No abstract

In a population‐based study including 35 218 infants born alive during the 15‐y period 1982–96, 360 (1%) were diagnosed as having a congenital heart defect (CHD). At a follow‐up 3–18 y after birth (median 9.5 y) 154 patients (42.8%) were spontaneously cured; of these, 142 (92.2%) had ventricular septal defects (VSDs). Forty‐two patients (11.7%) died, 22 of these (52.4%) during the neonatal period (0–28 d after birth). A total of 119 patients (33.1%) underwent therapeutic procedures (surgery, catheter interventions), 24 (20.2%) of whom died. Of the 95 children surviving therapeutic procedures, 54 (56.8%) had their defects completely repaired, while 41 (43.2%) had residual defects or cardiac sequelae, often of minor importance. In 69 children (19.2%) with persistent non‐operated defects, 43 (62.3%) had VSDs. A chromosomal disorder, syndrome or associated extracardiac malformation occurred in 72 children (20%). Conclusions: The study underlines the broad variety in severity of CHDs, with a high neonatal mortality rate as well as a high rate of spontaneous cure. It is estimated that 25% of infants born with a CHD will grow into adult age with persistent non‐operated defects, residual defects or cardiac sequelae after therapeutic procedures.

The study underlines the broad variety in severity of CHDs, with a high neonatal mortality rate as well as a high rate of spontaneous cure. It is estimated that 25% of infants born with a CHD will grow into adult age with persistent non-operated defects, residual defects or cardiac sequelae after therapeutic procedures.

In a population-based study of 35,218 infants born alive during the 15 years from 1982 to 1996, 353 (1%) were diagnosed as having a congenital heart defect, of whom 84 (24%) were diagnosed subsequent to discharge from hospital after birth (2.4/1000). Of these, 40 (48%) had a ventricular septal defect, 14 (17%) an atrial septal defect, 9 (11%) a patent arterial duct, 8 (10%) an aortic stenosis and 13 (15%) other defects. Compared with those in whom diagnosis was made before discharge, the group of patients with defects detected late had an increased prevalence of atrial septal defects, patent arterial duct and aortic stenosis, but less decreased prevalence of ventricular septal defects (p< 0.05). Median age at detection of the defects subsequent to discharge was 6 months (range 2 weeks-11 years). Seven patients (8%) presented with clinical symptoms of cardiac decompensation. The mortality rate was significantly lower in those in whom defects were detected late (1/84; 1%) as compared with those detected immediately after birth (37/269; 14%) (p < 0.05). The total rate for early detection was the same after using one clinical examination (8.2/1000) of newborns as our basic routine instead of two (7.1/1000) (p > 0.05). A substantial proportion of congenital cardiac malformations are detected after discharge from hospital after birth. Some patients with these lesions present with cardiac decompensation and are in need of medication and surgery. One clinical examination of newborns detects congenital malformations of the heart as efficient as two.

Meberg A, Otterstad JE, Frøland G, Sørland S, Nitter‐Hauge S. Increasing incidence of ventricular septal defects caused by improved detection rate. Acta Pzdiatr 1994;83:653–7. Stockholm. ISSN 0803–5253 In a population‐based study in childrcn born alive during the 10‐year period from 1982 to 1991 (n= 22 810), ventricular septal defects (VSDs) were diagnosed in 127 cases, an incidence of 5.6 per 1000. The incidence was significantly higher in the cohort of children born during the 6‐year period from 1986 to 1991 than among those born in the preceding 4‐year period, 1982–1985 (6.5 and 4.0 per 1000 respectively; p < 0.05). The increase was caused entirely by an increased detection rate of small defects in the muscular part of the interventricular septum after introducing echocardiography as a standard method for investigating suspect congenital heart defects in the neonatal period. This also explained entirely an increase in the total incidence of congenital hcart defects to 10.6 per 1000 in the last period from 8.4 per 1000 in the first, although this increase was not significant (p > 0.05). Morc children born in 1986–1991 had spontaneous closure of their VSDs (75.5%) than those born in 1982–1985 (51.5%) (p<0.05). In 69.3% of patients the VSDs closed during the first year of life. For the cohort born in 1986–1991, 84.6% of the defects located in the muscular part of the septum closed spontaneously. Small defects in the muscular part of the interventricular septum with spontaneous closure in early life may represent the tail of a normal developmental process, and not defects in the sense of malformations.