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[The role of inflammation in the pathogenesis of chronic heart failure]
R E Tokmachev1, A V Budnevsky1, A Ya Kravchenko1
1N.N. Burdenko Voronezh State Medical University, Ministry of Health of Russia, Voronezh, Russia.
Insights
Chronic heart failure (CHF) involves complex neurohumoral and immunoinflammatory pathways. Understanding cytokine roles, like interleukin-6 and tumor necrosis factor-alpha, is crucial for better CHF prognosis and treatment strategies.
Area of Science:
- Cardiology
- Immunology
- Pathophysiology
Background:
- The neurohumoral model offers insights into chronic heart failure (CHF) pathogenesis.
- Recent research indicates complex activation pathways within neurohumoral systems in CHF.
- Increased local hormone synthesis contributes to proinflammatory cytokine and proto-oncogene activation, leading to adverse effects.
Purpose of the Study:
- To review the concept of progressive chronic heart failure (CHF).
- To explore the immunoinflammatory concept of CHF pathogenesis.
- To detail the role, classification, and prognostic significance of cytokines in CHF.
Main Methods:
- Literature review of studies on CHF pathogenesis.
- Analysis of the role of neurohumoral systems and cytokines in CHF.
- Examination of the correlation between cytokine levels and CHF severity and prognosis.
Main Results:
- The immunoinflammatory concept highlights elevated interleukin-6 as a marker of poor prognosis in CHF.
- Tumor necrosis factor-alpha levels correlate directly with clinical severity and neurohumoral activity in decompensated CHF.
- Elevated plasma cytokine concentrations are linked to CHF occurrence and progression.
Conclusions:
- Cytokine aggression is a key component in CHF pathogenesis.
- Further research is needed to understand the impact of inflammation on heart failure progression.
- Targeting inflammatory components may offer novel therapeutic approaches for CHF.
Abstract:
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.
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