In recent years it has been demonstrated that both GH deficiency and excess include in their advanced clinical manifestations an impaired cardiovascular function, which may reduce life expectancy. This observation has allowed the investigation of the role played by the GH/IGF-I axis on cardiac structure and function. In particular, several recent experimental and clinical studies support the evidence implicating GH and/or IGF-I in the regulation of heart development. Acromegalic cardiomyopathy is characterized by myocardial hypertrophy with interstitial fibrosis, lymphomononuclear infiltration and areas of monocyte necrosis which often result in increased right and left ventricular mass and concentric hypertrophy. Conversely, patients with childhood or adulthood-onset GH deficiency (GHD) have a reduced left ventricular mass and ejection fraction and the indexes of left ventricular systolic function remained markedly depressed during exercise. In addition, a significant increase in the thickness of the vascular intima-media wall and a higher number of atheromatous plaques have been reported. These abnormalities of the cardiovascular system are partially reversed after normalization of GH and IGF-I levels, by octreotide in acromegaly or after GH replacement therapy in GHD patients. The evidence that GH is able to increase cardiac mass suggested its use in the treatment of idiopathic dilated cardiomyopathy. In a recent study on such patients, the administration of rhGH was demonstrated to increase myocardial mass and to reduce the size of the left ventricular chamber, resulting in an improvement in hemodynamics, myocardial energy metabolism and clinical status. These promising results might open a new field for GH treatment.