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Chronic heart failure (CHF) is a complex metabolic disorder with multiple interactions between the immune, neurohormonal and cardiovascular systems. That the progression of CHF is due to neurohormonal abnormalities is now considered to be established and has led to major therapeutic benefits. Many current therapies are also thought to exert a variety of immunological effects and this has been much less studied. This review aims to discuss interactions between immune pathways and neurohormonal abnormalities relevant to disease progression in CHF and to the development of cardiac cachexia. Cytokines, in particular tumour necrosis factor-a, have many interactive opportunities within a regulatory network of energy metabolism, immune function and neuroendocrine function. Inflammatory cytokines are known to contribute to the progression of CHF, being related to patients’ prognosis. Advanced CHF can be considered to be a state of chronic (low-grade) inflammation and ca tabolism. Anti-cytokine therapy could be successful in patients with proven immune abnormalities as in cardiac cachexia. In addition, anabolic therapies appear to be indicated in cachectic CHF patients. These novel approaches are certainly not without some risk and many of them are very expensive, which may limit their application to certain subgroups of patients. In the future it may not be enough to monitor only the cardiac function of patients; rather, the immune and neurohormonal status of patients may also need to be included to perform a complete assessment. Keywords: Chronic heart failure, cachexia, wasting, hormones, cytokines, endotoxin.

Imbalance of catabolic and anabolic pathways in chronic heart failure. Implications for the treatment of cardiac cachexia