18.2 Ventricular Septal Defect Closure

Ventricular Septal Defect Closure

ARRT Cardiac-Interventional Procedures 2.B.2 is ventricular septal defect (VSD) closure. Congenital holes and post-myocardial-infarction ventricular septal rupture (VSR) share a name and a device family; they do not share timing, tissue quality, or mortality. The Focus of Questions still applies: anatomy and pathophysiology, indications, contraindications, imaging, access, ultrasound, equipment, complications, and closure. This is a hybrid-OR case when conversion is a realistic plan (14.1).

Quick Answer: Congenital VSDs (especially muscular) are the usual percutaneous targets. Perimembranous defects sit next to the conduction system (AV block) and the aortic cusp. Post-MI VSD is a surgical emergency historically; percutaneous closure is for selected patients who cannot go to surgery or who have a residual leak after a patch. An arterial-venous rail is often built. Hemolysis follows a residual high-velocity jet. Staff a hybrid OR.

Anatomy and pathophysiology

The interventricular septum has a membranous portion (thin, superior, under the aortic and tricuspid valves, adjacent to the AV node and His bundle) and a large muscular portion.

Congenital VSD types (teaching):

• Perimembranous — most common congenital VSD; borders the membranous septum. Device rims sit near the conduction system and often near an aortic cusp.
• Muscular — completely bounded by muscle; mid-muscular, apical, or anterior. Better device real estate, farther from the His bundle and aortic valve.
• Inlet (AV canal) — next to the AV valves; usually surgical.
• Outlet / supracristal — under the great-artery valves; aortic cusp prolapse and AR; usually surgical.

A restrictive VSD is a high-pressure left-to-right jet (LV to RV). A large unrestrictive defect equalizes ventricular pressures and, over time, can produce pulmonary vascular disease. Cath-lab teaching still uses an oxygen step-up from RA to RV to locate a ventricular-level shunt (chapter 11).

Post-MI VSR is necrosis, not a congenital hole. Anterior rupture after a wraparound LAD infarct tends to be apical muscular. Inferior rupture after an RCA (or dominant LCx) infarct is basal, nearer the crux, and is worse surgically and percutaneously. Tissue at the edge is friable in the first days. That is why a device that holds in a chronic muscular VSD can embolize or tear in an acute infarct septum. Medical therapy alone has catastrophic mortality; the exam point is urgency, not an unpublished ARRT percentage.

Indications, contraindications, and timing

Congenital indications (teaching): a muscular (and selected perimembranous) VSD with a significant shunt, failure to thrive, RV volume/pressure overload, or residual defect after surgery, when rims will hold a device and valves are not committed to the defect.

Post-MI indications (teaching): historically a surgical emergency — patch repair, often with CABG, because waiting is not a strategy. Percutaneous closure is selected: prohibitive surgical risk, residual leak after a patch, or a more chronic post-infarct defect once the septum has scarred. It is not “always percutaneous first.”

Timing. Congenital elective cases wait for adequate weight and rims. Post-MI VSR classically appears about 3–7 days after transmural infarction (range teaching 1–14 days — not an unpublished ARRT cutoff). Acute necrotic rims argue for surgery or mechanical support as a bridge; delayed percutaneous closure is more realistic if the patient survives to a firmer septum. Do not treat day-2 VSR as a routine secundum-ASD device afternoon.

Contraindications: inlet/outlet defects that involve valves, active endocarditis, no landing zone, a defect so large the largest occluder will not sandwich, and a perimembranous defect whose device will pin the His bundle or aortic cusp when surgery is the better option. Inability to reverse or manage hemolysis if a residual jet is likely is a practical stop.

Imaging, access, ultrasound, and the AV rail

Imaging. TEE is the usual implant echo; ICE can help in adults. Left ventriculography (LAO cranial teaching view) profiles many VSDs. Biplane helps congenital work (14.1). Fluoro plus echo together — neither alone sizes a post-MI serpiginous rupture.

Access. Often both femoral arterial and femoral venous. A wire may pass LV → VSD → RV → PA or RA, then a snare from the venous side captures it, creating an arteriovenous rail (AV loop). The device delivery sheath then tracks from the vein (typically) across the defect while the rail keeps the path. Reverse rails exist. This is not a single 6 Fr radial PCI and it is not the PFO “cross the tunnel” story.

Ultrasound. Vascular ultrasound for the large venous and arterial sticks. TEE/ICE for rims, residual color, aortic regurgitation, and effusion. A new high-velocity residual jet is a hemolysis warning, not a “small leak that will remodel like a PFO.”

Equipment. Muscular VSD occluders (Amplatzer-class muscular teaching) have a longer waist for a thicker septum. Perimembranous-specific or ASD-like disks are used only when the operator accepts conduction and cusp risk. Post-MI defects may need oversized or dedicated post-infarct devices because the hole is irregular. Have a snare, surgical backup, and a hybrid OR.

Complications: AV block, aortic cusp, hemolysis, embolization

AV block is the perimembranous hallmark: the conduction axis runs at the posteroinferior margin. Heart block can be immediate or delayed (edema, device mass). Temporary pacing capability belongs in the room; some patients need a permanent pacemaker. Muscular apical defects are not immune to arrhythmia, but they are not the classic His-bundle lecture.

Aortic cusp proximity: a disk that crowds a right or non-coronary cusp produces aortic regurgitation. New AR after a perimembranous implant is a device problem, not incidental.

Hemolysis: a residual high-velocity jet through a small residual channel or around a malpositioned device shears red cells. Dark urine, falling hematocrit, rising LDH, and a noisy residual Doppler jet. Management is to close the residual leak (another device, surgery) or support until a tiny jet endothelializes — you do not ignore cola-colored urine after VSD closure.

Device embolization and residual shunt are the other two. Friable post-MI tissue embolizes more. Residual large shunt fails the indication. Tamponade from rail trauma or sheath perforation is an echo-now problem. Vascular injury from large arterial and venous sheaths is expected-risk, not a surprise.

Closure. Arterial large-bore preclose or surgical cutdown as planned; venous figure-of-8 or device. Hybrid conversion is sternotomy without moving the patient (14.1) if the device embolizes into a valve or the VSR cannot be sealed.

Table: etiology / timing / hallmark risk

Worked case

Day-5 anterior STEMI, new harsh holosystolic murmur, oxygen step-up RA to RV, shock. Historically this is a surgical emergency. If the heart team declares prohibitive operative risk, a hybrid OR percutaneous attempt with an AV rail and a muscular/post-infarct occluder is the selected path — not a table-suite PFO afternoon. If instead a teenager has an apical muscular VSD with adequate rims, femoral venous-arterial rail, TEE, and a muscular occluder are appropriate, and the conduction lecture is milder than a perimembranous case. New high-velocity residual color plus tea-colored urine the next day is hemolysis: residual jet, not a UTI. A perimembranous implant followed by a wide QRS and pauses is AV block — pace, do not assume the device “settled.”

Exam traps

• Treating post-MI VSR as an elective congenital device.
• Device-closing a primum-equivalent inlet VSD.
• Ignoring AV block risk on a perimembranous defect.
• Calling a residual high-velocity leak “trivial” when hemolysis is the named complication.
• Staffing post-MI VSD in a room that cannot convert to sternotomy.
• Forgetting the AV rail.