General · EdgepediaSeptember 17, 20267 min read

Atrial septal defect

An atrial septal defect (ASD) is an opening in the septum, the tissue wall dividing the heart's two upper chambers, known as the atria. This opening lets oxygen-rich blood move from the left atrium into the right atrium, the chamber that normally holds oxygen-poor blood.¹ The defect is present at birth, and the extra blood it sends to the right side of the heart and to the lungs determines most of its clinical course.¹

Key fact	Detail
What it is	A hole in the interatrial septum causing a left-to-right shunt and volume overload of the right atrium and right ventricle²
Frequency	About 6 to 10% of congenital heart disease cases; secundum ASD accounts for more than 90% of cases seen in adults²^•³
Main types	Ostium secundum (center of the septum), sinus venosus (posterior, near the vena cavae), and ostium primum (anteroinferior, a form of atrioventricular septal defect)²
Symptoms	Most children are asymptomatic; adults may develop exercise intolerance, dyspnea, fatigue, and atrial arrhythmias²
Physical sign	A grade 2 to 3/6 midsystolic murmur with a widely split, fixed second heart sound at the upper left sternal border²
Treatment	Observation for small defects; transcatheter device closure (possible in 85 to 90% of defects) or surgical repair for larger ones²
Long-term risk if unrepaired	Pulmonary hypertension, heart failure, paradoxical emboli, and atrial arrhythmias after age 20²

How the defect affects circulation

Every fetus has a normal opening between the atria, the foramen ovale, which lets blood bypass the lungs before birth; it usually closes or becomes very small within weeks or months after birth.¹ When the opening is larger than normal and fails to close, an ASD results; in most children the cause is unknown, though genetic factors sometimes play a role.¹

Because left atrial pressure exceeds right atrial pressure, blood shunts left to right, increasing volume in the right atrium and right ventricle and raising pulmonary blood flow.² Intracardiac pressures generally remain normal throughout childhood.² If a large shunt persists unrepaired, it can lead by the 30s or 40s to pulmonary artery hypertension, elevated pulmonary vascular resistance, and right ventricular hypertrophy; ultimately the shunt may reverse, producing a bidirectional shunt with cyanosis known as Eisenmenger syndrome, most commonly after age 40.² The atrial shunt can also allow venous microemboli to cross into the systemic circulation (paradoxical embolization), causing stroke or other arterial occlusion.²

Types and associated defects

ASDs are classified by location in the septum. An ostium secundum defect lies in the fossa ovalis, the central part of the septum, and is the type most often suitable for device closure. A sinus venosus defect sits posteriorly near the superior or inferior vena cava and is frequently associated with anomalous return of right pulmonary veins; an ostium primum defect occupies the anteroinferior septum and is a form of atrioventricular septal defect.² An ASD can also occur alone or with other heart defects such as anomalous pulmonary veins, pulmonary stenosis, tetralogy of Fallot, and ventricular septal defect.⁴ Most cases are isolated and sporadic, but some occur in genetic syndromes, for example Holt-Oram syndrome, and the combination of ASD with atrioventricular conduction disturbance may be associated with a mutation in the NKX2-5 homeobox gene.²

Symptoms and diagnosis

Most patients with small or moderate defects are asymptomatic, and even large ASDs may not cause symptoms in young children.² Larger shunts may cause slow weight gain in early childhood and, in older patients, exercise intolerance, exertional dyspnea, fatigue, or palpitations.² On examination the typical findings are a soft midsystolic murmur and a widely split, fixed second heart sound, though these may be absent in infants even with a large defect.²

Echocardiography with color flow and Doppler studies confirms the diagnosis, defines the defect's location and size, and assesses right-sided volume overload; chest x-ray and ECG provide supporting evidence.² In adults with an unrepaired ASD, the 2025 ACC/AHA guideline recommends cardiac MRI, transesophageal echocardiography, or cardiac CT to define defect size, morphology, rim anatomy, and pulmonary venous connections, and recommends assessing every adult with an unrepaired ASD for pulmonary arterial hypertension (PAH) to guide therapy and determine suitability for repair.⁵

