Post-myocardial infarction ventricular septal defect (post-MI VSD) is a rare but life-threatening complication, with an incidence of approximately 0.3% and high early mortality despite advances in reperfusion therapy. Management remains challenging and requires multidisciplinary decision-making. We conducted a narrative review of the literature through May 2024 using PubMed, Scopus, and Google Scholar, focusing on surgical, percutaneous, and mechanical circulatory support (MCS) strategies for post-MI VSD. A narrative approach was adopted due to the rarity of the condition, the heterogeneity of available evidence, and the predominance of registries and case series. Surgical repair remains the gold standard, employing approaches such as the Daggett, David, and double-patch infarct exclusion techniques. Delayed surgery (>7 days) in hemodynamically stable patients is associated with improved outcomes, whereas urgent intervention is warranted in refractory shock. Percutaneous closure, using dedicated or adapted occluder devices, offers an option for high-risk or unstable patients, either as definitive therapy or as a bridge to surgery, though residual shunts are more common. Hybrid procedures and novel beating-heart techniques have shown promise in selected cases. MCS, including intra-aortic balloon pump, veno-arterial extracorporeal membrane oxygenation, and Impella, facilitates hemodynamic stabilization, allowing myocardial recovery before repair. Overall, in-hospital mortality remains high, particularly in acute-phase interventions. In conclusion, management of post-MI VSD demands individualized strategies integrating patient stability, defect anatomy, and institutional expertise. While surgical closure offers superior long-term outcomes, percutaneous and hybrid approaches expand therapeutic options. Future studies should clarify optimal timing, refine patient selection, and evaluate the impact of advanced MCS strategies on survival and recovery.
Post-myocardial infarction (MI) ventricular septal defect (VSD) is a rare but severe mechanical complication of MI, with an incidence of approximately 0.3%. , Advances in percutaneous coronary intervention (PCI) have further reduced the frequency of this complication. However, despite significant progress in MI treatment over the past two decades, the prognosis for patients who develop post-MI VSD remains poor. The in-hospital mortality rate is approximately 55% for interventional treatment and 44% for surgical treatment. One-year postdischarge mortality ranges between 5% and 10%. Additionally, 94% of patients managed medically die within 30 days. Surgical closure is traditionally considered the gold standard, based on historical practices and expert consensus. , However, the procedure carries a high risk of perioperative mortality and postoperative complications. As an alternative, percutaneous transcatheter closure has emerged as a relatively new approach to VSD repair.
Methods
To identify relevant literature on the diagnosis and management of post-post-MI VSD, we conducted a comprehensive search of PubMed, Scopus, and Google Scholar through May 2024. The search strategy employed combinations of the following terms: “post-myocardial infarction ventricular septal defect,” “mechanical complications of myocardial infarction,” “surgical repair,” “percutaneous closure,” “mechanical circulatory support,” and “Impella,” “ECMO,” or “Amplatzer.” References from key articles and relevant guidelines by the European Society of Cardiology and American College of Cardiology/American Heart Association were also reviewed to ensure a thorough inclusion of pertinent studies.
Only English-language articles were included. We prioritized clinical trials, meta-analyses, registries, guidelines, and high-quality observational studies, as well as case series or reports when addressing emerging techniques or rare complications. Given the narrative nature of this review, no formal inclusion/exclusion criteria or systematic quality assessment tools were applied. Instead, studies were selected based on their relevance to current controversies, evolving management strategies, and emerging technologies in the treatment of post-MI VSD. This review was intentionally designed as a narrative synthesis. A systematic review approach was not considered appropriate due to the low incidence of post-MI VSD, the absence of randomized trials, and the substantial heterogeneity in study design, patient selection, timing of intervention, and outcome definitions across the available literature. Consequently, evidence is largely derived from retrospective series, registries, and expert consensus, which necessitate a critical, interpretative rather than quantitative methodology. Indeed, the review aimed not only to summarize available evidence but also to critically appraise unresolved issues such as optimal timing of intervention, patient selection, and the role of mechanical circulatory support in this complex clinical scenario.
