urmjУральский медицинский журналUral Medical Journal2949-4389Ural State Medical University10.52420/2071-5943-2024-23-1-46-59JPTCEUurmj-1425Research ArticleОригинальные статьи | Original articlesOriginal articlesМаркеры деградации коллагена при ремоделировании и диастолической дисфункции левого желудочка у пациенток с артериальной гипертензиейMarkers of Collagen Degradation in Remodeling and Diastolic Dysfunction of Left Ventricle in Patients with Arterial Hypertensionhttps://orcid.org/0000-0001-7312-415XШамбатовМ. А.ShambatovM. A.

Мураз Акбар оглы Шамбатов — аспирант кафедры фармакологии и клинической фармакологии

Екатеринбург

Muraz A. Shambatov — Postgraduate Student of the Department of Pharmacology and Clinical Pharmacology

Ekaterinburg

Muraz.shambatov@rambler.ruhttps://orcid.org/0000-0001-7826-9657ИзможероваН. В.IzmozherovaN. V.

Надежда Владимировна Изможерова — доктор медицинских наук, доцент, заведующий кафедрой фармакологии и клинической фармакологии

Екатеринбург

Nadezhda V. Izmozherova — Doctor of Sciences (Medicine), Associate Professor, Head of the Department of Pharmacology and Clinical Pharmacology

Ekaterinburg

nadezhda_izm@mail.ruhttps://orcid.org/0000-0001-6216-2468ПоповА. А.PopovA. A.

Артём Анатольевич Попов — доктор медицинских наук, доцент, заведующий кафедрой госпитальной терапии

Екатеринбург

Artem A. Popov — Doctor of Sciences (Medicine), Associate Professor, Head of the Department of Hospital Therapy

Ekaterinburg

art_popov@mail.ruhttps://orcid.org/0009-0005-8643-1825ГришинаИ. Ф.GrishinaI. F.

Ирина Фёдоровна Гришина — доктор медицинских наук, профессор, заведующий кафедрой поликлинической терапии

Екатеринбург

Irina F. Grishina — Doctor of Sciences (Medicine), Professor, Head of the Department of Polyclinic Therapy

Ekaterinburg

grishif@mail.ruhttps://orcid.org/0000-0003-2797-1926КудрявцеваЕ. В.KudryavtsevaE. V.

Елена Владимировна Кудрявцева — доктор медицинских наук, доцент, заведующий центральной научно-исследовательской лабораторией, доцент кафедры акушерства и гинекологии с курсом медицинской генетики

 Екатеринбург

Elena V. Kudryavtseva — Doctor of Sciences (Medicine), Associate Professor, Head of the Central Scientific Research Laboratory, Associate Professor of the Department of Obstetrics and Gynecology with Medical Genetics Course

Ekaterinburg

elenavladpopova@yandex.ruhttps://orcid.org/0000-0003-0966-9571БазарныйВ. В.BazarnyiV. V.

Владимир Викторович Базарный — доктор медицинских наук, профессор, главный научный сотрудник, руководитель отдела общей патологии и гистологической лаборатории центральной научно-исследовательской лаборатории

Екатеринбург,

Vladimir V. Bazarnyi — Doctor of Sciences (Medicine), Professor, Chief Researcher, Head of the General Pathology Department and Histological Laboratory of the Central Scientific Research Laboratory

Ekaterinburg

vlad-bazarny@yandex.ruhttps://orcid.org/0000-0002-4921-7222ПолушинаЛ. Г.PolushinaL. G.

Лариса Георгиевна Полушина — кандидат медицинских наук, старший научный сотрудник отдела общей патологии и гистологической лаборатории центральной научно-исследовательской лаборатории

Екатеринбург

Larisa G. Polushina — Candidate of Sciences (Medicine), Senior Researcher of the General Pathology Department and Histological Laboratory of the Central Scientific Research Laboratory

Ekaterinburg

polushina-larisa@bk.ruhttps://orcid.org/0000-0002-6092-3734КопёнкинМ. А.KopenkinM. A.

Максим Александрович Копёнкин — аспирант кафедры медицинской микробиологии и клинической лабораторной диагностики, младший научный сотрудник отдела общей патологии и гистологической лаборатории центральной научно-исследовательской лаборатории

Екатеринбург

Maksim A. Kopenkin — Postgraduate Student of the Department of Medical Microbiology and Clinical Laboratory Diagnostics, Junior Researcher of the General Pathology Department and Histological Laboratory of the Central Scientific Research Laboratory

