Atrial septal defects are relatively common congential cardiac malformations, but are difficult to diagnose prenatally due to problems differentiating the normal patent foramen ovale from an anatomic defect of the septum.
Many cases close spontaneously within 2 years of life, while persistence of a large defect, especially with evidence of right ventricular overload, is an indication for elective closure.
Open surgical approaches to closure have been replaced in most cases with minimally invasive transcatheter occlusion techniques.
While the medium-term outcome of such transcatheter occlusion techniques appears favorable, it will likely be some time before sufficient data are available to confirm long-term safety and efficacy.
Atrial septal defect (ASD) refers to a congenital malformation in the development of the interatrial septum. In embryonic life, the interatrial septum begins as a septum primum, growing from the atrial walls to the endocardial cushions, which contains a temporary opening known as the foramen primum (Romero et al., 1988). Subsequently, a septum secundum grows on the right side of the septum primum and contains a normal opening known as the foramen ovale. The lower part of the septum primum forms a flap valve for this foramen ovale. Soon after birth, increased left atrial pressure closes this flap, normally resulting in complete closure of the foramen ovale within 2 years of life (Kerut et al., 2006).
Three different types of ASDs are possible, depending on the location within the heart (Romero et al., 1988). An inlet ASD is located near the entrance of the superior vena cava; a secundum ASD occurs in the body of the interatrial septum; a primum or outlet ASD is located near the atrioventricular junction and usually behaves similarly to an AV canal defect (see Chapter 45). Secundum ASDs typically occur because of absence of the foramen ovale flap valve. ASDs usually cause no hemodynamic effects in utero because of the normal right-to-left shunting of blood across the patent foramen ovale. If an ASD persists after birth it may allow for a left-to-right shunt, which can result in congestive heart failure or pulmonary hypertension.
Because of the difficulties in differentiating ASDs from asymptomatic patency of the foramen ovale, the precise incidence of ASD in neonatal life is difficult to establish. A patent foramen ovale may be present in up to 30% of normal adults (Kerut et al., 2006). ASDs comprise 7.5% of all congenital cardiac malformations (Ferencz et al., 1987). In one population series, the incidence of ASD was 6 in 10,000 total births (Mitchell et al., 1971).
Prenatal sonographic diagnosis of ASD is problematic because the differentiation between a normal patent foramen ovale and true ASD may be difficult. The foramen ovale normally increases in size linearly with advancing ...