Hybrid Approach as a Salvage Strategy for Post–Myocardial Infarction Ventricular Septal Defect

Abstract

Background

Post–myocardial infarction ventricular septal defect (post-MI VSD) is a life-threatening complication of acute myocardial infarction, associated with high mortality if untreated. Advances in surgical repair and percutaneous closure have reduced its incidence, but post-MI VSD remains challenging to manage.

Case Summary

A 67-year-old man with an evolved inferior ST-segment elevation myocardial infarction developed cardiogenic shock. After the diagnosis of post-MI VSD, an initial surgical repair was performed. However, residual ventricular septal defect was detected, likely because of patch dehiscence, along with an additional serpiginous septal defect. After discussion within the heart team, a decision was made to proceed with percutaneous closure of the defect using an Amplatzer vascular plug II (Abbott), achieving an excellent clinical outcome.

Discussion

A hybrid approach combining surgery and percutaneous intervention for post-MI VSD demonstrates successful outcomes, especially when reoperation poses high risk. This approach could improve management and survival in complex post-MI VSD cases.

Graphical Abstract

History of Presentation

A 67-year-old man was transferred to our center with cardiogenic shock (Society for Cardiovascular Angiography and Interventions stage B) after an inferior ST-segment elevation myocardial infarction. Electrocardiogram showed ST-segment elevation in the inferior leads. Primary percutaneous coronary intervention was performed for acute mid–right coronary artery occlusion, treated with the implantation of a 2.75/28-mm XIENCE Skypoint drug-eluting stent (Abbott). A critical distal left anterior descending artery stenosis was also detected.

Take-Home Message

• •A hybrid approach for treating post-MI VSD offers successful outcomes and has the potential to improve survival, especially when used as a salvage strategy after failed surgical repair.

Past Medical History

The patient had hypertension, with no other known medical conditions.

Differential Diagnosis

Given the hemodynamic instability after ST-segment elevation myocardial infarction, the differential diagnosis included mechanical complications: ventricular septal defect (VSD), papillary muscle rupture, free wall rupture, left ventricular (LV) aneurysm, and malignant arrhythmias.

Investigations

Bedside transthoracic echocardiography (TTE) revealed a pseudoaneurysm in the mid-basal inferior wall, with a neck measuring approximately 2 cm, along with a basal–mid-interventricular septal defect and a serpiginous tract extending toward the right ventricle (RV) (Figure 1). Despite initiation of inotropes and intra-aortic balloon pump (IABP) support, the patient's condition worsened, with elevated lactate (4.5 mmol/L), oliguria, altered mental status, and norepinephrine requirement (0.2 μg/kg/min). The heart team determined there was a need for urgent surgical repair.

Figure 1.

Transthoracic Echocardiogram Showing Postmyocardial Interventricular Septal Defect

Management

The patient's chest was entered through median sternotomy. The pericardium was opened, and a large autologous pericardial patch was harvested. The procedure was carried out under cardiopulmonary bypass and aortic cross-clamp. Cardiac arrest and myocardial protection were obtained with an intermittent modified Calafiore cardioplegia. A single venous bypass graft was anastomosed to the left anterior descending artery. Subsequently, an inferior left ventriculotomy was performed, allowing for exploration of the VSD. No thrombi were identified. The defect was closed using a standard composite patch: an autologous pericardial patch on the LV side and a Sauvage patch on the RV side. The patch was secured on the left side of the interventricular septum with 3-0 prolene U-stitches with Teflon pledgets from the RV side, leaving a broad patch margin that was subsequently sutured to the LV wall using a continuous 4-0 prolene suture. The ventriculotomy was closed with a double-layer continuous 3-0 prolene suture reinforced with 2 external Teflon strips and 1 endoventricular strip along the left margin. Additional reinforcement was achieved with three 3-0 prolene stitches with Teflon pledgets. At the end of the procedure, the cardiopulmonary bypass was discontinued, and the patient remained on IABP support with adrenaline infusion.

