ROLE OF ENDOTOXIN AND SYSTEMIC INFLAMMATION IN CHRONIC HEART FAILURE PATHOGENESIS

Abstract

Aim. To study large intestine microbiocenosis, systemic inflammation activity, and the reaction of matrix metalloproteinases and tissue inhibitors of metalloproteinases (MMP-TIMP) at different stages of chronic heart failure (CHF). Material and methods. In 230 CHF patients, the following parameters were assessed: large intestine microbiocenosis, endotoxinemia, and plasma levels of tumor necrosis factor-α, C‑reactive protein, sE-selectin, MMP‑9, and TIMP‑4. Results. Progressing CHF was associated with more pronounced intestinal dysbiosis, increased endotoxinemia, activation of systemic inflammation, and MMPTIMP dysbalance. Conclusion. The pathogenetic CHD pathway starts with circulatory disturbances, which lead to increased endotoxinemia and subsequent activation of systemic inflammation. Inflammatory mediators – pro-inflammatory cytokines, intercellular adhesion molecules, and acute phase proteins – cause MMP-TIMP dysbalance, which, in turn, leads to myocardial remodelling, cardiac geometry changes, and advanced circulatory disturbances, completing the vicious circle (circulus vitiosus) of CHF progression.