Results
Pathophysiology
The first week following MI is the critical period for the development of post-MI VSD, occurring on average between 3 and 5 days after symptom onset. In the modern era of PCI, VSDs are predominantly observed in patients with ST-Elevation Myocardial Infarction. The anterior VSD is the predominant defect in most case series, with percentages ranging between 20% and 60%. , Several factors increase the risk of developing a post-MI VSD, including older age, female sex, and delayed reperfusion. In the absence of timely reperfusion, coagulative necrosis develops within the infarcted myocardium during the first 3 to 5 days post-MI. After the first 24 hours, neutrophils infiltrate the damaged area, releasing lytic enzymes that contribute to myocardial wall weakening and eventual rupture. In contrast, early ruptures are not primarily driven by neutrophil activity but rather by large intramural hematomas, which promote myocardial laceration. In patients who survive, fibrotic remodeling of the myocardial wall occurs over the following weeks.
The size of a VSD can vary from a few millimeters to several centimeters. Based on morphology, VSDs are classified into two types: simple VSD (a perforation that aligns at the same level on both sides of the septum) and complex VSD (extensive hemorrhage with irregular, serpiginous tracts within the necrotic tissue). In anterior MI, the septal rupture is typically apical and simple. Whereas in inferior MI, the rupture usually affects the basal inferior septum and is more often complex. , At the site of the septal rupture, a left-to-right shunt develops, leading to right ventricular (RV) volume overload, increased pulmonary blood flow, and enhanced venous return to the left heart chambers.
As left ventricular (LV) systolic function deteriorates, cardiac output (CO) decreases, prompting an increase in systemic vascular resistance (SVR). This, in turn, exacerbates the left-to-right shunt. The extent of the shunting is influenced by the size of the septal defect, pulmonary resistance, and SVR, and the functional status of both ventricles. Post-MI VSD typically manifests suddenly, often with signs and symptoms of heart failure, including dyspnea, orthopnea, hypotension, cool peripheries, and signs of pulmonary venous congestion. The holosystolic murmur produced by the left-to-right shunt is a key clinical finding. Additional auscultatory features may include a third heart sound and a split-second heart sound due to elevated pulmonary pressure.
Multimodality imaging
Different imaging modalities can be used in the assessment of post-MI VSD, each with specific advantages and limitations depending on the technique, the experience, and resources available at each institution.
Transthoracic echocardiography (TTE) with Doppler imaging is the first-line diagnostic modality ( Figure 1 ). However, conventional 2D TTE alone may only provide suggestive findings, such as thinned or focally absent myocardial tissue at the septum. Therefore, integrating color flow Doppler is crucial for both qualitative and quantitative assessment of the defect, allowing for precise shunt quantification (Qp:Qs), evaluation of LV and RV function, estimation of pulmonary artery pressure, and measurement of CO. Beyond diagnosing post-MI-VSD, TTE plays a crucial role in identifying key differential diagnoses that may coexist, such as acute mitral valve regurgitation secondary to papillary muscle rupture or contained free-wall rupture. These conditions carry significant prognostic and therapeutic implications, emphasizing the need for a thorough and systematic echocardiographic evaluation in patients presenting with post-MI complications. Transesophageal echocardiography (TEE) is recommended when TTE results are inconclusive ( Figure 2 ). TEE can provide more valuable information regarding the location and size of the defect, especially when integrated with 3D reconstruction.
Transthoracic echocardiographic evidence of a post-myocardial infarction ventricular septal defect ( arrows ) in the four-chamber view.
Transesophageal echocardiography demonstration of a post-myocardial infarction ventricular septal defect ( arrows ) in the four- ( A, B ) and three-chamber views ( B ).
