Atrial Septal Defect (ASD) — #1 Secundum ASD

Overview

Secundum atrial septal defect (ASD) is the most frequent type of interatrial communication and one of the most common congenital heart lesions overall.[1]PubMed The defect lies in the region of the fossa ovalis and permits a left-to-right shunt that typically increases in magnitude with age as systemic vascular resistance rises and right-sided compliance remains high.[1,2]PubMed+1

Most children with an isolated secundum ASD are asymptomatic, but chronic right-sided volume loading leads to progressive enlargement of the right atrium (RA), right ventricle (RV), and pulmonary arteries. Untreated patients have higher rates of exercise intolerance, supraventricular arrhythmias, RV dysfunction, pulmonary arterial hypertension, and ultimately reduced life expectancy compared with the general population.[1–3]PubMed+2Pure+2

Anatomy and pathophysiology

The true atrial septum is limited to the fossa ovalis and its muscular rim.[4]PubMed A secundum ASD represents a deficiency of tissue within this zone. Morphologic variants include:

• A single, well-circumscribed oval defect at the center of the fossa.
• Multiple fenestrations within a thin, aneurysmal septum.
• Large defects that extend toward the venae cavae or the atrioventricular (AV) valves.

Because left atrial (LA) pressure normally exceeds RA pressure, blood flows from left to right across the defect, increasing pulmonary blood flow (Qp) and RV preload. Systemic saturation is usually normal, but the sustained volume load produces: fixed splitting of the second heart sound, a pulmonary flow murmur, and RA/RV and main pulmonary artery dilation on imaging. Over decades, this physiology predisposes to atrial tachyarrhythmias and, in some, pulmonary vascular remodeling with pulmonary hypertension.[1–3,5]PMC+3PubMed+3Pure+3

Natural history and clinical presentation

Historical series of unrepaired ASDs show relatively low mortality in the first two decades, but a steep rise in the fourth and sixth decades due to heart failure, atrial fibrillation, pulmonary vascular disease, and stroke.[3]PubMed Adults may present with exertional dyspnea, reduced exercise tolerance, palpitations, paradoxical embolism, or incidentally detected RV enlargement on imaging.[2]Pure

The risk of pulmonary arterial hypertension increases with age and with larger defects, and is particularly important in women.[1,6]PubMed+1 Once severe, fixed pulmonary vascular disease develops, closure may no longer be safe or beneficial.

Indications and timing for closure

Current practice recommends closure of a secundum ASD when there is:

1. Hemodynamically significant left-to-right shunt—typically defined by right-sided chamber dilation and/or Qp:Qs ≥1.5:1.[2,5]Pure+1
2. Absence of severe, irreversible pulmonary vascular disease. In general, closure is favored when pulmonary vascular resistance (PVR) is <3 Wood units (WU), considered with caution when 3–5 WU, individualized when 5–8 WU, and avoided when PVR ≥8 WU or when a pulmonary vasodilator trial fails to demonstrate reversibility.[5,6]jtd.amegroups.org+1
3. No major contraindication to cardiopulmonary bypass or transcatheter intervention.

In children, elective closure is often performed in early school age to prevent long-standing RV volume overload and later arrhythmias. Earlier repair is chosen for large shunts, symptoms, or associated lesions.[1]PubMed In adults—even in middle or older age—closure generally improves symptoms and exercise capacity and reduces the incidence of new arrhythmias compared with medical management, although pre-existing atrial fibrillation may persist.[1,2]PubMed+1

Choice of closure technique

Transcatheter device closure

For most anatomically suitable secundum ASDs, transcatheter device closure has become the preferred approach worldwide. Large contemporary series and reviews suggest that approximately 80–90% of isolated secundum ASDs are amenable to percutaneous closure when adequate septal rims and venous access are present.[5,7,8]jtd.amegroups.org+2PMC+2

Key anatomical requirements include:

• Adequate rims (usually ≥5 mm) toward the superior and inferior venae cavae, coronary sinus, and AV valves.
• Absence of significant additional lesions (e.g., AV valve cleft, partial anomalous pulmonary venous return) that would mandate surgery.
• Defect size within the range of available devices.

Transcatheter closure has high procedural success and very low mortality in experienced centers, with shorter hospital stays, faster recovery, and comparable or lower complication rates than surgery.[7,9]PubMed+1 Major but rare complications include device embolization, cardiac erosion, and atrial arrhythmias, emphasizing the need for careful patient selection and long-term follow-up.[7,8]PMC+1

Health-economic analyses in adults show that, over about five years, transcatheter closure is at least as effective as surgical repair and is often cost-effective or cost-saving, largely due to shorter length of stay and fewer perioperative complications.[10]PubMed

Surgical repair

Surgical closure remains essential when:

• the defect is very large or multiple,
• septal rims are deficient (particularly posterior or inferior),
• there is associated pathology that requires repair (e.g., AV valve anomalies, partial anomalous pulmonary venous return, other congenital lesions), or
• prior device closure has failed or produced complications.

