At present, there is a growing body of evidence implicating growth hor
mone (GH) and/or insulin-like growth factor-I (IGF-I) in the intricate
cascade of events connected with the regulation of heart development
and hypertrophy. In addition, advanced clinical manifestations of abno
rmal GH levels almost always include impaired cardiac function, which
may reduce life expectancy. This finding is related both to a primary
impairment of heart structure and function and to metabolic changes su
ch as hyperlipidaemia, increased body fat and premature atherosclerosi
s. Acromegalic cardiomyopathy is better correlated with disease durati
on than with CH or IGF-I levels. Myocardial hypertrophy with interstit
ial fibrosis, lymphomononuclear infiltration and areas of monocyte nec
rosis often result in increased right and left ventricular mass concen
tric hypertrophy. Conversely, patients with childhood or adult-onset G
M deficiency (GHD) have a reduced left ventricular mass (LVM) and ejec
tion fraction (EF) and the indices of left ventricular systolic functi
on remained markedly depressed during exercise. Cardiac function is re
ported to improve during octreotide and GH replacement treatment in ac
romegaly and CHD, respectively. The evidence that GH can increase card
iac mass suggests its use in the treatment of idiopathic dilated cardi
omyopathy. In a recent study on such patients, the administration of r
ecombinant GH (rGH) was demonstrated to increase myocardial mass and r
educe the size of the left ventricular chamber, resulting in improved
haemodynamics, myocardial energy metabolism and clinical status.