена (-0,3 [-0,4; -0,1], р=0,002) и гомоцистеина: D -2,03 [-3,8; -0,2], p=0,03.
Заключение. Комбинация АГТ и СИПАП-терапии у пациентов с СОАС тяжелой степени и АГ позволяет не только достичь целевых значений АД, но и приводит к снижению маркеров активности воспалительного процесса и уменьшению проявлений эндотелиальной дисфункции.
Ключевые слова: СИПАП, артериальная гипертония, антигипертензивная терапия, синдром обструктивного апноэ сна, маркеры воспаления, эндотелиальная дисфункция.
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Materials and methods. The study included 43 male patients with severe OSA syndrome (Apnea–Hypopnea Index 52.4 [46.1; 58.6]) and AH (systolic blood pressure 144.0 [142.0; 156.0] mm Hg, diastolic blood pressure 90.9 [88.3; 93.5] mm Hg). Treatment with angiotensin-converting enzyme inhibitors, calcium antagonists, and thiazide-like diuretics was performed till target BP level measured with Korotkoff method was achieved. The patients who had reached target BP level (BP≤140/90 mm Hg) were randomized into two groups: group 1 included 23 patients who continued taking the AHT, group 2 included 22 patients who continued taking the AHT to which CPAP therapy was added. Peripheral blood lymphocyte immunophenotyping, cytokine panel test (IL-1β, IL-6, tumor necrosis factor a, IL-2Ra, sCD40L), adhesion molecule analysis (ICAM-1, VCAM-1), thromboxane B2, 6-keto-prostaglandin F1 alpha (6-keto-PGF1a), and endothelin-1 levels in blood serum were evaluated at admission, after target BP level achievement (2nd visit) and after 3 months of AHT or AHT+CPAP therapy (3rd visit). Flow-mediated dilation of brachial artery was assessed using reactive hyperemia test by D.Celermajer.
Results. Against the background of combined AHT the target BP level was achieved by 95% of patients. After target BP level achievement a significant decrease of IL-1β -0.16 [-0.5; 0], p=0.000 level and number of CD50+ cells (lymphocytes with inter-cellular adhesion molecule ICAM-3) from 2158.5 [1884.7; 2432.3] to 1949.6 [1740.9; 2158.3], p=0.050 were observed in patients with severe OSA associated with AH. There were no significant changes in vascular endothelial function observed in patients taking only AHT. Significant decrease of fibrinogen (-0.3 [-0.4; -0.1], p=0.002) and homocystein (-2.03 [-3.8; -0.2], p=0.03) levels was observed in patients taking both AHT and CPAP therapy.
Conclusion. The combination of AHT and CPAP therapy in patients with severe OSA and AH not only allows reaching the target BP level but also leads to inflammatory and endothelial dysfunction markers levels decrease.
Key words: CPAP, arterial hypertension, antihypertensive therapy, obstructive sleep apnea syndrome, inflammatory markers, endothelial dysfunction.
Полный текст
Список литературы
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26. Diefenbach K, Kretschmer K, Bauer S et al. Endothelin-1 Gene Variant Lys198. Asn and Plasma Endothelin Level in Obstructive Sleep Apnea. Cardiology 2009; 112: 62–8.
27. Mejza F, Kania A, Nastalek P et al. Systemic prostacyclin and thromboxane production in obstructive sleep apnea. Adv Med Sci 2016; 61 (1): 154–9. DOI: 10.1016/j.advms.2015.12.001.
28. Simpson PJ, Hoyos CM, Celermajer D et al. Effects of continuous positive airway pressure on endothelial function and circulating progenitor cells in obstructive sleep apnoea: a randomised sham-controlled study. Int J Cardiol 2013; 168 (3): 2042–8. DOI: 10.1016/j.ijcard.2013.01.166.
29. Monneret D, Tamisier R, Ducros V et al. Glucose tolerance and cardiovascular risk biomarkers in non-diabetic non-obese obstructive sleep apnea patients: Effects of long-term continuous positive airway pressure. Respir Med 2016; 112: 119–25. DOI: 10.1016/j.rmed.2016.01.015.
