Heart failure (HF) is a complex heterogeneous syndrome with immune, metabolic and neurohumoral
mechanisms interacting and leading to gradual heart contractility impairment. From the first study-to correlate
inflammation with HF, inflammation biomarkers have been the subject of intense inquiry in patients with various forms of
HF. Chronic HF (CHF) is strongly associated with inflammation in terms of pathogenesis, progression, severity and
prognosis. Inflammatory mediators participate in CHF pathophysiology in various ways like exerting direct impact on
cardiac myocytes, fibroblasts and β-adrenergic receptors leading to hypertrophy, fibrosis and impaired cardiac
contractility, respectively, or inducing apoptosis by stimulation of the proper genes. The anti-inflammatory effects of
classical heart failure therapeutic strategies such as ACEI and b-blockers are rather conflicting. Whether novel
immunomodulating and anti-inflammatory therapeutic approaches should be added to existing therapies in order to ensure
additional benefit to HF patients is under investigation. In this review, we summarize the pathophysiological link between
inflammatory processes and CHF, focusing on the role of novel and traditional inflammatory biomarkers and highlighting
novel anti-inflammatory therapeutic strategies.
Keywords: Anti-TNF therapy, biomarkers, chemokines, CRP, heart failure, inflammation, interleukins, TNF-α.
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