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

Ventricular septal defect (VSD) closure repairs a congenital opening in the interventricular septum that causes left-to-right blood shunting. Small defects may close spontaneously in infancy; haemodynamically significant VSDs require catheter-based device occlusion or open surgical patch repair.

Closure is indicated when the pulmonary-to-systemic flow ratio (Qp:Qs) exceeds 1.5:1, causing pulmonary hypertension, right ventricular volume overload, recurrent chest infections, or failure to thrive in infants. Large unrepaired VSDs risk Eisenmenger syndrome with irreversible pulmonary hypertension.

Catheter-based closure: an Amplatzer or similar occluder device is delivered via femoral vein under combined echocardiographic and fluoroscopic guidance. Surgical repair: via median sternotomy on cardiopulmonary bypass, the defect is directly patched with Dacron or autologous pericardium under direct vision.

Device closure: discharge in 1–2 days; 6 months antiplatelet therapy (aspirin) to promote device endothelialisation. Surgical repair: 5–7 days hospital stay with standard post-sternotomy recovery. Endocarditis prophylaxis is recommended for 6 months following successful closure.

Device closure risks: device embolisation (less than 1%), complete heart block (1–3% for perimembranous defects), residual shunt, and aortic regurgitation from device position. Surgical risks include heart block requiring pacemaker, haemorrhage, infection, and rarely residual defect.

Catheter-based device closure achieves greater than 95% procedural success in anatomically suitable perimembranous and muscular VSDs. Surgical patch repair achieves near-complete closure in approximately 98% of cases. Pulmonary pressures normalise in most patients with long-term excellent prognosis.