30. Steiropoulos P, Tsara V, Nena E et al. Effect of continuous positive airway pressure treatment on serum cardiovascular risk factors in patients with obstructive sleep apnea-hypopnea syndrome. Chest 2007; 132 (3): 843–51.
31. Hijmering ML, Stroes ES, Olijhoek J et al. Sympathetic activation markedly reduces endothelium-dependent, flow-mediated vasodilation. J Am Coll Cardiol 2002; 39 (4): 683–8.
32. Thijssen DHJ, Atkinson CL, Ono K et al. Sympathetic nervous system activation, arterial shear rate, and flow-mediated dilation. J Appl Physiol Pub 2014; 116 (10): 1300–7. DOI: 10.1152/japplphysiol.00110.2014.
2. Heinzer R, Vat S, Marques-Vidal P et al. Prevalence of sleep-disordered breathing in the general population: the Hypno Laus study. Lancet Respir Med 2015; 3: 310–8.
3. Parati G, Lombardi C, Hedner J et al. Recommendations for the management of patients with obstructive sleep apnoea and hypertension. Eur Respir J 2013; 41: 523–38.
4. Seif F, Patel SR, Walia HK et al.Obstructive sleep apnea and diurnal nondipping hemodynamic indices in patients at increased cardiovascular risk. J Hypertens 2014; 32: 267–75.
5. Cutler JA, Sorlie PD, Wolz M et al. Trends in hypertension prevalence, awareness, treatment, and control rates in United States adults between 1988–1994 and 1999–2004. Hypertension 2008; 52: 818–27.
6. Marin JM, Carrizo SJ, Vicente E et al. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005; 365: 1046–53.
7. Yaggi HK, Concato J, Kernan WN et al. Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med 2005; 353: 2034–41.
8. Narkiewicz K, van de Borne PJ, Montano N et al. Contribution of tonic chemoreflex activation to sympathetic activity and blood pressure in patients with obstructive sleep apnea. Circulation 1998; 97: 943–5.
9. Carlson JT, Hedner J, Elam M et al. Augmented resting sympathetic activity in awake patients with obstructive sleep apnea. Chest 1993; 103: 1763–8.
10. Imadojemu VA, Gleeson K, Quraishi SA et al. Impaired vasodilator responses in obstructive sleep apnea are improved with continuous positive airway pressure therapy. Am J Respir Crit Care Med 2002; 165: 950–3.
11. Kato M, Roberts-Thomson P, Phillips BG et al. Impairment of endothelium-dependent vasodilation of resistance vessels in patients with obstructive sleep apnea. Circulation 2000; 102: 2607–10.
12. Shamsuzzaman AS, Gersh BJ, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. JAMA 2003; 290: 1906–14.
13. Jelic S, Padeletti M, Kawut SM et al. Inflammation, oxidative stress, and repair capacity of the vascular endothelium in obstructive sleep apnea. Circulation 2008; 117: 2270–8.
14. Libby Р. Inflammation in Atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology 2012; 32: 2045–51.
15. Lavie L. Intermittent hypoxia: the culprit of oxidative stress, vascular inflammation and dyslipidemia in obstructive sleep apnea. Expert Rev Resp Med 2008; 2: 75–84.
16. Hotamisligil GS. Inflammation and metabolic disorders. Nature 2006; 444: 860–7.
17. Meigs JB, Larson MG, Fox CS et al. Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study. Diabetes Care 2007; 30: 2529–35.
18. Sung KC et al. High sensitivity C-reactive protein as an independent risk factor for esse.
19. Yudkin JS, Kumari M, Humphries SE, Mohamed-Ali V. Inflammation, obesity, stress and coronary heart disease: is interleukin-6 the link? Atherosclerosis 2000; 148: 209−14.
20. Balakhonova T.V. Ul'trazvukovoe issledovanie arterii u patsientov s serdechno-sosudistymi zabolevaniiami. Avtoref. dis. … d-ra med. nauk. M., 2002. [in Russian]
21. Chin K, Ohi M, Kita H et al. Effects of NCPAP therapy on fibrinogen levels in obstructive sleep apnea syndrome. Am J Respir Crit Care Med 1996; 153 (6 Pt. 1): 1972–6.
