СELLULAR IMMUNITY IN CHRONIC HEART FAILURE CAUSED BY ISCHEMIC ETIOLOGY

Abstract

The article summarizes the literature data on the pathogenetic effect of an increased level of pro-inflammatory cytokines on the progression of chronic heart failure (CHF) of ischemic origin. According to a number of modern researchers, immune activation and systemic inflammation play a key role in the pathogenesis of CHF [5]. According to this concept, there is an increase in the synthesis of pro-inflammatory cytokines that determine the evolution of left ventricular dysfunction. The content of cytokines in the blood plasma of patients with CHF, regardless of its etiology, significantly exceeds normal values [2]. However, the reasons for the activation of the immune system in CHF are not fully understood [2]. It has been suggested that the hyperproduction of pro-inflammatory cytokines, mainly tumor necrosis factor α (TNF-α), is mediated by high sympathetic adrenal activation [1].