Treatment of end-stage cardiac failure with growth hormone

Abstract

Human growth hormone (HGH) improves haemodynamics, myocardial energy metabolism, and clinical status in patients with moderate congestive heart failure. In addition, HGH reverses cachexia in patients with AIDS, malignancy, liver disease, and congestive cardiac failure, though this last patient was HGH-deficient due to hypopituitarism. It seems likely that the combined anabolic and cardiac effects of HGH would benefit patients with severe heart failure and cardiac cachexia. We report two patients with severe cardiac cachexia as a result of ischaemic heart disease who were treated with recombinant HGH (Somatropin, Serono, Australia). The first patient, a 59-year-old man, had had heart failure for more than 8 months and required intermittent support with inotropes despite digoxin, diuretics, and an angiotensin-converting enzyme (ACE) inhibitor. Before HGH treatment, he had generalised cachexia, was New York Heart Association class IV, wheel-chair bound, weighed 57·75 kg, and had body-mass index of 19·2 kg/m. The second patient, a 52-year-old man, developed severe heart failure subsequent to myocardial infarction, which persisted despite coronary artery bypass surgery. After 4 months in heart failure the patient was stabilised with maximally tolerated doses of digoxin, diuretics, an ACE inhibitor, and vasodilators. This patient also had generalised cachexia, was New York Heart Association class IV, weighed 55 kg, and had a body-mass index of 22 kg/m. The first patient received 14 units of recombinant HGH subcutaneously per day and was reassessed after 7 days, whereas the second patient received 10 units per day and was reassessed after 6 weeks. Measures from patient 2 were also collected 3 weeks after cessation of HGH. Body weight increased in both patients, along with the sum of 8 skinfolds and the sum of 9 muscle girths (table), suggesting that the weight gain was attributable to increased muscle bulk and subcutaneous adipose tissue. Patient 1 demonstrated improved grip strength and exercise duration during a maximal exercise test, whereas maximal strength measures on a variety of compound exercises, VO 2 max, and exercise duration improved substantially in patient 2. These data suggest improved functional capacity and exercise tolerance, which were maintained or continued to improve 3 weeks after cessation of therapy in patient 2. In addition, maximum heart rate during exercise increased in both patients, suggesting improved myocardial function which was confirmed in patient 2 by echocardiography, right-heart catheterisation, and gated blood pool scan. Following HGH therapy, patient 1 was successfully bridged to transplantation and patient 2 improved to such a degree that he was delisted. The results of these studies suggest that HGH administration to patients with severe heart failure and cardiac cachexia has a beneficial effect which may be sustained after stopping HGH. However, the results of these case studies must be interpreted with caution, since spontaneous improvement in functional and haemodynamic capacity cannot be ruled out. Nonetheless, we suggest that the present results provide support for a randomised placebo-controlled study of HGH in patients with severe heart failure.