Mixed acidosis persisted on postoperative day 1, requiring full inotropic and IABP support to maintain a mean arterial pressure of 70 to 75 mm Hg. A follow-up echocardiogram indicated aneurysmal remodeling of the inferior wall and a patched closure of the VSD. However, we noted residual VSD caused by a possible dehiscence of the patch, as well as an additional serpiginous communication from the midapical interventricular septum into the RV cavity (Video 1). LV function was moderately depressed, with an ejection fraction of 35% to 40%. Cardiac computed tomography confirmed closure of the VSD with the pericardial patch, revealing a continuity solution (approximately 5 × 6 mm) at the basal inferoseptal wall of the LV (Figure 2). The inferior wall exhibited significant thinning with an aneurysmal appearance. The patency of the venous graft to the left anterior descending artery and the stent in the mid-distal right coronary artery was also confirmed, with significant circumferential pericardial effusion (∼3 cm) observed.

Figure 2.

Cardiac Computed Tomography Showing Continuity Solution at the Basal Inferoseptal Wall of the Left Ventricle

Given the presence of significant residual shunts and the high risk associated with repeat cardiac surgery, a percutaneous closure of the residual VSD was performed. The interventional closure was performed under general anesthesia, with fluoroscopic and transesophageal echocardiography (TEE) guidance. Vascular access was obtained through both the right femoral artery and left femoral vein. LV angiography in the left anterior oblique view was performed and showed a VSD caused by LV patch dehiscence, with contrast accumulating in the interpatch space and then passing in the RV through a small fistulous tract (Figure 3). Through a transaortic approach, a right coronary angiographic catheter was introduced into the LV, and a hydrophilic guide wire was positioned in the VSD. Selective angiography confirmed the diagnosis of residual VSD caused by patch dehiscence. The hydrophilic guide wire was exchanged with a 0.035-inch extra-stiff guide wire (Cook Medical). The delivery sheath was then advanced on the guide wire and positioned at the VSD space between 2 pericardial patches. Under fluoroscopic and TEE guidance, a 16-mm type II Amplatzer vascular plug (Abbott) was deployed (Video 2). After deployment, the position and the stability of the device were assessed using TEE and fluoroscopy, and the device was released. Final LV angiography showed the correct position of the device, with a nonsignificant intradevice left-to-right shunt (Figure 4, Video 3).

Figure 3.

Ventricular Septal Defect Caused by Left Ventricular Patch Dehiscence, With Contrast Accumulating in the Interpatch Space and Subsequently Passing Into the Right Ventricle Through a Small Fistulous Tract

Figure 4.

Final Left Ventricular Angiography Showing the Correct Position of the Device

Outcome and Follow-Up

TTE on day 1 and cardiac computed tomography on day 3 (Figure 5, Figure 6, Figure 7) confirmed complete closure of the VSD, with no residual shunting. The patient was gradually weaned off IABP and inotropic support and was transferred to the cardiology ward for rehabilitation. After 36 days, the patient was discharged home in stable condition with preserved organ function.

Figure 5.

Device on Cardiac Computed Tomography

Figure 6.

CTA Images Showing the Ventricular Septal Defect Before and After Repair

Cardiac computed tomography showing (A) the interventricular septal defect (asterisk) and (B) the device (arrow).

Figure 7.

3-Dimensional Volume Rendering Semitransparency and Color Reconstruction

Discussion

Post–myocardial infarction (MI) VSD remains one of the most challenging mechanical complications of myocardial infarction, posing significant management challenges and affecting clinical outcomes. Although the incidence of post-MI VSD has markedly decreased to approximately 0.3%, the condition remains highly lethal, with a mortality rate approaching 100% if left untreated.^1,2 The clinical presentation is variable and depends on the size and location of the VSD. In patients with hemodynamic compromise, mechanical circulatory support can serve as a bridge to surgical repair, heart transplantation, or in selected cases, palliative care. The IABP remains the most widely used form of support, with preoperative insertion performed in approximately 65% of cases.³ It is recommended by both the European Society of Cardiology and American College of Cardiology/American Heart Association guidelines to improve hemodynamics and reduce left-to-right shunting.^4,5 However, its efficacy may be limited in cases with posterior VSD, which are often associated with more severe hemodynamic instability.⁶

