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European Heart Journal 1998 19(4):623-627; doi:10.1053/euhj.1997.0805
Copyright © 1998 by the European Society of Cardiology.
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Sympathetic deactivation by growth hormone treatment in patients with dilated cardiomyopathy

B. Capaldoa, G. Lembob, V. Rendinaa, C. Vigoritoa, R. Guidaa, A. Cuocoloa, S. Fazioa and L. Saccàaf1

a Department of Internal Medicine, Nuclear Medicine, University Federico II, Naples
b IRCCS, NEUROMED, Pozzilli, Isernia, Italy

accepted September 19, 1997

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±34ng.min–1; P<0·05). Basally, plasma aldosterone was 189±28 and 311±48pg.ml–1in the supine and upright position, respectively, and fell to 106±16 (P<0·01) and 182±29pg.ml–1(P<0·05) after growth hormone therapy. Growth hormone increased plasma volume from 3115±493ml to 3876±336ml (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.

Key Words: growth hormone • cardiomyopathy • sympathetic nervous system

f1 Correspondence: Luigi Saccà, MD, Medicina Interna, via Pansini 5, 80131—Napoli, Italy


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