The Cytokines and Heart Failure - A Review

Abstract

Heart Failure (HF) develops in several stages - the first stage is some disorder that places a hemodynamic burden on the myocardium or causes myocardial injury. The second stage is that of cardiac compensation, which involves neurohormonal activation to preserve cardiac output and tissue perfusion. And the final stage is the progression of HF, which is complex and is the result of the harmful effects of the compensatory mechanisms of the second stage; an immune-system activation manifested by increases in inflammatory cytokines, including tissue necrosis factor–alpha (TNF-á), soluble receptors of TNF-á (sTNFR1 and 2), interleukin (IL)-1, IL-6 and IL-10, and C-reactive protein (CRP). It has recently been recognized that elevated circulating levels of various proinflammatory cytokines (TNF- á, IL-1, IL-6) leading to free radical overproduction, as well as to cardiac myocyte and endothelial cell apoptosis, play a significant role in the pathophysiology of CHF. The extracellular domains of proinflammatory cytokine receptors (sTNFR1, sTNFR2 and sIL- 6R) are also elevated in CHF and provide more complete information on cytokine activation in this syndrome. This article reviews the contribution of inflammatory cytokines in the disease progression in patients with heart failure, their diagnostic as well as prognostic values and possibly therapeutic interventions on these biologic active molecules.

Key words: Cytokines; cytokine receptors; Heart failure.

DOI: http://dx.doi.org/10.3329/cardio.v3i2.9190

Cardiovasc. J. 2011; 3(2): 200-212