Cardiac computer tomography (CT) offers high-resolution imaging of the ventricular septum, enabling precise evaluation of defect margins, rim thickness, and tissue composition ( Figure 3 ). This modality is particularly useful in patients where echocardiographic windows are suboptimal. CT imaging allows for detailed three-dimensional reconstruction, aiding in the visualization of the defect in relation to surrounding structures. Additionally, CT can assist in procedural planning for percutaneous or surgical intervention by providing precise anatomical measurements, including defect diameter and myocardial integrity. Accurate sizing is crucial, as undersizing may lead to severe complications, including significant residual shunting and device embolization. However, radiation exposure and the need for contrast administration may limit its use in patients with renal impairment or those requiring multiple follow-up studies. Furthermore, it is important to achieve a heart rate of less than 60 beats per minute, as higher heart rates can degrade imaging quality.
Cardiac computed tomography evidence of a post-myocardial infarction ventricular septal defect ( arrows ) in the short-axis ( A, B ) and horizontal long-axis views ( C ).
Cardiac magnetic resonance (CMR) imaging provides a comprehensive anatomical and functional assessment, including precise quantification of the shunt volume and myocardial viability assessment, allowing for accurate estimation of VSD size. A study by Wang et al. has shown that CMR outperforms both echocardiography and conventional angiography in assessing shunt function across various defects, including supracristal VSDs, atrioventricular septal defects, and partial anomalous pulmonary venous return. The noninvasive nature of CMR for evaluating shunt function provides critical insights that can aid in treatment planning. However, its use may be limited in patients with renal insufficiency or those with implanted metallic devices. In addition, CMR may be challenging to perform in critically ill patients due to prolonged scan times and the requirement for patient stability and cooperation, as the exam requires breath-holding and remaining still.
Coronary angiography (CA) typically reveals a complete coronary obstruction without collateral circulation. Anterior and apical post-MI VSDs result from MI in the left anterior descending artery territory. Posterior VSDs are associated with inferior MI, sometimes due to proximal right coronary occlusion, which can lead to RV MI and subsequently VSD formation. In the GUSTO trial, anterior VSDs were more common than those localized in the inferior or lateral wall (70% vs 29%). However, inferior infarcts were more frequently associated with complex VSDs located in the basal inferior septum. Ventriculography ( Figure 4 ) is usually performed following CA to confirm the suspected diagnosis.
Ventriculography showing contrast medium passage ( arrows ) through a post-myocardial infarction ventricular septal defect.
Management
After post-MI VSD is diagnosed, treatment decisions should be made by a multidisciplinary Heart Team ( Figure 5 ). The choice of treatment modality and timing should be guided by the patient’s hemodynamic status, VSD characteristics, and underlying comorbidities.
Decision-making nodes in the management of post-myocardial infarction ventricular septal defects. CABG = coronary artery bypass grafting; ECMO = extracorporeal membrane oxygenation; IABP = intra-aortic balloon pump; PCI = Percutaneous Coronary Intervention; VAD = ventricular assist device; VSD = ventricular septal defect.
Surgical treatment
The repair of post-MI VSD relies on two main surgical techniques: the Daggett and David procedures. The Daggett technique, which can be performed using either a single or double patch, involves securing a patch over the defect and suturing it to both the RV and LV. In contrast, the David technique uses a pericardial or synthetic patch that is carefully sutured to the healthy, noninfarcted endocardium of both the interventricular septum and the anterolateral ventricular wall. This method effectively isolates the LV cavity from the infarcted myocardium, ensuring structural stability and reducing the risk of further rupture.
The approach to repairing a VSD varies depending on its location. For anterior VSDs, surgeons make an incision along the infarcted surface of the anterolateral LV, generally parallel to and 1 cm lateral to the left anterior descending. In contrast, the approach to posterior VSDs presents greater technical challenges due to their location, necessitating elevation of the heart to achieve adequate exposure. In these cases, the ventriculotomy is performed one cm lateral to the posterior descending artery, with careful attention given to preserving the mitral subvalvular apparatus to prevent additional complications.
