Impaired cardiovascular function, which may reduce life expectancy, has rec
ently been demonstrated both in GH deficiency and excess. Moreover, experim
ental and clinical studies support the evidence implicating GH and/or IGF-I
in the regulation of heart development. The existence of a specific acrome
galic cardiomyophathy characterized by myocardial hypertrophy with intersti
tial fibrosis, lympho-mononuclear infiltration and areas of monocyte necros
is which often result in biventricular concentric hypertrophy has been rece
nty demonstrated. By contrast, patients with childhood or adulthood-onset G
H deficiency (GHD) present with abnormalities of structure and function of
the left ventricle. In these patients, a significant increase in the vascul
ar intima-media thickness and an increased number of atheromatous plaques h
ave also been reported. The abnormalities of cardiovascular system could be
partially reverted by suppressing GH and IGF-I levels in acromegaly or aft
er GH remplacement therapy in GHD patients.
The evidence that GH is able to increase cardiac mass suggested its use in
the treatment of chronic heart failure of diverse etiologies. GH administra
tion was demonstrated to induce an improvement in hemodynamics and clinical
status in some patients. Although these data should be confirmed in double
-blind placebo controlled studies in larger series, the promising results o
pen new perspectives for GH treatment in humans.