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The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 9 3177-3183
Copyright © 1998 by The Endocrine Society

Original Studies

Acute Cardiovascular Effects of Insulin-Like Growth Factor I in Patients with Chronic Heart Failure1

Marc Y. Donath, Gabor Sütsch, Xia-Wei Yan, Bruno Piva, Hans-Peter Brunner, Yvonne Glatz, Jürgen Zapf, Ferenc Follath, E. Rudolf Froesch and Wolfgang Kiowski

Divisions of Endocrinology and Diabetes (M.Y.D., B.P., Y.G., J.Z., E.R.F.) and Cardiology (G.S., X.-W.Y., H.-P.B., F.F., W.K.), Department of Medicine, University Hospital, CH-8091 Zurich, Switzerland

Address all correspondence and requests for reprints to: Marc Donath, M.D., Division of Endocrinology and Diabetes, Department of Medicine, University Hospital, CH-8091 Zurich, Switzerland. E-mail: ndosam{at}usz.unizh.ch

Insulin-like growth factor I (IGF-I) enhances myofibrillar development in cardiomyocytes of rats in culture and in vivo. In addition, IGF-I has vasodilatory effects and improves cardiac function in healthy volunteers. This study was conducted to evaluate the acute hemodynamic effects of IGF-I in patients with chronic heart failure. Eight patients with chronic heart failure were randomized to receive recombinant human IGF-I (60 µg/kg) or placebo, iv, over 4 h in a cross-over, double blind study on 2 consecutive days. Electrocardiogram as well as systemic hemodynamics were continuously monitored over 7 h by flow-guided thermodilution and radial artery catheters. IGF-I was well tolerated by all patients, and no pathological changes on electrocardiogram were recorded. Compared with placebo, IGF-I increased the cardiac index by 27 ± 3.7% (±SE; P < 0.0005) and the stroke volume index by 21 ± 5.6% (P < 0.05), and decreased systemic vascular resistance by 28 ± 4.4% (P < 0.0002), right atrial pressure by 33 ± 9.0% (P < 0.003), and pulmonary artery wedge pressure by 25 ± 6.1% (P < 0.03). Mean systemic and pulmonary artery pressure as well as heart rate and pulmonary vascular resistance were not significantly influenced by IGF-I treatment. Insulin and C peptide levels were decreased by IGF-I, whereas glucose and electrolyte levels remained unchanged. Urinary levels of norepinephrine decreased significantly (P < 0.05) during IGF-I infusion. Thus, acute administration of IGF-I in patients with chronic heart failure is safe and improves cardiac performance by afterload reduction and possibly by positive inotropic effects. Further investigations to establish whether the observed acute effects of IGF-I are maintained during chronic therapy appear to be warranted.




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