cardiovascularКардиоваскулярная терапия и профилактикаCardiovascular Therapy and Prevention1728-88002619-0125«SILICEA-POLIGRAF» LLC10.15829/1728-8800-2012-5-11-17cardiovascular-1888Research ArticleАРТЕРИАЛЬНАЯ ГИПЕРТОНИЯARTERIAL HYPERTENSIONАртериальная гипертензия и синдром обструктивного апноэ сна: резистентность к лечению и роль дисфункции вегетативной нервной системыArterial hypertension and obstructive sleep apnoea syndrome: treatment resistance and the role of autonomic dysfunctionРостороцкаяВ. В.RostorotskayaV. V.

врач кардиолог, докторант

Тел.: (4822) 52-05-05, факс: (4822) 52-84-21

Cardio69@inbox.ruЭльгардтИ. А.ElgardtI. A.

главный врач

Тел.: (4822) 52-05-05, факс: (4822) 52-84-21

Cardio69@inbox.ruИвановА. П.IvanovA. P.

(контактное лицо) – научный руководитель диспансера, доцент кафедры внутренних болезней Тверской медицинской академии

Тел.: (4822) 52-05-05, факс: (4822) 52-84-21

Cardio69@inbox.ruСдобняковаН. С.SdobnyakovaN. S.

заместитель главного врача

Тел.: (4822) 52-05-05, факс: (4822) 52-84-21

Cardio69@inbox.ruТверской клинический кардиологический диспансер, ТверьTver Clinical Cardiology Dispanser, Tver2012201020121151117Copyright © Ростороцкая В.В., Эльгардт И.А., Иванов А.П., Сдобнякова Н.С., 20122012Ростороцкая В.В., Эльгардт И.А., Иванов А.П., Сдобнякова Н.С.Rostorotskaya V.V., Elgardt I.A., Ivanov A.P., Sdobnyakova N.S.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://cardiovascular.elpub.ru/jour/article/view/1888Цель

Цель. Оценить роль синдрома обструктивного апноэ сна (СОАС) при артериальной гипертензии (АГ) в развитии резистентности к проводимой медикаментозной терапии и влияние дисфункции вегетативной нервной системы (ВНС) как одного из возможных патофизиологических путей недостаточного снижения артериального давления (АД) при АГ + СОАС. Материал и методы. Изучено состояние 365 амбулаторных больных АГ, у 194 из которых регистрировался СОАС, а у 161 при наблюдении в течение 6-15 мес отсутствовал антигипертензивный эффект лечения. Использовались методы суточного мониторирования (СМ) АД и СМ ЭКГ и дыхания с анализом вариабельности сердечного ритма (ВСР). Результаты. Среди больных АГ + СОАС выявлено преобладание лиц с низкой приверженностью назначенному лечению АГ. Все показатели СМ АД в этой группе оказались выше, чем у больных АГ без СОАС, и эти различия еще более увеличились при наличии резистентности к лечению. Наиболее существенно при этом реагировал уровень пульсового АД и частоты сердечных сокращений. При анализе показателей ВСР выявлены их различные корреляции во временном и частотном диапазонах с индексом апноэ-гипопноэ (ИАГ) и с уровнем АД при СМ АД. Однако при многофакторном анализе корреляции сохранялись только между ИАГ и параметрами ВСР. Заключение. Наличие СОАС у больных АГ является фактором, отягчающим течение заболевания, наличие дисфункции ВНС может быть одним из механизмов развития резистентности к проводимому антигипертензивному лечению.

 

 

Aim. To study the role of obstructive sleep apnoea syndrome (OSAS) in the development of treatment resistance in patients with arterial hypertension (AH). To assess the effects of autonomic nervous system (ANS) dysfunction, as one of the potential pathophysiological mechanisms of inadequate blood pressure (BP) reduction in patients with AH and OSAS. Material and methods. The study included 365 ambulatory AH patients: 194 with OSAS and 161 with resistance to antihypertensive therapy after 6-15 months. The 24-hour BP monitoring (BPM) and 24-hour cardio-respiratory monitoring of electrocardiogram (ECG), with heart rate variability (HRV) analysis, were performed. Results. Among patients with AH and OSAS, most individuals had low antihypertensive therapy compliance. All parameters of 24-hour BPM in this group were lower than in OSAS-free hypertensives, and this difference was more pronounced in patients with lower treatment compliance, particularly for pulse BP and HR. HRV parameters correlated with apnoea-hypopnoea index (AHI) and BP levels during 24-hour BPM. However, in multivariate analyses, these correlations were observed only for HRV parameters and AHI. Conclusion. In AH patients, OSAS aggravates the clinical course of the disease. ANS dysfunction could be one of the mechanisms underlying the development of antihypertensive treatment resistance.

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The authors declare that there are no conflicts of interest present.