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, 23 (4), 205-11

Secundum Atrial Septal Defect in Adults: A Practical Review and Recent Developments

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Secundum Atrial Septal Defect in Adults: A Practical Review and Recent Developments

Joey M Kuijpers et al. Neth Heart J.

Abstract

Secundum atrial septal defect (ASDII) is a common congenital heart defect that causes shunting of blood between the systemic and pulmonary circulations. Patients with an isolated ASDII often remain asymptomatic during childhood and adolescence. If the defect remains untreated, however, the rates of exercise intolerance, supraventricular arrhythmias, right ventricular dysfunction and pulmonary arterial hypertension (PAH) increase with patient age, and life expectancy is reduced. Transcatheter and surgical techniques both provide valid options for ASDII closure, the former being the preferred method. With the exception of those with severe and irreversible PAH, closure is beneficial to, and thus indicated in all patients with significant shunts, regardless of age and symptoms. The symptomatic and survival benefits conferred by defect closure are inversely related to patient age and the presence of PAH, supporting timely closure after diagnosis. In this paper we review the management of adult patients with an isolated ASDII, with a focus on aspects of importance to the decision regarding defect closure and medical follow-up.

Figures

Fig. 1
Fig. 1
a ECG of a 38-year-old woman with an ASDII. Mild right-axis deviation, rsR’ pattern in lead V1 reminiscent of a partial right bundle branch block. There is no further evidence of right ventricular hypertrophy. b Detail of lead aVF from an ECG of a 31-year-old man with an ASD, showing a notch on the R wave: crochetage
Fig. 2
Fig. 2
Flow diagram of the factors involved in the decision concerning defect closure in adults with an ASDII. RV right ventricle, PAP pulmonary artery pressure, PE paradoxical embolism, OPS orthodeoxia-platypnoea syndrome, PVR pulmonary vascular resistance, Qp/Qs pulmonary-to-systemic flow ratio, WU Woods unit, SVR systemic vascular resistance. *either at baseline or after pulmonary vasodilator challenge or targeted pretreatment. **unless severe left ventricular dysfunction and/or mitral insufficiency are present. ¥ class of recommendation and level of evidence
Fig. 3
Fig. 3
Transthoracic echocardiogram from a patient with an ASDII, showing clear left-to-right shunting through an open defect (small white arrow) and right-atrial enlargement. The previously implanted closure device has embolised to the left ventricle (large white arrow)
Fig. 4
Fig. 4
Synthetic ASDII closure device, the Amplatzer Septal Occluder (AGA Medical Corporation, Plymouth, MN), which was retracted after attempted implantation. The metal wires and synthetic meshwork are clearly seen. Entangled in the device is the Chiari network, which hampered device deployment

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