A refinement of the David technique, known as the double-patch technique, offers further reinforcement, particularly for anterior VSDs. This method involves suturing a properly tailored bovine pericardial patch to the healthy endocardium surrounding the infarcted area in both the septum and lateral ventricular wall. A second, smaller patch is then applied directly over the VSD and secured with running sutures to prevent right-to-left shunting while the primary patch reinforces the structural integrity of the repair. This modification can also be employed for posterior VSDs, where additional support is often necessary due to the complexity of the defect.
One of the greatest challenges in VSD repair is the fragility of the infarcted myocardium in the acute phase, which makes it prone to tearing and recurrent defects. To improve surgical outcomes, meticulous debridement of necrotic tissue is essential, even if it requires enlarging the defect to reach healthy myocardium. Despite these advances, operative mortality remains high, ranging from 40% to 90% if the surgical approach is performed within 7 days of MI-VSD occurrence. However, it decreases to 10% to 40% when surgery is performed after 7 days. Preoperative prognostic factors associated with in-hospital mortality are reduced ventricular systolic function, cardiogenic shock, inferior infarction, the need for inotropic support, and total occlusion of the infarct-related artery. Long-term survival is similarly dependent on the preservation of RV function and the extent of residual LV function after surgical closure. Factors such as age, preoperative cardiac arrest, the need for percutaneous revascularization, and postoperative requirements for intra-aortic balloon pump (IABP) and extracorporeal membrane oxygenation (ECMO) were independently linked to early mortality in a retrospective multicenter international cohort study.
In recent years, emerging techniques have been developed to improve the success rates of VSD repair. One such approach is the “beating-heart butterfly” technique, a novel method specifically designed for basal post-MI VSDs. This technique involves the use of a double-layered pericardial patch, which is sewn to the intact septum while the heart continues to beat under cardiopulmonary bypass. A small study described its application in four patients, all of whom received mechanical circulatory support (MCS). Among them, three also underwent coronary artery bypass grafting before VSD repair, while one received PCI before surgery. Additionally, one patient required bioprosthetic tricuspid valve replacement. This open-chest procedure was associated with 100% one-year survival in all patients.
Another innovative strategy is the hybrid technique, which combines infarct exclusion with the use of a patch and a nitinol-mesh septal occluder implanted under direct vision rather than percutaneously. By integrating both surgical and device-based approaches, this method enhances defect closure while providing additional structural support. In a study of 24 patients with predominantly posterior post-MI VSDs, those who underwent the hybrid approach demonstrated stable or improved RV function, despite similar survival rates to those who received traditional patch-only repair. While no intraoperative mortality was reported in either group, the hybrid technique appears to offer significant advantages in preserving RV function.
Finally, a novel technique involving the use of two patches, referred to as the “embankment technique,” was described in a case series of 11 patients. In this approach, the BioGlue surgical adhesive was utilized between the two patches, resulting in no observed residual shunts or embolic events caused by glue leakage into the LV in any of the patients.
