Вісник проблем біології і медицини (Sep 2020)
GENDER ANALYSIS OF CHRONIC SYSTEMIC INFLAMMATION INDICATORS IN PATIENTS WITH ISCHEMIC HEART DISEASE
Abstract
For many years in a row, the leading cause of death worldwide is coronary heart disease (CHD) – 1.7 million people a year. The prevalence of diseases of the circulatory system in women as of 2018 was 1.3 more than in men. Over the last decade, mortality mortality due to diseases of the circulatory system in women has increased by 14%. Given the peculiarities of the prevalence, course, mortality from HSC in men and women, based on differences in hormonal metabolism at different ages, the susceptibility of modified and unmodified risk factors, etc., the study of gender aspects of coronary heart disease is relevant and timely.Objective: to study and compare the indicators of systemic inflammation in patients with stable coronary artery disease, depending on gender. Object and research methods. An open clinical study was carried out in which 99 patients aged 57 + 7.2 years old with a diagnosis of Сoronary Heart Disease (CHD): stable angina pectoris, II FC, CH 0-I, 51 men (group 1) and 48 women (group 2) took part. The patients underwent laboratory studies to determine the levels of cytokines involved in the process of inflammation and circulating endothelial microparticles with markers of inflammatory endothelial activation CD32 and C40 in the blood. Results. In CHD patients of both sexes an increased content of proinflammatory cytokines – IL-1β and TNFα was found, the level of anti-inflammatory cytokine IL-10 did not differ significantly from these healthy individuals. The pool of CD32+ CD40+ microparticles circulating in the bloodstream was significantly larger than in healthy individuals. There were no gender differences in the values of the studied indicators. Conclusions. In patients with stable CHD, the level of systemic inflammation and inflammatory activation of the endothelium is increased and does not have gender specificity, which may indicate the universality of the proinflammatory response in CHD, as well as the nonspecific influence of risk factors and agents of vascular lesion on the activation of chronic systemic inflammation.
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