Changing medical and surgical practices alter the incidence and persistence of GF in congenital heart disease. Clinic records of 900 pediatric cardiac pts. were reviewed to determine incidence of past and present GF. Pts. with functional murmurs, primary arrhythmias, and bicuspid aortic valves were excluded. GF was defined as height, weight, or weight for height more than 2 SD below mean. 300 pts. had a history of GF. Of these, 133 had resolved GF, 21% of whom had had a probable non-cardiac cause (prematurity, neurologic abnormality, etc.). In 105 others, 41% had had closure of a ventricular septal defect(VSD), 14% repair of tetralogy, 11% of atrial septal defect(ASD), 9% of transposition (TGV). Of 167 pts. with persistent GF, 51%(86 pts.) had probable non-cardiac causes: 41 with chromosomal abnormality, 8 with rubella, 6 with major neurologic deficits. Of 81 pts. remaining, 18 had VSD's(4pre-op,2post-op,12 considered small). 14 had had tetralogy or double outlet right ventricle; all had undergone definitive repair. 18 patients had persistent GF despite palliation for complex cyanotic heart disease.Although GF is common in congenital heart disease, it may be caused by non-cardiac conditions--which preclude growth despite cardiac surgery. Excluding non-cardiac GF, poor growth persists in less than 10% of pts. after repair of VSD, ASD, coarctation and transposition. It persists in 25% of pts. after repair of conotruncal abnormalities and in 75% of pts. palliated for complex cyanotic heart disease.