Ekaterinburg

maximkopenkin@yandex.ruУральский государственный медицинский университетРоссияUral State Medical UniversityRussian Federation2024060320242314659Copyright © Шамбатов М.А., Изможерова Н.В., Попов А.А., Гришина И.Ф., Кудрявцева Е.В., Базарный В.В., Полушина Л.Г., Копёнкин М.А., 20242024Шамбатов М.А., Изможерова Н.В., Попов А.А., Гришина И.Ф., Кудрявцева Е.В., Базарный В.В., Полушина Л.Г., Копёнкин М.А.Shambatov M.A., Izmozherova N.V., Popov A.A., Grishina I.F., Kudryavtseva E.V., Bazarnyi V.V., Polushina L.G., Kopenkin M.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.umjusmu.ru/jour/article/view/1425Введение

Введение. Ремоделирование миокарда — последствие или предиктор развития ряда сердечно-сосудистых заболеваний. Ключевой процесс в ремоделировании миокарда — деградация волокон коллагена, опосредуемая активностью матриксных металлопротеиназ и их тканевого ингибитора.

Цель исследования — выявить ассоциации между сывороточной концентрацией матричной металлопротеиназы 9 (ММП-9) и тканевого ингибитора металлопротеиназ 1 типа (ТИМП-1), структурно-геометрическим ремоделированием миокарда и диастолической дисфункцией у пациенток с артериальной гипертензией.

Материалы и методы

Материалы и методы. В одномоментное исследование включены 84 женщины в постменопаузе. Ремоделирование миокарда левого желудочка (ЛЖ) оценивали по результатам эхокардиографии в соответствии с классификацией Ганау (англ. Ganau). У женщин с нормальными значениями индекса массы миокарда ЛЖ (ИММЛЖ) определялись следующие типы ремоделирования ЛЖ: нормальная геометрия (НГ) ЛЖ — при относительной толщине стенки (ОТС) ≤0,42; концентрическое ремоделирование (КР) ЛЖ — при ОТС >0,42. У пациентов со значениями ИММЛЖ выше нормальных выделяли два типа ремоделирования: в случае, если значение ОТС превышало 0,42, то верифицировали концентрическую гипертрофию (КГ) ЛЖ; если значение ОТС было менее 0,42 — эксцентрическую гипертрофию (ЭГ) ЛЖ. Диастолическую функцию ЛЖ оценивали с помощью тканевой допплерографии посредством оценки трансмитрального кровотока с использованием показателей максимальной скорости раннего диастолического наполнения и предсердной систолы, времени замедления раннего диастолического наполнения. Диастолическую дисфункцию (ДД) ЛЖ определяли при наличии трех любых критериев из четырех: скорость движения медиальной части митрального кольца в раннюю диастолу e` (септальная) <7 см/с и (или) e` (боковая) <10 см/с; Е/e` > 14; индексированный объем ЛП >34 мл/м 2; скорость трикуспидальной регургитации >2,8 см/с. ДД I степени (или замедленная релаксация) определяли при Е/А ≤ 0,8 и скорости E ≤ 50 см/с. При наличии как минимум двух критериев из перечисленных: E/e` > 14; объемный индекс левого предсердия ≥34 мл/м 2; скорость трикуспидальной регургитации >2,8 м/с, — определяли II степень ДД (псевдонормальный тип). При Е/А > 2 определяли III степень ДД (рестриктивный тип). Иммунохимический анализ сыворотки включал в себя определение сывороточной концентрации ММП-9 и TИМП-1 методом твердофазного гетерогенного иммуноферментного анализа. Статистическая обработка данных проводилась с помощью пакета Statistica 13.0. Данные представлены в виде — медиана (Q1–Q3). Различия оценивали с использованием непараметрических критериев Манна — Уитни и Крускала — Уоллиса. Различия признавались значимыми при уровне p < 0,05.

Результаты

Результаты. Медиана концентрации ММП-9 в выборке составила 2 295,00 (923,60–4 114,00) нг/мл, ТИМП — 1–17 010,00 (16 780,00–17 170,00) нг/мл. При оценке морфометрических вариантов ремоделирования миокарда левого желудочка установлено, что нормальную геометрию имели 29 пациенток (35 %), у 6 (7 %) выявлено концентрическое ремоделирование миокарда, в 21 случае (25 %) выявлена концентрическая гипертрофия миокарда, в 28 (33 %) установлена эксцентрическая гипертрофия миокарда. При оценке структуры сердечно-сосудистых заболеваний и медикаментозной терапии статистически значимых различий у пациенток с различными вариантами ремоделирования миокарда не выявлено. Выявлены статистически значимые различия сывороточной концентрации ММП-9 у пациенток с различными структурно-геометрическими вариантами ремоделирования. ДД ЛЖ выявлена у всех пациенток, включенных в исследование: I степень выявлена у 25 пациенток (30 %), II степень определена в 59 случаях (70 %). При оценке структуры коморбидной патологии и медикаментозной терапии статистически значимых различий у пациенток с различной степенью ДД ЛЖ не выявлено. Посредством непараметрического критерия Манна — Уитни определены статистически значимые различия значений ММП-9 у пациенток с I и II степенями ДД.

