Congenital left ventricular pressure overload is associated with "excessive" hypertrophy that leads to subnormal afterload (wall stress), permitting enhanced ventricular ejection performance. Whether congenital right ventricular pressure overload is associated with a similar phenomenon is uncertain. It is also unknown whether supranormal ejection performance affects only the overloaded ventricle or is a general process affecting both ventricles. Conflicting data exist about whether the hypertrophic process associated with pressure overload is induced primarily by local loading conditions or by neuroendocrine influences. If the former postulate is true, the hypertrophic response should be confined to the overloaded ventricle; if the latter is true, one might predict that both ventricles would be affected by a less specific response to circulating catecholamines. To help resolve these issues, both right and left ventricular performance was examined in seven patients with isolated congenital pulmonary stenosis (average pulmonary pressure gradient 78 ± 13 mm Hg), six patients with isolated congenital aortic stenosis (average gradient 80 ± 10 mm Hg) and six normal subjects. Right ventricular ejection fraction was increased in patients with pulmonary stenosis (61 ± 2%) compared with the value in normal subjects (53 ± 2%, p < 0.01) and in patients with aortic stenosis (50 ± 3%, p = 0.007). Left ventricular ejection fraction was increased in patients with congenital aortic stenosis (84 ±4%) compared with the value in normal subjects (70 ± 4%, p < 0.01) and in patients with congenital pulmonary stenosis (65 ± 2%, p < 0.002). Thus, patients with congenital right ventricular pressure overload had enhanced right ventricular ejection performance with normal left ventricular ejection performance in contrast to those with congenital left ventricular pressure overload, who had enhanced left ventricular performance but normal right ventricular performance. These findings are consistent with the hypothesis that local loading is a key determinant of the congenital hypertrophic response.