肥胖在冠状病毒疾病炎症发展和心力衰竭进展中的作用

O. Samchuk, O.S. Kapustynska, E.Ya. Sklyarov E.Ya.
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引用次数: 0

摘要

关联组织起着复杂的生理作用,因此可能发展为新冠肺炎和心力衰竭。目的是评估病毒性疾病合并肥胖和心力衰竭患者的定义和心肌生物标志物。材料和方法。对89名冠状病毒新冠肺炎和心力衰竭患者进行了检查。所有患者都接受了人体测量和体重指数计算、一般临床治疗、反应蛋白、铁蛋白、降钙素原、白细胞介素-6水平以及心肌标志物NTproBNP和肌钙蛋白I。结果。在89名患者中,60.7%的病例被诊断为肥胖和超重(分别为41.6%和19.1%),只有39.3%的体重在正常范围内。在新冠肺炎肺炎和心力衰竭的肥胖背景下,新冠肺炎肺炎和非肥胖性心力衰竭患者的C反应蛋白水平统计增加(87.79±16.16毫克/升)(48.79±8.3;毫克/升p=0.036)。注意到肥胖患者防毒面具上肌钙蛋白I水平的统计值(0.04(0.00;0.09))(0.01(0.00;0.05)纳克/毫升;p=0.024)。新冠肺炎肺炎和心力衰竭肥胖患者体内C反应蛋白的增长证实了脂肪组织在诱导和维持中的重要作用。位于心脏厚度的异位脂肪库也可能参与心肌炎症变化的发展,这是肌钙蛋白I生长的实验室迹象。
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THE ROLE OF OBESITY IN THE DEVELOPMENT OF INFLAMMATION AND PROGRESSION OF HEART FAILURE IN CORONAVIRUS DISEASE
Relevance. Tissue plays a complex physiological role and may therefore progress to COVID-19 and heart failure. Objective is to evaluate the definition and myocardial biomarkers in a patient with viral disease in combination with obesity and heart failure. Materials and methods. 89 patients with coronavirus COVID-19 and heart failure were examined. All patients underwent anthropometric measurements and calculation of body mass index, general clinical treatment, levels of reactive protein, ferritin, procalcitonin, interleukin-6, as well as myocardial markers NTproBNP and troponin I. Results. Among 89 patients, obesity and overweight were diagnosed in 60.7% of cases (41.6% and 19.1%, respectively) and only 39.3% of the weight was in the normal range. Against the background of obesity on COVID-19 pneumonia and heart failure, a statistical increase in the level of C-reactive protein (87.79 ± 16.16 mg / l) was found in patients with COVID-19 pneumonia and non-obesity heart failure (48.79 ± 8.3; mg / l p = 0.036). The statistical value of the level of troponin I (0.04 (0.00; 0.09) on a gas mask in obese patients was noted) (0.01 (0.00; 0.05) ng / ml; p = 0.024). Conclusion. The growth of C-reactive protein in the body with obesity in pneumonia COVID-19 and heart failure confirms the important role of adipose tissue in induction and maintenance. Ectopic fat depots located in the thickness of the heart may also be involved in the development of inflammatory changes in the myocardium, a laboratory sign that is the growth of troponin I.
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