Idiopathic dilated cardiomyopathy is characterized by progressive dilatation of the left and sometimes the right ventricle with compensatory wall thickening [1]. No definitive therapy is available for this disease. The observation that growth hormone (GH) is a physiologic regulator of myocardial growth and performance [2] provided a rationale for the use of GH to treat idiopathic dilated cardiomyopathy.

The first patient was a man with idiopathic dilated cardiomyopathy in whom cardiac transplantation was contraindicated because of disseminated prostate cancer.

The second patient was a 68-year-old man admitted to the hospital with heart failure. Echocardiography revealed dilated cardiomyopathy. The results of coronary angiography were normal, and the hemodynamic data are shown in Table 1. Endomyocardial biopsy showed no myocarditis, and results of serologic tests for viral infection and blood cultures were negative. The patient presented with idiopathic dilated cardiomyopathy. Three years earlier, he had received a diagnosis of a prostate neoplasm; cardiac transplantation was contraindicated because of prostate cancer.

Despite furosemide and warfarin therapy, cardiac function deteriorated over 4 years. Treatment was attempted with recombinant GH (16 units daily, subcutaneously, at 23 pm). Within days, the peripheral perfusion increased and dyspnea was alleviated. Recombinant GH treatment was discontinued after a year. After this year of treatment, the patient had improved hemodynamically, echocardiographically, and clinically. The patient remains asymptomatic 3 years after the end of the treatment.

Growth hormone activates cardiac cell growth without changing collagen content or capillary density [3]. By reducing energy expenditure, GH may improve the thermodynamic efficiency of cardiac contractility. Our patient's catheterization and echocardiographic data show an increase in myocardial mass and improved cardiac function. Fazio and colleagues [4] recently showed that the improvement in cardiac variables tended to wane 3 months after the discontinuation of GH therapy. In our patient, the improvement remains after 3 years. Our longer duration of the treatment (12 months in our study compared with 3 months in the study by Fazio and colleagues) and our higher dose (16 compared with 14 units per day) may have contributed to the observed differences between our case and the report of Fazio and colleagues. Further investigation of GH in the treatment of dilated cardiomyopathy is warranted.