DYNAMIC CHANGES IN CARDIOVASCULAR RISK BIOMARKERS AND CYTOKINES OF MYOCARDITIS-FREE PATIENTS WITH DECOMPENSATED HEART FAILURE AND ISCHEMIC SYSTOLIC DYSFUNCTION

The development and progression of heart failure is associated with a variety of pathophysiological mechanisms, of particular interest is the study of the inflammatory response as a fundamental link in the pathogenesis of CHF and its main component – decompensation. An open, non-randomized, prospective study was carried out to evaluate the clinical and morphological features of subclinical inflammation in patients with acute decompensation of ischemic chronic heart failure with a reduced ejection fraction. The study included 25 patients with decompensated ischemic CHF with left ventricular ejection fraction < 40% aged 35 to 75 years (60.12±9.3 y. o.). In this study the dynamics of the serum content of C-reactive protein (CRP), N-terminal fragment of the brain natriuretic peptide precursor protein (NT-proBNP), soluble ST2(sST2), insulin-like growth factor-1 receptor (IGF-1R), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-α (TNFα) was performed by multiplex immunoassay using the FLEXMAP 3D. All studied patients were divided into two groups depending on the diagnosed myocarditis: patients with no signs of myocarditis and patients with myocarditis. It was found that in the group of patients with diagnosed myocarditis there was an increased content of CRP, IGF-1R, IL-6 and IL-10, TNFα compared to the group of patients without myocarditis. The median concentrations of the NT-proBNP and sST2 in both groups did not differ. At the follow-up visit a year later, there was a decrease in the content of CRP, NT-proBNP, IL-6 in both groups. In the group of patients with myocarditis, an increase in the content of sST2, IGF-1R, IL-10 was observed. Thus, the study carried out in dynamics revealed significant differences in the degree of changes in the serum activity of pro- and anti-inflammatory cytokines and biomarkers of cardiovascular risk in patients with decompensated heart failure with systolic dysfunction with diagnosed myocarditis and in its absence

IMMUNE RESPONSE IN DECOMPENSATED CHRONIC HEART FAILURE OF ISCHEMIC ORIGIN

Recently, a significance has been established, for the role of inflammation in the pathology of chronic heart failure (CHF). It is well known that raised level of circulating pro-inflammatory cytokines in ischemic CHF patients correlate with the severity and prognosis of the disease. Monocytes play key role in an inflammatory cascade and are the main source of pro-, as contra-inflammatory cytokines. Disbalance of physiological inflammation in alteration and healing of the myocardium might lead to formation of pathological chronic inflammation. In the article, the role of monocytes discussed, and of inflammation, in CHF and its decompensation. The kinds of cytokines observed with their role in inflammation. Also, the analysis presented, of the drugs used for modulation of immune response in CHF

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 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

Pseudo-coronary scenario of inflammatory viral cardiomyopathy

Cardiomyopathy is one of the most severe and complicated cardiovascular diseases which leads to development of acute and chronic heart failure. The progress in molecular biochemistry and genetics allows to significant enhancement of its diagnostics. New data has confirmed that cardiomyopathies represent a comple

Pseudo-coronary scenario of inflammatory viral cardiomyopathy

Cardiomyopathy is one of the most severe and complicated cardiovascular diseases which leads to development of acute and chronic heart failure. The progress in molecular biochemistry and genetics allows to significant enhancement of its diagnostics. New data has confirmed that cardiomyopathies represent a comple