22. Wu SQ, Liao QC, Xu XX et al. Effect of CPAP therapy on C-reactive protein and cognitive impairment in patients with obstructive sleep apnea hypopnea syndrome. Sleep Breath 2016.
23. Sun L, Chen R, Wang J et al. Association between inflammation and cognitive function and effects of continuous positive airway pressure treatment in obstructive sleep apnea hypopnea syndrome. Zhonghua Yi Xue Za Zhi 2014; 94 (44): 3483–7.
24. Markin A.V., Tseimakh I.Ia., Nagaitsev V.M. Otsenka vyrazhennosti sistemnogo vospaleniia u patsientov s sindromom obstruktivnogo apnoe sna. Meditsina i obrazovanie v Sibiri. 2013; 6. [in Russian]
25. Libby P. Inflammation in atherosclerosis. Nature 2002; 420 (6917): 868–74.
26. Diefenbach K, Kretschmer K, Bauer S et al. Endothelin-1 Gene Variant Lys198. Asn and Plasma Endothelin Level in Obstructive Sleep Apnea. Cardiology 2009; 112: 62–8.
27. Mejza F, Kania A, Nastalek P et al. Systemic prostacyclin and thromboxane production in obstructive sleep apnea. Adv Med Sci 2016; 61 (1): 154–9. DOI: 10.1016/j.advms.2015.12.001.
28. Simpson PJ, Hoyos CM, Celermajer D et al. Effects of continuous positive airway pressure on endothelial function and circulating progenitor cells in obstructive sleep apnoea: a randomised sham-controlled study. Int J Cardiol 2013; 168 (3): 2042–8. DOI: 10.1016/j.ijcard.2013.01.166.
29. Monneret D, Tamisier R, Ducros V et al. Glucose tolerance and cardiovascular risk biomarkers in non-diabetic non-obese obstructive sleep apnea patients: Effects of long-term continuous positive airway pressure. Respir Med 2016; 112: 119–25. DOI: 10.1016/j.rmed.2016.01.015.
30. Steiropoulos P, Tsara V, Nena E et al. Effect of continuous positive airway pressure treatment on serum cardiovascular risk factors in patients with obstructive sleep apnea-hypopnea syndrome. Chest 2007; 132 (3): 843–51.
31. Hijmering ML, Stroes ES, Olijhoek J et al. Sympathetic activation markedly reduces endothelium-dependent, flow-mediated vasodilation. J Am Coll Cardiol 2002; 39 (4): 683–8.
32. Thijssen DHJ, Atkinson CL, Ono K et al. Sympathetic nervous system activation, arterial shear rate, and flow-mediated dilation. J Appl Physiol Pub 2014; 116 (10): 1300–7. DOI: 10.1152/japplphysiol.00110.2014.
2. Heinzer R, Vat S, Marques-Vidal P et al. Prevalence of sleep-disordered breathing in the general population: the Hypno Laus study. Lancet Respir Med 2015; 3: 310–8.
3. Parati G, Lombardi C, Hedner J et al. Recommendations for the management of patients with obstructive sleep apnoea and hypertension. Eur Respir J 2013; 41: 523–38.
4. Seif F, Patel SR, Walia HK et al.Obstructive sleep apnea and diurnal nondipping hemodynamic indices in patients at increased cardiovascular risk. J Hypertens 2014; 32: 267–75.
5. Cutler JA, Sorlie PD, Wolz M et al. Trends in hypertension prevalence, awareness, treatment, and control rates in United States adults between 1988–1994 and 1999–2004. Hypertension 2008; 52: 818–27.
6. Marin JM, Carrizo SJ, Vicente E et al. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005; 365: 1046–53.
7. Yaggi HK, Concato J, Kernan WN et al. Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med 2005; 353: 2034–41.
8. Narkiewicz K, van de Borne PJ, Montano N et al. Contribution of tonic chemoreflex activation to sympathetic activity and blood pressure in patients with obstructive sleep apnea. Circulation 1998; 97: 943–5.
