Modern approaches to treatment of patients with decompensated chronic heart failure: the role of inflammation in the pathogenesis of decomposition

It was established that in patients with chronic heart failure (CHF), including CHF with reduced ejection fraction, as well as acute decompensated CHF, the level of serum inflammatory markers was increased. Moreover, experimental studies have shown repeatedly that activation of mechanisms of immune...

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Published in:Bi͡u︡lletenʹ Sibirskoĭ medit͡s︡iny Vol. 17; no. 4; pp. 238 - 253
Main Authors: Kruchinkina, E. V., Ryabova, T. R., Batalov, R. E., Ryabov, V. V.
Format: Journal Article
Language:English
Russian
Published: Siberian State Medical University (Tomsk) 01-01-2018
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Summary:It was established that in patients with chronic heart failure (CHF), including CHF with reduced ejection fraction, as well as acute decompensated CHF, the level of serum inflammatory markers was increased. Moreover, experimental studies have shown repeatedly that activation of mechanisms of immune response in the myocardium provokes left ventricular remodeling and progression of left ventricular dysfunction. Nonetheless, clinical studies of anti-inflammatory drugs, including those aimed at blockage of cytokines have been neutral or negative with respect to the primary end points of the trials, and in some patients, resulted in worsening CHF or death. This review discusses variants of the types of inflammation in the myocardium, their immune mediators involved in the pathogenesis of CHF and its progression. Mechanisms of the pathogenesis of inflammatory cardiomyopathy leading to HF are discussed. A more precise conclusion about inflammatory phenotype in myocardial tissue, which will identify therapeutic targets in the treatment of CHF is necessary. Additionally, the review presents modern data about tactics for managing patients with acute decompensation of CHF with systolic dysfunction, which includes optimal medication, invasive and device therapy.
ISSN:1682-0363
1819-3684
DOI:10.20538/1682-0363-2018-4-238-253