The classic model of Chronic Heart Failure (CHF) is rooted in the overexpression of neurohormonal molecules.
To complement this paradigm, increasing evidence indicates that a variety of hormones may be down-regulated in CHF
patients. The list includes growth hormone (GH) and its tissue effector insulin-like growth factor-1 (IGF-1).
The GH/IGF-1 axis regulates cardiac growth, stimulates myocardial contractility, and influences the vascular system. The
relationship between the GH/IGF-1 axis and the cardiovascular system has been extensively demonstrated in numerous
studies in animals models and confirmed by the cardiac derangements secondary to both GH excess and deficiency in
Impaired activity of the GH/IGF-1 axis in CHF has been described by several independent groups and includes a wide
array of abnormalities, including low IGF-1 levels, GH deficiency (GHD), and GH resistance that may be related to the
severity of heart disease. According to several observations, these derangements are associated with poor clinical status
Since the first study of GH therapy in CHF in 1996, several placebo-controlled trials have been conducted with conflicting
results. These discordant findings are likely explained by the degree of CHF-associated GH/IGF-1 impairment that may
impact on individual responsiveness to GH administration.
Biological actions of GH and IGF-1, cardiovascular implication of GH deficiency and GH excess, relation between
somatotrophic axis and CHF are discussed. Results from trials of GH therapy, emerging therapeutic strategies, safety
issues, and lack in evidence are also reported.