Background Cardiac hypertrophy is a physiologic response thatallows the heart to adapt to an excess hemodynamic load. Wehypothesized that inducing cardiac hypertrophy with recombinanthuman growth hormone might be an effective approach to the treatmentof idiopathic dilated cardiomyopathy, a condition in which compensatorycardiac hypertrophy is believed to be deficient.
Methods Seven patients with idiopathic dilated cardiomyopathyand moderate-to-severe heart failure were studied at base line,after three months of therapy with human growth hormone, andthree months after the discontinuation of growth hormone. Standardtherapy for heart failure was continued throughout the study.Cardiac function was evaluated with Doppler echocardiography,right-heart catheterization, and exercise testing.
Results When administered at a dose of 14 IU per week, growthhormone doubled the serum concentrations of insulin-like growthfactor I. Growth hormone increased left-ventricular-wall thicknessand reduced chamber size significantly. Consequently, end-systolicwall stress (a function of both wall thickness and chamber size)fell markedly (from a mean [±SE] of 144±11 to85±8 dyn per square centimeter, P<0.001). Growth hormoneimproved cardiac output, particularly during exercise (from7.4±0.7 to 9.7±0.9 liters per minute, P = 0.003),and enhanced ventricular work, despite reductions in myocardialoxygen consumption (from 56±6 to 39±5 ml per minute,P = 0.005) and energy production (from 1014±100 to 701±80J per minute, P = 0.002). Thus, ventricular mechanical efficiencyrose from 9±2 to 21±5 percent (P = 0.006). Growthhormone also improved clinical symptoms, exercise capacity,and the patients' quality of life. The changes in cardiac sizeand shape, systolic function, and exercise tolerance were partiallyreversed three months after growth hormone was discontinued.
Conclusions Recombinant human growth hormone administered forthree months to patients with idiopathic dilated cardiomyopathyincreased myocardial mass and reduced the size of the left ventricularchamber, resulting in improvement in hemodynamics, myocardialenergy metabolism, and clinical status.
Source Information
From the Department of Internal Medicine, University Federico II, Naples, Italy.
Address reprint requests to Dr. Saccà at Medicina Interna, Via Pansini 5, 80131-Naples, Italy.
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