9. Carlson JT, Hedner J, Elam M et al. Augmented resting sympathetic activity in awake patients with obstructive sleep apnea. Chest 1993; 103: 1763–8.
10. Imadojemu VA, Gleeson K, Quraishi SA et al. Impaired vasodilator responses in obstructive sleep apnea are improved with continuous positive airway pressure therapy. Am J Respir Crit Care Med 2002; 165: 950–3.
11. Kato M, Roberts-Thomson P, Phillips BG et al. Impairment of endothelium-dependent vasodilation of resistance vessels in patients with obstructive sleep apnea. Circulation 2000; 102: 2607–10.
12. Shamsuzzaman AS, Gersh BJ, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. JAMA 2003; 290: 1906–14.
13. Jelic S, Padeletti M, Kawut SM et al. Inflammation, oxidative stress, and repair capacity of the vascular endothelium in obstructive sleep apnea. Circulation 2008; 117: 2270–8.
14. Libby Р. Inflammation in Atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology 2012; 32: 2045–51.
15. Lavie L. Intermittent hypoxia: the culprit of oxidative stress, vascular inflammation and dyslipidemia in obstructive sleep apnea. Expert Rev Resp Med 2008; 2: 75–84.
16. Hotamisligil GS. Inflammation and metabolic disorders. Nature 2006; 444: 860–7.
17. Meigs JB, Larson MG, Fox CS et al. Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study. Diabetes Care 2007; 30: 2529–35.
18. Sung KC et al. High sensitivity C-reactive protein as an independent risk factor for esse.
19. Yudkin JS, Kumari M, Humphries SE, Mohamed-Ali V. Inflammation, obesity, stress and coronary heart disease: is interleukin-6 the link? Atherosclerosis 2000; 148: 209−14.
20. Балахонова Т.В. Ультразвуковое исследование артерий у пациентов с сердечно-сосудистыми заболеваниями. Автореф. дис. … д-ра мед. наук. М., 2002. / Balakhonova T.V. Ul'trazvukovoe issledovanie arterii u patsientov s serdechno-sosudistymi zabolevaniiami. Avtoref. dis. … d-ra med. nauk. M., 2002. [in Russian]
21. Chin K, Ohi M, Kita H et al. Effects of NCPAP therapy on fibrinogen levels in obstructive sleep apnea syndrome. Am J Respir Crit Care Med 1996; 153 (6 Pt. 1): 1972–6.
22. Wu SQ, Liao QC, Xu XX et al. Effect of CPAP therapy on C-reactive protein and cognitive impairment in patients with obstructive sleep apnea hypopnea syndrome. Sleep Breath 2016.
23. Sun L, Chen R, Wang J et al. Association between inflammation and cognitive function and effects of continuous positive airway pressure treatment in obstructive sleep apnea hypopnea syndrome. Zhonghua Yi Xue Za Zhi 2014; 94 (44): 3483–7.
24. Маркин А.В., Цеймах И.Я., Нагайцев В.М. Оценка выраженности системного воспаления у пациентов с синдромом обструктивного апноэ сна. Медицина и образование в Сибири. 2013; 6. / Markin A.V., Tseimakh I.Ia., Nagaitsev V.M. Otsenka vyrazhennosti sistemnogo vospaleniia u patsientov s sindromom obstruktivnogo apnoe sna. Meditsina i obrazovanie v Sibiri. 2013; 6. [in Russian]
25. Libby P. Inflammation in atherosclerosis. Nature 2002; 420 (6917): 868–74.
26. Diefenbach K, Kretschmer K, Bauer S et al. Endothelin-1 Gene Variant Lys198. Asn and Plasma Endothelin Level in Obstructive Sleep Apnea. Cardiology 2009; 112: 62–8.
27. Mejza F, Kania A, Nastalek P et al. Systemic prostacyclin and thromboxane production in obstructive sleep apnea. Adv Med Sci 2016; 61 (1): 154–9. DOI: 10.1016/j.advms.2015.12.001.
28. Simpson PJ, Hoyos CM, Celermajer D et al. Effects of continuous positive airway pressure on endothelial function and circulating progenitor cells in obstructive sleep apnoea: a randomised sham-controlled study. Int J Cardiol 2013; 168 (3): 2042–8. DOI: 10.1016/j.ijcard.2013.01.166.
