巨细胞病毒抗体水平与慢性心力衰竭的进展

S. Shilov, E. N. Berezikova, S. Mayanskaya, I. V. Pankova, B. B. Pinkhasov, A. A. Popova, D. Z. Tabdaeva, A. D. Vikhreva
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摘要

本研究探讨了巨细胞病毒(CMV)IgG滴度与促炎细胞因子TNF-α和IL-1β浓度之间的关系,以及观察24个月期间慢性心力衰竭(CHF)失代偿患者住院后的预后。材料和方法我们对 132 名因缺血性病因导致 CHF 失代偿而住院的患者(年龄 59.0 [54.0; 63.5] 岁,中位数 [下四分位数;上四分位数])进行了研究。患者在 CHF 失代偿稳定后出院,被纳入研究范围。随后,对患者进行为期24个月的前瞻性监测。纳入研究后,测定 TNF-α、IL-1β 血浆浓度,出院前和 24 个月后测定 CMV IgG 抗体滴度。结果显示患者群中 CMV IgG 抗体滴度为 1356 [835; 1931] 单位/毫升。患者被分为 1、2 和 3 三组,抗体滴度分别为小于 923、923 至 1811 和大于 1811 单位/毫升(每组 44 人)。与三等分 1 的患者相比,三等分 3 组的患者更有可能患有 IV 功能分级的慢性阻塞性肺疾病(p = 0.025),而且促炎细胞因子的含量更高(TNF-α 为 p = 0.001,IL-1β 为 p = 0.019),在 24 个月的观察期间,因慢性阻塞性肺疾病失代偿而住院、慢性阻塞性肺疾病功能分级恶化和死亡的人数也更多。结论是与抗体水平较低的患者相比,CHF 患者的 CMV IgG 水平越高,促炎细胞因子的浓度就越高,CHF 失代偿发作后 24 个月内发生不良心血管事件的风险也越高。在慢性阻塞性肺疾病患者免疫抑制的背景下,受 CMV 感染影响的炎症过程的活性很可能是心血管病变进展和死亡的重要诱因。
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Cytomegalovirus antibody level and progression of chronic heart failure
This study demonstrates the relationship between IgG titer to cytomegalovirus (CMV) and the proinflammatory cytokine TNF-α and IL-1β concentration, the prognosis after hospitalization of patients due to decompensation of chronic heart failure (CHF) during 24 months of observation. Material and methods. We examined 132 patients with CHF of ischemic etiology (age 59.0 [54.0; 63.5] year, median [lower quartile; upper quartile]), hospitalized for CHF decompensation. Patients were included in the study after stabilization of CHF decompensation before discharge from the hospital. Subsequently, patients were prospectively monitored for 24 months. Upon inclusion in the study, TNF-α, IL-1β plasma concentration was determined, before discharge from the hospital and after 24 months – the titer of IgG antibodies to CMV. Results. The titer of IgG to CMV in the cohort of patients was 1356 [835; 1931] units/ml. Patients were divided into tertiles 1, 2 and 3 with an antibody titer of less than 923, from 923 to 1811 and more than 1811 units/ml, respectively (44 persons in each group). Individuals from the tertile 3 group were more likely to have IV functional class CHF (p = 0.025), and also had a higher content of pro-inflammatory cytokines (p = 0.001 for TNF-α and p = 0.019 for IL-1β), and the number of hospitalizations due to decompensation of CHF, worsening functional class of CHF and deaths during 24 months of observation than in patients of tertile 1. Conclusions. With an increased level of IgG to CMV in patients with CHF, there is an increase in the concentration of pro-inflammatory cytokines and the risk of adverse cardiovascular events within 24 months after an episode of CHF decompensation compared to patients with lower antibody levels. The activity of the inflammatory process, which is influenced by CMV infection, on the background of immunosuppression in patients with CHF, is likely an important trigger for the progression of cardiovascular pathology and mortality.
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