Sympathetic deactivation by growth hormone treatment in patients with dilated cardiomyopathy

Aims. We examined the effects of growth hormone administration on the sympathetic nervous system in patients with idiopathic dilated cardiomyopathy. Background. Growth factor therapy is emerging as a new potential option in the treatment of heart failure. Although growth hormone provides functional benefit in the short term, it is unknown whether it affects the sympathetic nervous system, which plays a role in the progression of heart failure. Methods. Seven patients with idiopathic cardiomyopathy received 3 months treatment with recombinant human growth hormone (0.15-0.20 IU. kg^-1. week^-1). Standard medical therapy was unchanged. Myocardial norepinephrine release, both at rest and during submaximal physical exercise, plasma aldosterone, and plasma volume were measured before and after growth hormone treatment. Myocardial norepinephrine release was assessed from arterial and coronary venous plasma concentrations of unlabelled and tritiated norepinephrine and coronary plasma flow (thermodilution). Results. Growth hormone induced a significant fall in myocardial norepinephrine release in response to physical exercise (from 180 ± 64 to 99 ± 34 ng. min^-1; P <0.05). Basally, plasma aldosterone was 189 ± 28 and 311 ± 48 pg. ml^-1 in the supine and upright position, respectively, and fell to 106 ± 16 (P <0.01) and 182 ± 29 pg. ml^-1 (P <0.05) after growth hormone therapy. Growth hormone increased plasma volume from 3115 ± 493 ml to 3876 ± 336 ml (P <0.05), whereas serum sodium and potassium concentrations were unaffected. Conclusions. The data demonstrate that growth hormone administration to patients with idiopathic cardiomyopathy reduces myocardial sympathetic drive and circulating aldosterone levels. This neurohormonal deactivation may be relevant to the potential, long-term use of growth hormone in the treatment of patients with heart failure.