29. Monneret D, Tamisier R, Ducros V et al. Glucose tolerance and cardiovascular risk biomarkers in non-diabetic non-obese obstructive sleep apnea patients: Effects of long-term continuous positive airway pressure. Respir Med 2016; 112: 119–25. DOI: 10.1016/j.rmed.2016.01.015.
30. Steiropoulos P, Tsara V, Nena E et al. Effect of continuous positive airway pressure treatment on serum cardiovascular risk factors in patients with obstructive sleep apnea-hypopnea syndrome. Chest 2007; 132 (3): 843–51.
31. Hijmering ML, Stroes ES, Olijhoek J et al. Sympathetic activation markedly reduces endothelium-dependent, flow-mediated vasodilation. J Am Coll Cardiol 2002; 39 (4): 683–8.
32. Thijssen DHJ, Atkinson CL, Ono K et al. Sympathetic nervous system activation, arterial shear rate, and flow-mediated dilation. J Appl Physiol Pub 2014; 116 (10): 1300–7. DOI: 10.1152/japplphysiol.00110.2014.
________________________________________________
2. Heinzer R, Vat S, Marques-Vidal P et al. Prevalence of sleep-disordered breathing in the general population: the Hypno Laus study. Lancet Respir Med 2015; 3: 310–8.
3. Parati G, Lombardi C, Hedner J et al. Recommendations for the management of patients with obstructive sleep apnoea and hypertension. Eur Respir J 2013; 41: 523–38.
4. Seif F, Patel SR, Walia HK et al.Obstructive sleep apnea and diurnal nondipping hemodynamic indices in patients at increased cardiovascular risk. J Hypertens 2014; 32: 267–75.
5. Cutler JA, Sorlie PD, Wolz M et al. Trends in hypertension prevalence, awareness, treatment, and control rates in United States adults between 1988–1994 and 1999–2004. Hypertension 2008; 52: 818–27.
6. Marin JM, Carrizo SJ, Vicente E et al. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005; 365: 1046–53.
7. Yaggi HK, Concato J, Kernan WN et al. Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med 2005; 353: 2034–41.
8. Narkiewicz K, van de Borne PJ, Montano N et al. Contribution of tonic chemoreflex activation to sympathetic activity and blood pressure in patients with obstructive sleep apnea. Circulation 1998; 97: 943–5.
9. Carlson JT, Hedner J, Elam M et al. Augmented resting sympathetic activity in awake patients with obstructive sleep apnea. Chest 1993; 103: 1763–8.
10. Imadojemu VA, Gleeson K, Quraishi SA et al. Impaired vasodilator responses in obstructive sleep apnea are improved with continuous positive airway pressure therapy. Am J Respir Crit Care Med 2002; 165: 950–3.
11. Kato M, Roberts-Thomson P, Phillips BG et al. Impairment of endothelium-dependent vasodilation of resistance vessels in patients with obstructive sleep apnea. Circulation 2000; 102: 2607–10.
12. Shamsuzzaman AS, Gersh BJ, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. JAMA 2003; 290: 1906–14.
13. Jelic S, Padeletti M, Kawut SM et al. Inflammation, oxidative stress, and repair capacity of the vascular endothelium in obstructive sleep apnea. Circulation 2008; 117: 2270–8.
14. Libby Р. Inflammation in Atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology 2012; 32: 2045–51.
15. Lavie L. Intermittent hypoxia: the culprit of oxidative stress, vascular inflammation and dyslipidemia in obstructive sleep apnea. Expert Rev Resp Med 2008; 2: 75–84.
16. Hotamisligil GS. Inflammation and metabolic disorders. Nature 2006; 444: 860–7.
17. Meigs JB, Larson MG, Fox CS et al. Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study. Diabetes Care 2007; 30: 2529–35.
18. Sung KC et al. High sensitivity C-reactive protein as an independent risk factor for esse.
19. Yudkin JS, Kumari M, Humphries SE, Mohamed-Ali V. Inflammation, obesity, stress and coronary heart disease: is interleukin-6 the link? Atherosclerosis 2000; 148: 209−14.
