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Aim. To compare the effect of 12-month pharmacotherapy with a betablocker (BB) (bisoprolol and nebivolol) and a combination of BB with a mineralocorticoid receptor antagonist (bisoprolol+eplerenone, nebivolol+eplerenone) on following fibrosis markers: matrix metalloproteinases 1 and 9 (MMP-1, MMP-9) and tissue inhibitor of MMP-1 (TIMP-1) in patients with heart failure with mid-range ejection fraction (HFmrEF) of ischemic origin.Material and methods. The study included 135 patients, including 40 (29,6%) women and 95 (70,4%) men aged 45-60 years (mean age, 53,1±5,7 years). Patients were randomized into subgroups based on pharmacotherapy with BB (bisoprolol or nebivolol) and their combination with eplerenone. The enzyme-linked immunosorbent assay was used to determine the level of MMP-1, MMP-9, TIMP-1 (ng/ml) using the commercial test system “MMP-1 ELISA”, “MMP-9 ELISA”, “Human TIMP-1 ELISA” (“Bender Medsystems “, Austria).Results. In patients with HFmrEF of ischemic origin, there were following downward changes in serum level of myocardial fibrosis markers, depending on the therapy: bisoprolol  — MMP-1 decreased by 35% (p<0,01), MMP-9  — by 56,3% (p<0,001), TIMP-1  — by 17,9% (p<0,01); nebivolol  — MMP-1 decreased by 45% (p<0,001), MMP-9  — by 57,1% (p<0,001), TIMP-1  — by 30,1% (p<0,01); combination of bisoprolol with eplerenone  — MMP-1 decreased by 43% (p<0,001), MMP-9  — by 51,2% (p<0,001), TIMP-1  — by 25,1% (p<0,01); combination of nebivolol with eplerenone  — MMP-1 decreased by 53% (p<0,001), MMP-9 — by 64,3% (p<0,001), TIMP-1 — by 39% (p<0,01). In patients with NYHA class I HFmrEF after 12-month therapy, the decrease in MMP-1 level was 39,9% (p<0,01), MMP-9  — 57,5% (p<0,001). In class II, the decrease in MMP-1 level was 47% (p<0,001), MMP-9 — 49,7% (p<0,001). A significant decrease in TIMP-1 level was revealed in patients with class I by 29% (p<0,01), in patients with class II by 27,1% (p<0,01) compared with the initial data.Conclusion. A significant decrease in the levels of myocardial fibrosis markers (MMP-1, MMP-9, TIMP-1) was demonstrated in patients with HFmrEF of ischemic origin receiving long-term pharmacotherapy. The most pronounced effect was determined in patients with NYHA class I HF.

лее высокую концентрацию инсулина (∆17%), лептина (∆33%) в крови у женщин, чем мужчин. У женщин выявлено более высокое содержание липопротеидов низкой плотности (∆12%) и более низкое содержание липопротеидов высокой плотности (∆10%), чем у мужчин. Заключение: Таким образом, у женщин с СНпФВ ишемического генеза на фоне метаболического синдрома отмечается наиболее выраженное по сравнению с мужчинами абдоминальное ожирение, ассоциированное с более высокими уровнями лептина крови и инсулинорезистентности, более высоким уровнем липопротеидов низкой плотности и более низким содержанием липопротеидов высокой плотности. Ключевые слова: сердечная недостаточность; промежуточная фракция выброса; пожилой возраст; метаболический синдром Для цитирования: Гостева ЕВ. Гендерные особенности метаболических нарушений у пожилых больных с сердечной недостаточностью с промежуточной фракцией выброса. Научные результаты биомедицинских исследований. 2020;6(2):249-260.

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Aim. To compare the effect of angiotensin II receptor blocker therapy (azilsartan, telmisartan) on fibrosis and immune inflammation markers in hypertensive patients with chronic kidney disease (CKD) after ischemic stroke (IS).Material and methods. The study included 76 hypertensive patients aged 60-74 years (mean age, 66±5 years) with CKD after IS. Patients were randomly divided into following pharmacotherapy groups: 38 patients — telmisartan group; 36 patients — azilsartan group. The control group consisted of 20 hypertensive people (mean age, 63±2 years) without a history of CKD and IS. The levels of matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were determined by enzyme-linked immunosorbent assay (ELISA Kit, USA). The levels of interleukin-1β (IL-1β), tumor necrosis factor α (TNF-α), interferon γ (INF-γ), monocytic chemoattractant protein 1 (MCP-1) were assessed using Vector-Best kit (Russia).Results. Six-month azilsartan therapy led to a decrease in the levels of MMP-9 by 19,9% (p<0,01), TIMP-1 by 7,5% (p<0,05), IL-1β by 7,8%, TNF-α by 13,5%, INF-γ by 7,1%, MCP-1 by 13% (p<0,05). Telmisartan therapy was associated with a decrease in the levels of MMP-9 by 39,1% (p<0,01), TIMP-1 by 16,4%, IL-1β by 10,1% (p<0,05), TNF-α by 20,8% (p<0,01), INF-γ by 14,6% (p<0,05), MCP-1 by 21,3% (p<0,01). Intergroup comparison revealed more pronounced changes in the levels of MMP-9 by 19,2% (p<0,01), TIMP-1 by 7,2% (p<0,05), TNF-α by 7,3% (p<0,05), INF-γ by 7,5% (p<0,05), and MCP-1 by 8,3% (p<0,05) when using telmisartan compared to azilsartan. When using telmisartan, the increase in glomerular filtration rate (GFR) was 14,2% (p<0,05) higher compared to azilsartan.Conclusion. Six-month telmisartan therapy in hypertensive patients with CKD after stroke was accompanied by a more pronounced decrease in markers of myocardial fibrosis (MMP-9, TIMP-1) and immune inflammation (TNF-α, INF-γ, MCP-1) compared with azilsartan, as well as with more pronounced improvement in renal function.