rpcardioRational Pharmacotherapy in CardiologyРациональная Фармакотерапия в Кардиологии1819-64462225-3653«SILICEA-POLIGRAF» LLC10.20996/1819-6446-2021-08-05rpcardio-2542Research ArticlePOINT OF VIEWТОЧКА ЗРЕНИЯObstructive sleep apnea and cardiovascular comorbidity: common pathophysiological mechanisms to cardiovascular diseaseОбструктивное апноэ сна и сердечно-сосудистая коморбидность: общность патофизиологических механизмовhttps://orcid.org/0000-0002-4982-628XАгальцовМ. В.AgaltsovM. V.

Михаил Викторович Агальцов

Москва

Michail V. Agaltsov 

Moscow

agaltsov@rambler.ruhttps://orcid.org/0000-0002-4453-8430ДрапкинаО. М.DrapkinaO. M.

Драпкина Оксана Михайловна

eLibrary SPIN 4456-1297

Москва

Oxana M. Drapkina

eLibrary SPIN 4456-1297

Moscow

Национальный медицинский исследовательский центр терапии и профилактической медициныРоссияNational Medical Research Center for Therapy and Preventive MedicineRussian Federation202102092021174594605Copyright © Agaltsov M.V., Drapkina O.M., 20212021Агальцов М.В., Драпкина О.М.Agaltsov M.V., Drapkina O.M.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.rpcardio.online/jour/article/view/2542

Obstructive sleep apnea (OSA) is associated with many cardiovascular and metabolic diseases. Sleep apnea causes intermittent hypoxemia, chest pressure fluctuations and a reaction from the cerebral cortex in the form of a short awakening during sleep (EEG-activation). The consequences of pathological pathways are studied in experimental models involving cell cultures, animals, and healthy volunteers. At present, the negative impact of intermittent hypoxemia on a variety of pathophysiological disorders of the heart and blood vessels (vascular tone fluctuations, thickening of the intimamedia complex in the vascular wall, direct damaging effect on the myocardium) has a great evidence base. Two other pathological components of OSA (pressure fluctuations and EEG-activation) can also affect cardiovascular system, mainly affecting the increase in blood pressure and changing cardiac hemodynamics. Although these reactions are considered separately in the review, with the development of sleep apnea they occur sequentially and are closely interrelated. As a result, these pathological pathways trigger further pathophysiological mechanisms acting on the heart and blood vessels. It is known that these include excessive sympathetic activation, inflammation, oxidative stress and metabolic dysregulation. In many respects being links of one process, these mechanisms can trigger damage to the vascular wall, contributing to the formation of atherosclerotic lesions. The accumulated data with varying degrees of reliability confirm the participation of OSA through these processes in the formation of cardiovascular disorders. There are factors limiting direct evidence of this interaction (sleep deprivation, causing similar changes, as well as the inability to share the contribution of other risk factors for cardiovascular diseases, in particular arterial hypertension, obesity, which are often associated with OSA). It is necessary to continue the study of processes that implement the pathological effect of OSA on the cardiovascular system.

Обструктивное апноэ сна (ОАС) ассоциировано со многими сердечно-сосудистыми (ССЗ) и метаболическими заболеваниями. Остановка дыхания во сне вызывает преходящую гипоксемию, колебания давления в грудной клетке и реакцию со стороны коры головного мозга в виде короткого пробуждения (ЭЭГ-активация). Последствия патологических реакций изучаются с помощью экспериментальных моделей: на клеточных культурах, животных и здоровых добровольцах. В настоящее время большую доказательную базу имеет отрицательное влияние преходящей гипоксемии на разнообразные нарушения функции сердца и сосудов (колебания сосудистого тонуса, утолщение комплекса интима-медиа сосудистой стенки, прямое повреждающее действие на миокард). Остальные патологические компоненты ОАС (колебания давления и ЭЭГ-активация) также могут воздействовать на кардиоваскулярную систему, в основном, влияя на повышение артериального давления и изменяя сердечную гемодинамику. Хотя в обзоре эти реакции рассматриваются раздельно, при развитии апноэ во сне они происходят последовательно и тесно взаимосвязаны. В результате эти патологические реакции запускают дальнейшие патофизиологические механизмы, действующие на сердце и сосуды. Известно, что к ним относятся избыточная активация симпатической нервной системы, окислительный стресс с воспалительными реакциями и метаболическая дизрегуляция. Во многом являясь звеньями одного процесса, эти механизмы могут запускать повреждение сосудистой стенки, способствуя формированию ее атеросклеротических повреждений. Накопленные данные с той или иной степенью достоверности подтверждают участие ОАС в формировании сердечно-сосудистых нарушений. Существуют причины, ограничивающие прямые доказательства влияния ОАС на сердечно-сосудистую систему (депривация сна, вызывающая аналогичные изменения, а также трудность разграничения влияния других факторов риска развития ССЗ, в частности, артериальной гипертензии или ожирения, которые часто ассоциированы с ОАС). Необходимо продолжение изучения процессов, реализующих патологическое влияние ОАС на сердце и сосуды.

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