Tokmachev R E, Budnevsky A V, Kravchenko A Ya
N.N. Burdenko Voronezh State Medical University, Ministry of Health of Russia, Voronezh, Russia.
Ter Arkh. 2016;88(9):106-110. doi: 10.17116/terarkh2016889106-110.
The review considers the main points of the concept of progressive chronic heart failure (CHF). The neurohumoral model of CHF pathogenesis could create novel approaches to treating these patients. However, recent studies have shown that the ways of activating the neurohumoral systems in CHF are much more complex. The increased local synthesis of hormones causes the activation of proinflammatory cytokines and proto-oncogenes, which have a number of negative effects. Multiple studies have formulated the immunoinflammatory concept of CHF pathogenesis, according to which the increased concentration of interleukin-6 is a marker of poor prognosis in CHF, and the level of tumor necrosis factor-α directly correlates with the severity of its clinical manifestations and the activity of the neurohumoral background in decompensation. The review gives a classification of cytokines and describes the reasons for their elevated plasma concentration, their possible role in the occurrence and progression of CHF, and their prognostic significance. The pathogenesis of CHF, which includes cytokine aggression, requires further studies of the effect of the inflammatory component on the course of heart failure.
本综述探讨了进行性慢性心力衰竭(CHF)概念的要点。CHF发病机制的神经体液模型可能为治疗这些患者创造新方法。然而,最近的研究表明,CHF中激活神经体液系统的方式要复杂得多。激素局部合成增加会导致促炎细胞因子和原癌基因激活,产生许多负面影响。多项研究提出了CHF发病机制的免疫炎症概念,根据该概念,白细胞介素-6浓度升高是CHF预后不良的标志物,肿瘤坏死因子-α水平与CHF临床表现的严重程度以及失代偿时神经体液背景的活性直接相关。本综述对细胞因子进行了分类,并描述了其血浆浓度升高的原因、在CHF发生和发展中的可能作用及其预后意义。CHF的发病机制,包括细胞因子攻击,需要进一步研究炎症成分对心力衰竭病程的影响。