The Impella device (Abiomed) enables direct LV unloading and limits shunt volume. However, its use carries risks, including hemolysis, stroke, and the potential for right-to-left shunting, particularly in the presence of RV dysfunction. Venoarterial extracorporeal membrane oxygenation (VA-ECMO), while effective in improving systemic perfusion and end-organ function, increases LV afterload, which may worsen pulmonary congestion and impede myocardial recovery. In such cases, LV venting strategies are necessary.

Recently, combined support strategies such as ECMO with Impella (ECMELLA) or left atrial VA-ECMO (LAVA-ECMO) have shown encouraging results in case series, allowing for patient stabilization and delayed repair.⁷ Similarly, transvalvular LV-assist devices have been used to stabilize patients, improve end-organ perfusion, and delay surgical repair under better conditions.⁸

Despite promising data from case reports and retrospective series, prospective evidence remains limited. Surgical and percutaneous repair are the main treatment options, both carrying substantial risks. A retrospective multicentric study of 362 patients who underwent post-MI VSD closure reported procedural success in 79.4% of percutaneous cases and 88.3% of surgical cases, with higher in-hospital mortality in the percutaneous group (55% vs 44.2%) but fewer complications.⁹ The European guidelines and consensus statement recommend delayed surgery—ideally >7 days from diagnosis—whenever feasible, often supported by temporary mechanical circulatory support.^1,4 Emergency surgery is generally reserved for patients with refractory shock or unmanageable RV dysfunction.^1,4

Operative mortality in early surgery remains high (40%-90%), but this risk decreases significantly when surgery is delayed >7 days (10%-40%).¹ In our case, several factors—including profound hemodynamic compromise, complex anatomy, and partial RV involvement—necessitated immediate surgical repair despite the high risks associated with early intervention. In fact, the acute nature of the infarcted tissue is a major challenge in early repair, given its friability and susceptibility to tearing.

Although early surgical intervention was unavoidable, the initial repair proved only partially effective and required subsequent percutaneous optimization. The use of a type II Amplatzer vascular plug was particularly suitable in this context given its flexibility, low radial force, and ease of repositioning—features that are advantageous in fragile, postsurgical tissue. In this case, the device's large waist and right disc were deployed within the interpatch space, and the left disc was positioned on the left side of the ventricular septum, effectively sealing the VSD entry point and anchoring the device. This configuration allowed for successful closure despite the presence of patch dehiscence, which had created an interpatch cavity communicating with the LV and a narrow fistulous tract leading to the RV. Finally, a 2024 consensus statement supports a hybrid approach in selected cases of post-MI VSD.¹ In a study involving 24 patients—primarily with posterior defects—the hybrid technique preserved or improved RV function compared with patch-only repair, with similar survival rates.¹⁰ This approach may be especially valuable when redo surgery carries prohibitive risk. In our patient, a mild improvement in RV function was noted after the hybrid procedure.¹

Conclusions

This case illustrates the complexity of managing post-MI VSD in the setting of hemodynamic instability. Early surgical repair, while sometimes unavoidable, is associated with high procedural risk owing to tissue fragility, and it may result in incomplete closure. A hybrid approach that combines surgical and percutaneous techniques, supported by timely mechanical circulatory support, can be effective in selected patients. The involvement of a multidisciplinary heart team is critical to guide decision-making and optimize outcomes. Given the rarity and severity of this condition, further research is needed to define standardized treatment strategies and improve long-term prognosis.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Appendix

Video 1

Residual Ventricular Septal Defect: Color Doppler Echocardiography Demonstrates a Left-to-Right Regurgitant Jet From the Left Ventricle to the Right Ventricle

Video 2

Deployment of Left Disc of Device on the Left Side of the Ventricular Septum

Video 3

Final Left Ventricular Angiography Showing the Correct Position of the Device