تعيين المستويات البلازمية لبعض الواصمات الالتهابية لدى مرضى فشل القلب

Abstract EN

Persistent inflammation, involving increased levels of inflammatory cytokines and Galectin-3, seems to play a pathogenic role in heart failure (HF), by influencing heart contractility, inducing hypertrophy and promoting apoptosis, contributing to myocardial remodeling.

Aim: This study aimed to investigate the relationship between circulating levels of some cytokines (tumor necrosis factor-α, and interleukin-6) and the fibrosis marker Galectin-3 in patients with HF.

Materials and methods: The study included 122 HF patients and 22 normal controls.

HF patients were divided into two groups: mild HF (n=40 patients) and severe HF (n=82 patients).

Plasma cytokine levels (TNF-α, IL-6) and Galectin-3 levels were measured by ELISA.

Results: Concentrations of inflammatory cytokines (IL-6 and TNF-α) were significantly higher in heart failure patients than in normal controls, with Galectin-3 concentrations also significantly higher in heart failure patients than control group.

Increased Galectin-3 concentrations were compatible with severity of heart failure.

A significant correlation was found between IL-6 and Galectin-3 concentrations (r = 0.16; P = 0.0001), and also significant correlation was found between TNF-α and Galectin-3 (r = 0.09; P = 0.00011).

Conclusion: Our results show that Inflammation Markers: IL-6, TNF-α, and Galectin-3 levels were markedly elevated in patients with HF.

This study found that inflammatory cytokines levels significantly correlate with galectin-3 levels, which suggests the role of the inflammatory process in the pathogenesis of myocardial fibrosis.