Natural history and when to close

Small defects often close on their own: most defects under 3 mm that are centrally located close spontaneously, and many between 3 mm and 8 mm close by age 3 years; these probably represent stretched patent foramina ovalia rather than true secundum ASDs.² Ostium primum and sinus venosus defects do not close spontaneously.² No medication makes an ASD smaller or close faster.¹

Moderate-to-large defects, meaning those with right ventricular volume overload on echocardiography, should be closed, typically between ages 2 and 6 years.² In adults, the 2025 guideline recommends closure when there is a significant left-to-right shunt (Qp:Qs ≥1.5, the ratio of pulmonary to systemic blood flow) with right ventricular dilation, in the absence of PAH (pulmonary vascular resistance ≤2 Wood units) or significant left ventricular disease.⁵ When PAH is present with PVR of 5 to 8 Wood units, closure can be considered beneficial only if targeted pulmonary hypertension therapy brings PVR below 5 Wood units.⁵ In established Eisenmenger physiology, closure should not be performed, because it increases morbidity and mortality.⁵ Closure is also indicated in adults with known or suspected paradoxical embolism regardless of defect size, in the absence of significant PAH or left ventricular disease.⁶

Closure methods and outcomes

Surgical closure was the only interventional treatment from 1952 until percutaneous closure was introduced by King and Mills in the mid-1970s; percutaneous closure is now the treatment of choice for most secundum ASDs.⁷ Transcatheter closure with commercial devices is possible in 85 to 90% of defects when anatomic features are favorable, such as adequate rims of septal tissue and safe distance from the aortic root, pulmonary veins, and tricuspid annulus; sinus venosus and ostium primum defects are not amenable to device closure and require surgery.²

Comparative evidence. A 2026 meta-analysis of 36 observational studies found a pooled procedural success rate of 95% for both approaches combined; in adults, transcatheter success was 97% versus 98% for surgery, and transcatheter closure produced shorter hospitalization (mean difference −3.86 days) and fewer major complications (risk ratio 0.58).⁸ A meta-analysis of six studies comparing minimally invasive surgery with device closure found higher treatment efficacy for surgery (99.8% versus 97.3%) but more complications (16.2% versus 7.1%) and longer hospital stays (5.6 versus 1.3 days), with more residual shunts after the transcatheter approach (3.9% versus 0.95%).⁹ Observational data also show percutaneous closure with lower rates of early complications, atrial flutter or fibrillation, thromboembolism, stroke, and all-cause mortality over 4-year follow-up.⁷ Among transcatheter devices, a network meta-analysis found no differences in device embolization or clinical outcomes between devices, though follow-up residual shunt was higher with the HELEX septal occluder than the AMPLATZER septal occluder (odds ratio 2.92).¹⁰

When repaired during childhood, perioperative mortality approaches zero and long-term survival approaches that of the general population.² Even when the defect is first diagnosed in adulthood, closure of large defects is beneficial.¹ After closure, most patients need no long-term medication beyond about six months, endocarditis precautions are not needed beyond six months after repair, and the long-term outlook is described as excellent.¹

History

The first intracardiac surgical procedure was performed by F. John Lewis in 1952, repairing an ASD using moderate hypothermia and caval inflow occlusion.¹¹ In 1953 John Gibbon Jr. performed the first successful application of the heart-lung machine, repairing an ASD in a young woman, an operation that marked the birth of open-heart surgery.¹¹ The first successful transcatheter ASD closure was performed by Terry Dean King in 1975, part of the earliest wave of transcatheter procedures that also included Rashkind's balloon atrial septostomy in 1966.¹¹^•¹² Four decades of device development in shape, material, and implantation technique have since made percutaneous closure the current treatment of choice in most secundum ASD cases.⁷

References

Topic: Encyclopedia › Life and health › Human health and medicine › Diseases and injuries › Cardiovascular and blood conditions › Heart conditions › Congenital and genetic heart conditions › Septal, shunt, and simple obstructive lesions › Atrial septal defects

Initially written Sep 17, 2026 · Reviewed: Sep 30, 2026; Oct 21, 2026 · Edited: Sep 30, 2026; Oct 21, 2026 · Last review: Oct 21, 2026

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