Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp lthough primary cardiac hypertrophy can result from genetic abnormalities, most cases in the clinical situation are secondary to pressure or volume overload, to mutations of sarcomere proteins, or to loss of contractile mass because of a prior infarction. 1 When cardiac hypertrophy persists for a long time without intensive care, the resulting deterioration in diastolic function often leads to congestive heart failure. 2 Great advances in surgical techniques and medical management of congenital heart diseases have dramatically improved the survival of affected patients over the past decades. However, with many patients with congenital heart disease now surviving until adulthood, right ventricular hypertrophy (RVH) has drawn much attention. 3 It is well known that several congenital heart diseases often cause RVH, even though various surgical or interventional corrections have been developed. Examples are pressure overload RVH caused by right ventricular (RV) outflow tract obstruction after total correction of tetralogy of Fallot, pulmonary stenosis, the atrial switch operation for transposition of the great arteries, and congenitally corrected transposition of the great arteries, and systemic RVH after the Fontan operation. Other conditions are volume overload RVH caused by atrial septal defect, tricuspid regurgitation, and pulmonary regurgitation. 3,4 Development of RVH should be carefully monitored and both medical prevention and treatment should be considered.Currently, afterload-reducing agents, β-adrenergic blockers, inotropics, and diuretics are used in the treatment of cardiac dysfunction, including cardiac hypertrophy. It is widely accepted that several angiotensin-converting enzyme (ACE) inhibitors have clinical benefits in the treatment of left ventricular hypertrophy (LVH) 5-7 but there is much debate over the ideal medical management of RVH 4 because the primary