Ventricular Septal Defect (VSD) Closure — Procedure Guide, Recovery & Risks | MyMedicPlus

Ventricular septal defect (VSD) closure is a procedure to repair a congenital or acquired opening in the interventricular septum — the muscular and fibrous wall dividing the right and left ventricles — which causes an abnormal left-to-right shunt of oxygenated blood back to the pulmonary circulation, creating volume overload of the right heart and pulmonary vasculature. VSDs are the most common congenital heart defect, occurring in approximately 3.5 per 1,000 live births, and are classified by anatomical location: perimembranous VSDs (70-80% of cases, adjacent to the aortic valve in the membranous septum), muscular VSDs (5-20%, within the muscular septum, may be multiple), outlet/supracristal VSDs (5-7%, beneath the pulmonary valve), and inlet/atrioventricular canal-type VSDs (5-8%). The haemodynamic significance of a VSD depends on its size and the pulmonary-to-systemic resistance ratio; small VSDs (Qp:Qs below 1.5:1) are haemodynamically insignificant and may close spontaneously during childhood. Large VSDs cause significant left-to-right shunting (Qp:Qs above 2:1), resulting in pulmonary hypertension, biventricular volume overload, left ventricular dilatation, recurrent lower respiratory tract infections, failure to thrive in infants, and — if untreated — irreversible pulmonary vascular disease (Eisenmenger syndrome) in which the shunt reverses to right-to-left, causing chronic cyanosis and precluding further repair. Transcatheter device closure and open surgical repair are the two principal treatment modalities.

VSD closure is indicated when the pulmonary-to-systemic blood flow ratio (Qp:Qs) exceeds 1.5:1, indicating that more than half as much additional blood is flowing through the lungs as through the body — placing significant volume overload on the right ventricle and pulmonary arteries. Specific indications include infants with large VSDs causing failure to thrive, recurrent lower respiratory tract infections, cardiac failure, or severe pulmonary hypertension; children with moderate VSDs and right ventricular volume overload on echocardiography; and perimembranous or muscular VSDs of haemodynamic significance in adults. Urgent closure is required in post-infarction VSDs (acute VSD from myocardial infarction causing acute left-to-right shunt and cardiogenic shock). VSDs in the perimembranous position adjacent to the aortic valve may also require closure to prevent progressive aortic regurgitation even when the shunt is modest. Echocardiography, cardiac catheterisation, and CT angiography assess anatomy and haemodynamic significance to guide the optimal intervention.

Transcatheter device closure is performed in a cardiac catheterisation laboratory under general anaesthesia with continuous TOE (transoesophageal echocardiography) and fluoroscopic guidance. Femoral venous access is established; a long sheath is advanced across the VSD from right to left ventricle under fluoroscopy and echocardiographic guidance. A self-expanding double-disc nitinol mesh device (Amplatzer Muscular VSD Occluder, Figulla Flex II, or PFM Nit-Occlud) of appropriate diameter is loaded into the delivery system, advanced through the sheath, and deployed across the VSD: the left ventricular disc is expanded in the left ventricular cavity first, the device is then pulled back to seat against the left side of the septum, and the right ventricular disc is opened against the right side. TOE confirms correct positioning, absence of significant residual shunt, and preserved aortic valve function before the device is released from the cable. Open surgical VSD repair is performed via median sternotomy under cardiopulmonary bypass with cardiac arrest using cardioplegia. The right atrium is opened for perimembranous and inlet VSDs (via the tricuspid valve to access the membranous septum); the right ventricle is opened for outlet and muscular VSDs. Small VSDs are closed with interrupted pledgeted 4-0 Prolene sutures through the defect edges directly. Larger VSDs require a Dacron or pericardial patch sutured circumferentially around the defect rim, ensuring no sutures are placed through the conduction tissue at the inferior border of perimembranous VSDs (risk of complete heart block). Total bypass time for isolated VSD repair is 30-60 minutes.

Transcatheter device closure achieves greater than 95% procedural success in haemodynamically suitable muscular and perimembranous VSDs, eliminating the left-to-right shunt and restoring normal haemodynamics without the morbidity of open-heart surgery, cardiopulmonary bypass, or sternotomy. Surgical patch repair achieves near-complete closure (less than 2% residual shunt) in approximately 98% of cases and remains the definitive approach for all anatomically unsuitable VSDs and post-infarction defects. Following successful closure of a significant VSD, right ventricular volume overload resolves over weeks to months, pulmonary artery pressures normalise in most patients without established irreversible pulmonary vascular disease, exercise tolerance improves markedly, and risk of arrhythmia from chronic right heart dilation is substantially reduced. Long-term prognosis after timely VSD closure is excellent, with life expectancy approaching that of the general population.

Transcatheter device closure of perimembranous and muscular VSDs carries procedure success rates of greater than 95% in experienced interventional centres, with low major complication rates. Device embolisation occurs in under 1% of procedures and requires urgent surgical retrieval. Complete atrioventricular block (CAVB) — requiring permanent pacemaker implantation — complicates approximately 1-3% of perimembranous VSD device closures, arising from pressure necrosis or inflammation of the conduction tissue by the device disc; the risk is influenced by defect proximity to the bundle of His and device oversizing. Aortic regurgitation from device impingement on the right coronary cusp of the aortic valve occurs in 1-3% of cases and may be progressive, occasionally requiring device retrieval and surgical repair. Residual shunt through or around the device occurs in 5-15% at 24 hours, but the majority (80-85%) close spontaneously by 6 months as tissue grows through the mesh. Open surgical repair carries perioperative risks including complete heart block (3-5% for perimembranous VSDs), residual VSD patch leak requiring re-exploration (1-2%), and standard open cardiac surgery risks including stroke, infection, and bleeding. Pulmonary hypertensive crisis in the early post-operative period is managed with inhaled nitric oxide.

After transcatheter device closure, patients are typically discharged within 1–2 days following overnight monitoring for arrhythmia and haemodynamic stability. Low-dose aspirin (antiplatelet therapy, 3–5 mg/kg/day) is prescribed for 6 months to prevent thrombus formation on the device surface while it becomes covered with endothelium. Infective endocarditis antibiotic prophylaxis is recommended for 6 months following complete device coverage. Strenuous exercise and contact sports are restricted for 6 weeks. A follow-up echocardiogram at 1 and 6 months documents device position, residual shunt, and any effect on adjacent cardiac structures. Following surgical patch repair, hospital stay is 5–7 days including post-sternotomy monitoring. Full sternal healing takes 6–8 weeks; driving and heavy lifting are restricted during this period. Long-term cardiac follow-up with echocardiography at 1–2 year intervals is recommended for all closed VSDs.