Experimental and clinical studies have recently demonstrated that the growth hormone-insulin-like growth factor-I (GH-IGF-I) system is involved in the regulation of cardiac structure and function. Patients with acromegaly have an increased propensity of developing cardiovascular complications, such as ventricular hypertrophy with interstitial fibrosis. Conversely, patients with GH deficiency can exhibit ventricular dysfunction, increased vascular thickness, and an increased number of atheromatous plaques. In both groups of patients these abnormalities may be partially reverted by normalizing GH-IGF-I levels. In experimental or human chronic heart failure (CHF), GH administration increases ventricular mass and cardiac performance and reduces pulmonary vascular resistance. The mechanism by which this occurs is still unclear, but seems to involve calcium channels and non-endothelium-mediated vasodilatation. Randomized trials studying CHF patients contradict these results, highlighting that, in patients with heart failure, the response to GH therapy appears to be variable, and is probably influenced either by acquired GH resistance or by baseline levels of hormones. Due to the small number of patients examined to date, larger, randomized, controlled studies are needed.
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