Обсуждение

Обсуждение. В патофизиологических условиях протеолитические свойства ММП-9 способствуют стимуляции иммунного ответа, инициируя и усугубляя прогрессирование заболевания. Оценка сывороточной концентрации ММП-9 и ТИМП-1 у пациентов с артериальной гипертензией может являться маркером ремоделирования ЛЖ.

Заключение

Заключение. Выявлено повышение сывороточной концентрации матриксной металлопротеиназы 9 типа и снижение концентрации тканевого ингибитора матриксных металлопротеиназ 1 типа у пациенток с артериальной гипертензией, ремоделированием миокарда и диастолической дисфункцией ЛЖ. Концентрация ММП-9 ассоциирована со степенью диастолической дисфункции и структурно-геометрическим типом ремоделирования ЛЖ.

Introduction

Introduction. Myocardial remodeling is a consequence or predictor of several cardiovascular diseases. The key process in myocardial remodeling is the degradation of collagen fibers, mediated by the activity of matrix metalloproteinases and their tissue inhibitor.

The aim of this study was to evaluate serum levels of matrix metalloproteinase type 9 and tissue inhibitor of matrix metalloproteinase type 1 in female patients with arterial hypertension, myocardial remodeling, and diastolic dysfunction.

Materials and methods

Materials and methods. A cross-sectional study that included 84 postmenopausal women. All patients underwent echocardiography. Left ventricular remodeling was assessed according to Ganau classification, and diastolic function was evaluated using transmittal flow parameters. Serum analysis included the determination of MMP-9 and TIMP-1 levels using an enzyme-linked immunosorbent assay.

Results

Results. The median concentration of MMP-9 in the sample was 2 295.00 (923.60–4 114.00) ng/ml, TIMP — 1–17 010.00 (16 780.00–17 170.00) ng/ml. When evaluating the echocardiographic parameters of the patients included in the study, changes were revealed that indicate structural and functional remodeling of the LV and DD. 29 patients (35 %) had normal geometry, 6 patients (7 %) had concentric myocardial remodeling, 21 patients (25 %) had concentric myocardial hypertrophy, 28 cases (33 %) had eccentric myocardial hypertrophy. Statistically significant changes in the activity of MMP-9 and TIMP-1 were revealed in patients with various structural and geometric variants of remodeling. DD was detected in all patients included in the study: I degree was detected in 25 patients (30 %), II degree was determined in 59 cases (70 %). Using one-way analysis of variance, statistically significant differences in the level of MMP-9 in patients with grades I and II DD were determined. MMP-9 and MMP-9/TIMP-1 in patients with grade II DD are significantly higher than in patients with grade I.

Discussion

Discussion. Under pathophysiological conditions, the proteolytic properties of MMP-9 contribute to the stimulation of the immune response, initiating pathogenesis and aggravating the progression of the disease. Evaluation of the activity of MMP-9 and TIMP-1 in patients with arterial hypertension may be a marker of myocardial remodeling.

Conclusion

Conclusion. An increase in the activity of matrix metalloproteinase type 9 and a decrease in the activity of a tissue inhibitor of matrix metalloproteinases type 1 were revealed in patients with arterial hypertension, myocardial remodeling and LV diastolic dysfunction. The level of MMP-9 is associated with the degree of diastolic dysfunction and the structural-geometric type of LV remodeling.

матриксная металлопротеиназа 9тканевой ингибитор матриксных металлопротеиназдиастолическая сердечная недостаточностьсердечная недостаточностьсохранная фракция выбросатрансторакальная эхокардиографиянедифференцированная дисплазия соединительной тканиmatrix Metalloproteinase 9tissue Inhibitor of Metalloproteinasesdiastolic Heart Failurepreserved ejection fractiontransthoracic echocardiographyundifferentiated Connective Tissue DysplasiaReferencesFrangogiannis NG, Smith CW, Entman ML. The inflammatory response in myocardial infarction. Cardiovascular Research. 2002;53(1):31–47. DOI: https://doi.org/10.1016/S0008-6363(01)00434-5.Frangogiannis NG, Smith CW, Entman ML. The inflammatory response in myocardial infarction. Cardiovascular Research. 2002;53(1):31–47. DOI: https://doi.org/10.1016/S0008-6363(01)00434-5.Yabluchanskiy A, Ma Y, Iyer RP, Hall ME, Lindsey ML. Matrix metalloproteinase-9: Many shades of function in cardiovascular disease. Physiology. 2013;28(6):391–403. 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The authors declare that there are no conflicts of interest present.