Surgery is performed under cardiopulmonary bypass through a right atriotomy. Small defects may be closed directly with sutures, but larger or multiple defects are usually closed with an autologous pericardial (or occasionally synthetic) patch to avoid distortion of the surrounding structures. Outcomes of isolated surgical closure in otherwise healthy patients are excellent, with operative mortality near zero in contemporary series.[1,5]PubMed+1

Meta-analyses comparing percutaneous and surgical closure confirm similar long-term efficacy in eliminating the shunt; transcatheter closure offers fewer early complications and a shorter hospitalization, whereas surgery provides a definitive solution without device-related issues.[7,9]PubMed+1

Surgical anatomy: triangle of Koch and conduction tissue

When surgery is chosen, meticulous attention to the AV conduction system is crucial. The AV node lies within the triangle of Koch, bordered by:

1. the tendon of Todaro
2. the septal leaflet of the tricuspid valve, and
3. the ostium of the coronary sinus.

The node is located near the apex of this triangle, just superior and anterior to the coronary sinus, close to the posteroinferior rim of many secundum ASDs.[4]PubMed When anchoring a patch along this margin, the surgeon keeps sutures:

• superficial rather than deep into the septal myocardium, and
• slightly “tricuspid-ward,” following the hinge line of the septal leaflet.

This strategy avoids direct injury to the AV node and His bundle while still providing secure fixation of the patch. Awareness of the nearby coronary sinus and the tendon of Todaro helps orient the surgeon and reinforces respect for the conduction axis.

Postoperative course and long-term outcomes

After uncomplicated closure—whether device or surgical—most patients experience:

• regression of RA and RV dilation over months to years,
• improved exercise tolerance, and
• elimination of the risk of paradoxical embolism related to the ASD.[1,2,5]PubMed+2Pure+2

Long-term surveillance focuses on:

• Residual or recurrent shunt, which is uncommon but should be excluded by echocardiography.
• Atrial arrhythmias, particularly in patients who were older at the time of closure or had long-standing volume overload; some may require ongoing rhythm or rate control and anticoagulation.[2,5]Pure+1
• Sinus node and AV conduction after surgical closure near the triangle of Koch.
• Device-related issues (erosion, thrombus, endocarditis, nickel allergy) in percutaneous cases, though these are rare and usually emerge early if at all.[7,8]PMC+1

Overall, timely closure of a hemodynamically significant secundum ASD—by device or surgery—restores near-normal life expectancy and quality of life in most patients, provided pulmonary vascular disease has not progressed to an irreversible stage.[1–3,5–7]PMC+5PubMed+5Pure+5

References

[1] Geva T, Martins JD, Wald RM. Atrial septal defects. Lancet. 2014;383(9932):1921-1932.

[2] Kuijpers JM, Mulder BJM, Bouma BJ. Secundum atrial septal defect in adults: a practical review and recent developments. Neth Heart J. 2015;23(4):205-211.

[3] Campbell M. Natural history of atrial septal defect. Br Heart J. 1970;32(6):820-826.

[4] Naqvi N, McCarthy KP, Ho SY. Anatomy of the atrial septum and interatrial communications. J Thorac Dis. 2018;10(Suppl 24):S2837-S2847.

[5] Fraisse A, Latchman M, Sharma SR, Bayburt S, Amedro P, di Salvo G, Baruteau AE. Atrial septal defect closure: indications and contra-indications. J Thorac Dis. 2018;10(Suppl 24):S2874-S2881.

[6] Jain S, Dalvi B. Atrial septal defect with pulmonary hypertension: when/how can we consider closure? J Thorac Dis. 2018;10(Suppl 24):S2890-S2898.

[7] Faccini A, Butera G. Atrial septal defect (ASD) device trans-catheter closure: limitations. J Thorac Dis. 2018;10(Suppl 24):S2923-S2930.

[8] Muroke V, Sipola P, Magga J, et al. Outcome of transcatheter atrial septal defect closure in a nationwide cohort. Ann Med. 2023;55(1):615-623.

[9] Butera G, Biondi-Zoccai G, Sangiorgi G, et al. Percutaneous versus surgical closure of secundum atrial septal defects: a systematic review and meta-analysis of currently available clinical evidence. EuroIntervention. 2011;7(3):377-385.

[10] Mylotte D, Ossei-Gerning N, O’Donnell C, et al. Long-term cost-effectiveness of transcatheter versus surgical closure of secundum atrial septal defect in adults. Int J Cardiol. 2014;172(1):109-114.