Chronic heart failure represents a leading cause of mortality and health care expenditure in developed countries. In the last 20 years, medical therapy of heart failure has dramatically changed thanks to the introduction of agents able to significantly reduce the neurohormonal hyperactivation that underpins the syndrome, and to the growing opportunities of electrical therapies. Although major advances in terms of improved survival and quality of life have been achieved, the reduction in the burden of heart failure is still the primary goal of cardiovascular societies. In the last decades, other research lines have also grown to complement the neurohormonal paradigm. It is increasingly evident that several hormonal systems are down-regulated or impaired in patients with heart failure, including growth and thyroid hormones, androgens and insulin. These abnormalities could be considered interrelated and linked, in turn, to the neurohormonal and cytokine hyperactivation. Since most of these alterations provide prognostic information, these new lines of evidence support the extension of the classical neurohormonal scheme to a more comprehensive pathophysiological model that includes multiple hormonal and metabolic deficiencies. This chapter examines the evidence in support of this concept. Preliminary experience concerning targeted hormonal supplementation or metabolic modulation is also briefly reviewed in this article.
ASJC Scopus subject areas