20Бета-адренореактивность эритроцитов и прогрессирование хронической сердечной недостаточности у пациентов, перенесших инфаркт миокарда Гарганеева А. А., Александренко В. А., Кужелева Е. А., Реброва Т. Ю.Цель. Выявление ассоциации бета-адренореактивности эритроцитов с прогрессированием хронической сердечной недостаточности (ХСН) у пациентов, перенесших инфаркт миокарда (ИМ). Материал и методы. Проведен анализ бета-адренореактивности по изменению осморезистентности эритроцитов под влиянием адреноблокатора у 50 пациентов с ХСН через 6 мес. после перенесенного ИМ для определения уровня активности симпато-адреналовой системы. Результаты. На основании проведенного исследования была установлена частота прогрессирования ХСН в виде увеличения функционального класса (ФК) ХСН после индексного ИМ, которая в анализируемой когорте ставила 26% (n=13). Все пациенты были разделены на 2 группы в зависимости от наличия или отсутствия прогрессирования ХСН в постинфарктном периоде. При определении бета-адренореактивности было выявлено, что у пациентов с прогрессирующей ХСН уровень показателя β-АРМ составил 58,8 (50,9;78,0) усл. ед., что значительно превышало аналогичный показатель у пациентов со стабильным течением заболевания (46,8 (38,0;66,3) усл. ед., p=0,025). Был проведен ROC-анализ, позволивший установить уровень показателя β-АРМ ≥49,53 усл. ед. "точкой отсечения", которую можно рассматривать в качестве маркера прогрессирования ХСН у пациентов, перенесших ИМ, при чувствительности -92,3% и специфичности -62,2%. Данный уровень β-АРМ ассоциирован более чем с пятикратным увеличением риска прогрессирования ХСН у пациентов, перенесших ИМ (ОШ 5,48; 95% ДИ 1,28-23,37; p=0,024). Заключение. У больных ХСН, перенесших ИМ, наблюдается снижение адренореактивности мембран эритроцитов, что отражается увеличением показателя β-АРМ выше условной принятой нормы в 20 усл. ед. При этом, при прогрессирующей ХСН β-АРМ значительно увеличивается по сравнению со стабильным течением заболевания. Установлена "точка отсечения" показателя β-АРМ ≥49,53 усл. ед., которая позволяет предсказывать прогрессирование ХСН с высокой чувствительностью и специфичностью.Ключевые слова: адренореактивность, хроническая сердечная недостаточность, инфаркт миокарда, симпато-адреналовая система.
Aim. to evaluate long term outcomes of acute myocardial infarction (MI), based on the populational registry. Material and methods. In the study, the survived post-MI patients were included, in the year 2007 registered in database of MI (n=439). Prospective observation was done during 5 years after index event. In the case of fatal outcome the protocols were analyzed, of pathology studies and summaries of forensic autopsies; relatives were interviewed and the witnesses of clinical cases. For statistics, the software "Statistiсa" V.10 was applied. Results. Mortality among patients included into the study, was 11% in one year post MI, and 35% at 5 years. In overall structure of the causes of fatal outcomes there were cases of second MI -37%. Chronic coronary heart disease was found as a cause of death in 21%, and in 2% there was fatal stroke; in 5% pulmonary embolism, and in 5% sudden cardiac death. In 17% causes of death were not related to cardiovascular pathology. Conclusion.Patients after MI do demonstrate high level of mortality in 5 year outcomes. Leading causes of fatal outcomes during first 2 years are recurrent acute coronary events, acute strokes, thromboembolism.
Objective. To identify associations of beta-adrenoreactivity with stage of chronic heart failure (CHF) in patient with previousmyocardial infarction (MI).Material and Methods. A total of 50 patients with CHF underwent an analysis of adrenoreactivity based on the changes in red blood cellosmoresistance in the presence of adrenergic blocker to determine the activity of the sympathoadrenal system a year after MI.Results. Higher levels of beta-adrenoreactivity (β-ARM) were characteristic of patients with CHF of higher gradations: 61.8(47.5;74.8) с.u. in patients with stage IIA CHF versus 48.7 (39;65.2) с.u. in patients with stage I CHF, p=0.037.Conclusion. These results may suggest the diagnostic value of the indicator of adrenoreactivity and its possible use as a newbiomarker for assessing the severity of CHF in patients with previous myocardial infarction.
Objective: To study the association of beta-adrenergic reactivity index of erythrocyte membranes with polymorphisms of the beta-1-adrenergic receptor gene ADRB1 (Ser49Gly and Arg389Gly).Material and methods: the study included 62 patients with myocardial infarction (MI) — 49 men (median age of 58.0 (47.5; 64.5) years) and 13 women (median age of 76.0 (61.5; 81.0) years). All patients underwent analysis of beta-adrenoreactivity of erythrocyte membranes using the BETA-ARM AGAT reagent kit within the first 6 hours from the onset of MI. The patients were divided into 2 groups depending on the value of the beta-adrenergic reactivity index (β-ARM). The first group (n = 11) included patients with a normal P-ARM level (from 2 to 20 conventional units). The second group (n = 51) consisted of patients with increased values of β-ARM (more than 20 standard units). Genetic analysis for the determination of ADRB1 gene polymorphisms (Ser49Gly and Arg389Gly) was carried out by isolating DNA from peripheral blood leukocytes (Wizard Genomic DNA Purification Kit) with PCR amplification and further electrophoretic detection. Statistical processing of the obtained data was carried out using Statistica 10 software and the demo version of IBM SPSS Statistics 20.0.Results: patients with elevated β-APM values were characterized by higher levels of myocardial necrosis markers in the blood (CPK, CPK-MB, and troponin I) in acute myocardial infarction than for patients of the first group (p = 0.009, p = 0.032 and p = 0.001, respectively). In addition, the second group of patients was characterized by a more frequent development of acute left ventricular failure (33.3%, p = 0.026), as well as a history of arterial hypertension before the development of index MI (90.2%, p = 0.044). With regard to the Arg389Gly polymorphism, significant differences were found among patients with normal and increased P-APM values in the acute period of MI. Thus, the second group of patients consisted mainly of carriers of the 1165CC genotype of the ADRB1 gene (n = 29, 56.9%, p = 0.043). The carriage of the 1165G allele was much more often observed among patients of the first group (81.8%; OR = 5.93; CI 1.16-30.25; p = 0.043).Conclusion: an association of the 1165CC genotype of the Arg389Gly polymorphism of the ADRB1 gene with increased β-APM values in acute MI was established. The detected associations may indicate a possible genetic predisposition to SAS hyperactivation, and also indicate the need for further study of polymorphisms and the level of expression of the ADRB1 gene in patients with high individual values of β-APM established in the acute period of MI.
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