cardiovascularКардиоваскулярная терапия и профилактикаCardiovascular Therapy and Prevention1728-88002619-0125«SILICEA-POLIGRAF» LLC10.15829/1728-8800-2012-3-102-112cardiovascular-1839Research ArticleОБЗОРЫREVIEWSОптимальная стратегия лечения пациентов с артериальной гипертонией и атеросклерозом: фокус на олмесартана медоксомилOptimal therapeutic strategy for treating patients with hypertension and atherosclerosis: focus on olmesartan medoxomilМасонР. П.MasonR. P.Гарвардская медицинская школа, Бостон; Элюсида Ресерч, БеверлиUnited States201220062012113102112Copyright © Масон Р.П., 20122012Масон Р.П.Mason R.P.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/1839

Сердечно-сосудистые заболевания (ССЗ) являются одной из основных причин смертности во всем мире. В США на их долю приходится более одной трети всех смертей. В основе развития ССЗ лежит атеросклероз – хронический воспалительный процесс, который проявляется клинически в виде коронарной болезни сердца (КБС), поражения сонных или периферических артерий. Ожидается, что к 2020г атеросклероз станет ведущей причиной смертности во всем мире. Это подчеркивает важность разработки новых терапевтических подходов, которые способны замедлять прогрессирование атеросклеротического процесса или приводить к его обратному развитию. Причиной атерогенеза является повреждение эндотелия, обусловленное окислительным стрессом (ОС), который, в свою очередь, ассоциируется с такими факторами сердечно-сосудистого риска (ССР), как сахарный диабет (СД), гипертензия (АГ), курение, дислипидемия (ДЛП), ожирение (Ож) и метаболический синдром (МС). Поскольку ренин-ангиотензин-альдостероновая система (РААС) играет ключевую роль в процессе сосудистого воспаления, терапия АГ препаратами, блокирующими действие РААС (ингибиторами ангиотензин-превращающего фермента (ИАПФ) и блокаторами рецепторов к ангиотензину II (БРА)), способна уменьшать выраженность воспалительной реакции и замедлять прогрессирование атеросклероза. Снижение биодоступности оксида азота (NO) играет важную роль в патогенезе эндотелиальной дисфункции (ЭД) и АГ. Таким образом, препараты, повышающие биодоступность NO и уменьшающие выраженность ОС (например, ИАПФ и БРА), могут оказывать антиатеросклеротическое действие. В ранее выполненных исследованиях было продемонстрировано, что блокада ангиотензиновых рецепторов 1 типа при приеме БРА улучшает функцию эндотелия и препятствует атерогенезу. У пациентов с АГ БРА олмесартана медоксомил обеспечивает эффективное снижение артериального давления (АД), а также выраженное подавление действия РААС. Согласно результатам проспективных рандомизированных исследований, олмесартана медоксомил обладает целым рядом благоприятных сосудистых эффектов, что проявляется в замедлении прогрессирования атеросклеротического поражения коронарных артерий у пациентов со стабильной стенокардией (исследование OLIVUS); снижении уровней маркеров воспаления у больных АГ и доклиническим микровоспалением (EUTOPIA); положительной динамике толщины комплекса «интима-медия» (ТКИМ) сонных артерий (СА) и объема атеросклеротической бляшки у пациентов с диагностированным атеросклерозом (MORE); а также обратном развитии ремоделирования сосудов у больных АГ 1 ст. (VIOS). Несмотря на то, что в этих исследованиях не изучалось влияние терапии на СС исходы, отмеченный положительный эффект олмесартана медоксомила на частоту суррогатных конечных точек позволяет предположить, что в данных клинических группах пациентов этот препарат способен уменьшать частоту СС событий.

Cardiovascular (CV) disease is a major factor in mortality rates around the world and contributes to more than one-third of deaths in the US. The underlying cause of CV disease is atherosclerosis, a chronic inflammatory process that is clinically manifested as coronary artery disease, carotid artery disease, or peripheral artery disease. It has been predicted that atherosclerosis will be the primary cause of death in the world by 2020. Consequently, developing a treatment regimen that can slow or even reverse the atherosclerotic process is imperative. Atherogenesis is initiated by endothelial injury due to oxidative stress associated with CV risk factors including diabetes mellitus, hypertension, cigarette smoking, dyslipidemia, obesity, and metabolic syndrome. Since the renin– angiotensin–aldosterone system (RAAS) plays a key role in vascular inflammatory responses, hypertension treatment with RAAS-blocking agents (angiotensin-converting enzyme inhibitors [ACEIs] and angiotensin II receptor blockers [ARBs]) may slow inflammatory processes and disease progression. Reduced nitric oxide (NO) bioavailability has an important role in the process of endothelial dysfunction and hypertension. Therefore, agents that increase NO and decrease oxidative stress, such as ARBs and ACEIs, may interfere with atherosclerosis. Studies show that angiotensin II type 1 receptor antagonism with an ARB improves endothelial function and reduces atherogenesis. In patients with hypertension, the ARB olmesartan medoxomil provides effective blood pressure lowering, with inflammatory marker studies demonstrating significant RAAS suppression. Several prospective, randomized studies show vascular benefits with olmesartan medoxomil: reduced progression of coronary atherosclerosis in patients with stable angina pectoris (OLIVUS); decreased vascular inflammatory markers in patients with hypertension and micro- (pre-clinical) inflammation (EUTOPIA); improved common carotid intima-media thickness and plaque volume in patients with diagnosed atherosclerosis (MORE); and resistance vessel remodeling in patients with stage 1 hypertension (VIOS). Although CV outcomes were not assessed in these studies, the observed benefits in surrogate endpoints of disease suggest that RAAS suppression with olmesartan medoxomil may potentially have beneficial effects on CV outcomes in these patient populations.

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