Percutaneous management
Percutaneous repair of post-MI VSDs has emerged as a promising alternative for patients considered high-risk for open-heart surgery. It can also serve as definitive therapy for closing residual defects postsurgery or as a bridge to surgical repair, allowing time for tissue healing and rupture remodeling, thereby potentially making the defect more amenable to surgical closure. Currently used devices for post-MI VSD closure include the “Amplatzer Post-Infarct Muscular VSD Occluder”, which is specifically designed for this purpose, as well as the off-label use of the “Amplatzer Muscular VSD Occluder,” originally designed for congenital muscular VSDs. ,,, Additionally, various manufacturers produce atrial septal defect (ASD) occluders, which are primarily designed for ASD closure, but can be adapted for VSD closure in selected cases. While the Amplatzer Post-Infarct Muscular VSD device is available in larger sizes than the Muscular VSD device (up to 24 mm), making it more suitable for larger post-MI VSDs, the Muscular VSD device and ASD occluders may be more appropriate for smaller post-MI VSDs (less than 18 mm). In cases of small, serpiginous, or multiple-tract postinfarct VSDs, a self-centering patent foramen ovale occluder device may be considered. ,,
The transcatheter procedure is performed under general anesthesia with TEE guidance. Vascular access is typically obtained via both the femoral artery and vein, with access site selection based on the defect’s location. Inlet and mid-muscular defects may be approached through the right jugular vein, whereas outlet defects are more commonly accessed through the femoral vein. Standard antibiotic prophylaxis and systemic heparinization are administered, aiming for an activated clotting time greater than 250 seconds. LV angiography, performed in a left anterior oblique view, is utilized to visualize the post-infarct VSDs. Typically, a hydrophilic wire is advanced from the LV to the RV, across the VSD, and into the pulmonary trunk. The wire is then snared and exteriorized through venous access, usually through the femoral or jugular vein, creating a complete arteriovenous loop. Over this rail, a shuttle sheath is guided into the interventricular septum, and the occluder is then deployed. After deployment, device position and stability, as well as any residual shunt is assessed with TEE and fluoroscopy. If the device is unstable or interferes with other structures, the device is retrieved and repositioned. In cases of significant residual shunt due to an incomplete coverage of the post-infarct VSDs from the device or multiple post-infarct VSDs, the device may be retrieved and exchanged with a larger device or additional devices may be used to completely close the defect. While residual shunt in proximity to the original device or with deficient rim favors the use of a larger device, additional post-infarct VSDs distant from the original device are preferably closed with the use of additional devices.
Another recent procedure is the DEXTER (Direct Externalization and Enmeshment to the Right Ventricular Moderator Band) technique, described in two patients with post-MI apical VSDs. Both were treated with an innovative transcatheter approach, which involves closing the defect by positioning a device in the RV moderator band, resulting in an immediate hemodynamic improvement.
Optimal timing and choice of surgical vs percutaneous management
The optimal timing for the repair of post-MI VSDs remains a complex and contentious issue. Notably, neither the United States nor European guidelines provide a specific timeframe for post-MI VSD repair. ,, The European guidelines recommend, when feasible, a delayed surgical repair beyond 7 days from diagnosis. This approach may involve the use of noninvasive or invasive systems such as veno-arterial ECMO (VA-ECMO) or other temporary percutaneous circulatory assist devices. They advocate for prompt surgical intervention if refractory shock persists or if RV dysfunction becomes unresponsive.
Given the high mortality risk associated with surgery performed during the acute phase, along with instances where hemodynamic instability necessitates urgent intervention, transcatheter repair has emerged as a possible salvage modality for critically ill patients. This approach can potentially stabilize hemodynamics, allowing for surgical correction of the VSD after myocardial fibrosis has developed. , A recent meta-analysis of 12 single-arm studies involving 284 patients highlighted that transcatheter closure could serve as a rescue option for patients with post-MI VSD during the acute phase. However, as known for surgical repair, the analysis indicated that closure during the chronic phase was more effective and associated with lower mortality, though the findings must be interpreted with caution due to potential selection bias and the small sample size.
Despite promising procedural success rates, ranging from 80% to 100%, with an average of 89%, hospital mortality remains high, and complications are common with percutaneous repair. These include device embolization, arrhythmias, hemolysis, and incomplete defect closure, often necessitating surgical intervention. A particularly severe complication is LV rupture, which can occur either immediately postoperatively or during device manipulation and positioning, potentially leading to fatal outcomes. However, studies suggest that patients who survive the immediate post-procedural period tend to have a favorable long-term prognosis. In a study of 15 patients, Zhang et al. reported a hospital discharge survival rate of 73.3%. Over a follow-up period of approximately 250 days, all but one patient demonstrated favorable survival outcomes. Another study assessed 30-day outcomes based on the timing of percutaneous closure: patients treated within 14 days (acute phase) had a 57.1% survival rate, while those treated after 14 days (nonacute phase) showed improved survival at 76.9%.
