Growth hormone (GH), probably acting indirectly through locally produced insulin-like growth factor I, stimulates myocardial hypertrophy and increases myocyte contractility. In experimental models insulin-like growth factor I appears to be a key regulator of ventricular hypertrophy. Many adults with growth hormone deficiency (GHD) have reduced left ventricular mass, a lower ejection fraction, and reduced exercise tolerance. Elevated serum lipid levels, increased visceral fat, and early atheroma formation may contribute to an increased mortality rate from cardiovascular disease in these persons, but GH replacement therapy appears to correct many of these abnormalities. GH excess (acromegaly) results in cardiac hypertrophy that can progress to cardiac failure. Treatment with octreotide at least partially reverses cardiac hypertrophy and dysfunction. GH treatment may induce beneficial cardiac hypertrophy in adults without GHD who have dilated cardiomyopathy. Significant cardiac dysfunction has not been reported in children with GHD who are treated with GH, nor have adverse cardiac effects been reported with GH in short children without GHD, including those with Turner syndrome. We now have extensive experience with the therapeutic use of GH in children with cardiac structural abnormalities (e.g., Turner and Noonan syndromes, congenital heart disease), and such use appears to be safe. Furthermore, cardiac complications of GH in children without cardiac disease are rare. Continued observation to ensure that GH therapy has no long-term effects on cardiac anatomy or function in children is necessary.