20. Balakhonova T.V. Ul'trazvukovoe issledovanie arterii u patsientov s serdechno-sosudistymi zabolevaniiami. Avtoref. dis. … d-ra med. nauk. M., 2002. [in Russian]
21. Chin K, Ohi M, Kita H et al. Effects of NCPAP therapy on fibrinogen levels in obstructive sleep apnea syndrome. Am J Respir Crit Care Med 1996; 153 (6 Pt. 1): 1972–6.
22. Wu SQ, Liao QC, Xu XX et al. Effect of CPAP therapy on C-reactive protein and cognitive impairment in patients with obstructive sleep apnea hypopnea syndrome. Sleep Breath 2016.
23. Sun L, Chen R, Wang J et al. Association between inflammation and cognitive function and effects of continuous positive airway pressure treatment in obstructive sleep apnea hypopnea syndrome. Zhonghua Yi Xue Za Zhi 2014; 94 (44): 3483–7.
24. Markin A.V., Tseimakh I.Ia., Nagaitsev V.M. Otsenka vyrazhennosti sistemnogo vospaleniia u patsientov s sindromom obstruktivnogo apnoe sna. Meditsina i obrazovanie v Sibiri. 2013; 6. [in Russian]
25. Libby P. Inflammation in atherosclerosis. Nature 2002; 420 (6917): 868–74.
26. Diefenbach K, Kretschmer K, Bauer S et al. Endothelin-1 Gene Variant Lys198. Asn and Plasma Endothelin Level in Obstructive Sleep Apnea. Cardiology 2009; 112: 62–8.
27. Mejza F, Kania A, Nastalek P et al. Systemic prostacyclin and thromboxane production in obstructive sleep apnea. Adv Med Sci 2016; 61 (1): 154–9. DOI: 10.1016/j.advms.2015.12.001.
28. Simpson PJ, Hoyos CM, Celermajer D et al. Effects of continuous positive airway pressure on endothelial function and circulating progenitor cells in obstructive sleep apnoea: a randomised sham-controlled study. Int J Cardiol 2013; 168 (3): 2042–8. DOI: 10.1016/j.ijcard.2013.01.166.
29. Monneret D, Tamisier R, Ducros V et al. Glucose tolerance and cardiovascular risk biomarkers in non-diabetic non-obese obstructive sleep apnea patients: Effects of long-term continuous positive airway pressure. Respir Med 2016; 112: 119–25. DOI: 10.1016/j.rmed.2016.01.015.
30. Steiropoulos P, Tsara V, Nena E et al. Effect of continuous positive airway pressure treatment on serum cardiovascular risk factors in patients with obstructive sleep apnea-hypopnea syndrome. Chest 2007; 132 (3): 843–51.
31. Hijmering ML, Stroes ES, Olijhoek J et al. Sympathetic activation markedly reduces endothelium-dependent, flow-mediated vasodilation. J Am Coll Cardiol 2002; 39 (4): 683–8.
32. Thijssen DHJ, Atkinson CL, Ono K et al. Sympathetic nervous system activation, arterial shear rate, and flow-mediated dilation. J Appl Physiol Pub 2014; 116 (10): 1300–7. DOI: 10.1152/japplphysiol.00110.2014.
Авторы
Е.М.Елфимова*, А.В.Рвачева, М.И.Трипотень, О.В.Погорелова, Т.В.Балахонова, К.А.Зыков, А.Ю.Литвин
Институт клинической кардиологии им. А.Л.Мясникова ФГБУ «Российский кардиологический научно-производственный комплекс» Минздрава России. 121552, Россия, Москва, ул. 3-я Черепковская, д. 15а
*eelfimova@gmail.com
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
*eelfimova@gmail.com
Институт клинической кардиологии им. А.Л.Мясникова ФГБУ «Российский кардиологический научно-производственный комплекс» Минздрава России. 121552, Россия, Москва, ул. 3-я Черепковская, д. 15а
*eelfimova@gmail.com
________________________________________________
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
*eelfimova@gmail.com
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