A comprehensive assessment of both surgical and transcatheter closure techniques for post-MI VSD was conducted in a retrospective review involving 362 patients who underwent a total of 416 interventions (131 percutaneous and 231 surgical) across 16 centers in the United Kingdom from 2010 to 2021. The procedural success rates were 79.4% for percutaneous closures and 88.3% for surgical closures. The overall in-hospital mortality rate was 48.1%, with a higher mortality rate observed in the percutaneous group compared to the surgical group (55.0% vs 44.2%, p = 0.048). Despite this, the surgical group had a greater risk of complications, including stroke, renal replacement therapy, and pneumonia. Five-year all-cause mortality rates showed no significant difference between the two groups. Multivariate analysis indicated that PCI of the infarct-related artery was associated with in-hospital mortality, while the severity of coronary artery disease in non-culprit lesions influenced long-term mortality outcomes.
A residual shunt remains a common long-term complication following both procedures, with a higher incidence associated with the transcatheter approach. Yi et al. suggest that using a device larger than the measured VSD diameter may enhance closure outcomes, specifically recommending an occluder approximately 1.5 times the VSD diameter to reduce the incidence of residual shunts.
In a meta-analysis of seven retrospective observational studies involving 603 patients, the comparison between surgical and percutaneous repair of post-MI VSD revealed that surgical closure was associated with significantly lower short-term mortality and a reduced incidence of residual shunts or the need for reintervention. Specifically, the relative risk for short-term mortality was 1.21 (95% confidence interval: 1.00 to 1.46, p = 0.05), while the relative risk for residual shunts or reintervention was 2.68 (95% confidence interval: 1.46 to 4.91, p = 0.001) for percutaneous closure compared to surgical closure.
From a Heart Team perspective, management can be stratified according to clinical presentation. In acutely unstable patients with cardiogenic shock, immediate stabilization with mechanical circulatory support is paramount, and definitive repair should not be postponed on the basis of arbitrary time thresholds. In subacute patients stabilized with MCS, a period of optimization may allow tissue consolidation and facilitate delayed surgical or staged percutaneous closure. In chronic-phase stable patients, elective surgery generally provides the most durable results, while percutaneous or hybrid strategies may be considered in selected high-risk cases. Importantly, current ESC and ACC/AHA guidelines do not define precise timing cut-offs, and the frequently cited “>7 days” threshold is derived from observational series rather than randomized evidence; therefore, this concept should not delay intervention in patients with persistent shock or end-organ hypoperfusion.
Appropriateness and timing for coronary revascularization
Another challenge in managing these patients is defining the appropriateness and ideal timing for revascularization of the culprit lesion. Before proceeding with PCI, careful assessment should be made in cases of suspected mechanical complications from a MI. This is particularly important in patients with post-MI VSDs, as the concomitant use of P2Y12 inhibitors may hinder or delay a surgical strategy due to potential hemorrhagic complications related to antiplatelet therapy. According to the European Society of Cardiology guidelines, in patients presenting more than 48 hours after symptom onset, operators should refrain from performing PCI on completely occluded vessels. While revascularization of noninfarcted coronary arteries is suggested to benefit in preventing further deterioration of LV function, the risk of reperfusion injury and suture entrapment due to ventriculotomy closure cannot be overlooked. In a more recent and broader UK registry analysis, which included patients treated with both surgical and percutaneous approaches, PCI of the infarcted coronary artery was associated with higher mortality. These findings, largely derived from observational registry data, do not establish causality but support a cautious approach to routine culprit-lesion PCI. Therefore, decisions regarding revascularization should be individualized within the Heart Team, carefully balancing the potential benefits of myocardial salvage against the risks of surgical postponement and bleeding related to P2Y12 therapy.
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