Contemporary Management of Post-MI Ventricular Septal Rupture

Ventricular septal rupture (VSR) remains a devastating complication following acute myocardial infarction (MI). Surgical repair is the definitive treatment, but it is challenging and associated with high morbidity and mortality. The availability of mechanical support and percutaneous closure has significantly altered the treatment paradigm. In this review, we outline the current management of this dreaded complication.

How Often Do We See It?

The incidence of VSR has decreased from 1-3% following ST-segment elevation MI in the pre-reperfusion era to 0.17-0.31% following primary percutaneous coronary intervention.1-6 Optimal reperfusion of the infarct-related artery prevents development of VSR by salvaging myocardium and limiting infarct expansion. In contrast, late reperfusion remains associated with increased risk of mechanical complications.3 The rarity of clinical presentation results in a lack of medical and surgical expertise in the identification and management of VSR. Given the dismal outcomes, transfer to high-volume centers should be considered when the diagnosis is established.

Pathophysiology and Timing

The timing and presentation of VSR is closely related to the underlying pathophysiology. Universally, patients with VSR present with a transmural infarction, resulting from complete occlusion of any coronary vessel subtending a portion of the septum.6,7 The Becker and van Mantgem classification of free wall rupture usually correlates with clinical presentation.1,8 Becker type 1 ruptures are slit-like tears through normal thickness myocardium, occurring abruptly within 24 hours of an MI, typically related to intramural hematomas dissecting through tissue planes. These typically occur in the setting of a relatively small inferior MI involving the margins of the posterior descending artery distribution, likely due to the shear stress generated by the adjacent hyperkinetic myocardium supplied by the non-infarct left anterior descending (LAD) artery. Such VSRs can be present either at or shortly after clinical presentation. Becker type 2 ruptures typically result sub-acutely from erosion of infarcted myocardium and are associated with neutrophilic infiltration and coagulation necrosis. Becker type 3 ruptures result from perforation of thinned aneurysmal myocardium in the late phase post-MI and occur more frequently in the absence of reperfusion therapy.8 VSR in these settings occurs sub-acutely or late after the index infarction. As a result, there is a bimodal distribution of time to rupture with VSR diagnosis occurring within hours or within 3-5 days or even later of the index MI.4,6,7

Older age, female gender, prior stroke, ST-segment elevation, elevated cardiac markers, higher heart rate, lower blood pressure, higher Killip class, and delayed or lack of reperfusion are all associated with increased likelihood of developing post-infarct VSR.3,7 The LAD and the right coronary arteries are the most common infarct-related arteries leading to septal rupture (42 and 46%, respectively, of all VSRs in the SHOCK [Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock] registry).7 Anterior and inferior infarctions contribute roughly equally to the VSR burden.2,5,7,9 Anterior infarctions typically result in apical VSRs.1 These defects are relatively simple, occurring at the same level on both sides of the septum. In contrast, inferior infarctions more commonly result in complex ruptures, taking serpiginous routes through a hemorrhagic and necrotic basal inferoposterior septum. On imaging with computed tomography and magnetic resonance imaging, LAD VSRs were smaller, had thinner margins, and were more likely surrounded entirely by septum. In contrast, right coronary artery VSRs were more likely complex with associated intramyocardial dissection and involvement of the free wall.10

Presentation and Diagnosis

VSR results in left-to-right shunting, right ventricular (RV) volume and pressure overload, increased pulmonary venous return, and secondary left-sided volume overload. The degree of shunting, or shunt fraction (Qp/Qs), is determined by the relative vascular resistances in the systemic and pulmonary beds. The left-to-right shunt results in a harsh, systolic murmur heard throughout the precordium, often loudest at the left sternal border, associated with a palpable thrill. Signs of increased right-sided flow may include an accentuated pulmonic component of the second heart sound, left and/or right S3 gallop, tricuspid regurgitation, and a mid-diastolic rumble from increased trans-mitral flow. Depending on the size of the index infarction, degree of shunting, and RV dysfunction, patients with VSR may manifest with relative hemodynamic stability or frank cardiogenic shock. In stable patients, the presence of a murmur or findings of routine echocardiography may be the only clues to the diagnosis. Patients with cardiogenic shock manifest with hypotension, cold clammy peripheries, oliguria, and frank pulmonary edema. When the RV is involved, especially in the setting of an inferior infarction, hepatic dysfunction and coagulopathy may also be noted.

Transthoracic and Doppler echocardiography are essential to diagnosing the presence, size, and hemodynamic impact of VSR and helping establish the diagnosis while excluding other etiologies of hemodynamic instability. Transesophageal echocardiography may be necessary if surface images are limited and is especially useful in inferior MI when percutaneous closure is contemplated. On occasion, when faced with unexplained hemodynamic instability in the catheterization laboratory, left ventriculography will help confirm the presence of VSR. Pulmonary artery catheterization will reveal a step-up in oxygen saturation in the RV and can be used to calculate the Qp/Qs.


Surgical closure is the definitive treatment for post-infarction VSR. Arnaoutakis et al. reported on surgical outcomes in 2,876 VSR patients from the Society of Thoracic Surgeons National Database.11 They found an overall in-hospital or 30-day mortality of 42.9%, the highest of any cardiac surgeries, with a sharp decrease in mortality with delay in repair: 54.1% with repair within 7 days from MI versus 18.4% after 7 days. Selection and survivorship bias confound the observations of increased survival with delayed repair (Figure 1).1 Risk factors for operative mortality include age, female gender, shock, inferior infarction, pre-operative intra-aortic balloon pump use, pre-operative dialysis, mitral insufficiency, redo cardiac surgery, emergent surgery, and timing of repair.11

Figure 1: Mortality and Timing of Repair

Figure 1
Published series suggest a graded decline in mortality with greater delay in VSR repair. This ubiquitous finding is likely both a true association due to increased stability of peri-infarct myocardium rending repair more successful as well as an artifact from survivorship bias. Reproduced with permission from Jones et al.1

The optimal timing of definitive surgical repair remains elusive. Although the 2013 American College of Cardiology and American Heart Association guidelines recommended emergent surgical repair regardless of hemodynamic status, the timing of surgery in the setting of VSR remains controversial and should be individualized (Figure 2).12 In hemodynamically stable patients with preserved end-organ function and favorable anatomy, early corrective surgery should be considered because sudden and unpredictable hemodynamic compromise is often noted. Delayed surgery in hemodynamically stable patients may be considered when surgical anatomy is complex and there is concern regarding tissue fragility and the ability to perform definitive repair. The perceived benefit of delayed surgery, although fraught with bias, does have a mechanistic basis. Following infarction, metalloproteinase activity and tissue breakdown peak by day 7, whereas deposition of new collagen begins by days 2-4; necrotic myocytes are entirely replaced by collagen by 28 days.13 Therefore, delay might facilitate successful repair by allowing friable tissue to organize, strengthen, and become well-differentiated from surrounding healthy tissue. In this scenario, close follow-up in the intensive care unit may be considered to enable tissue healing and promote chances of definitive repair. Watchful waiting in this group of patients may also be appropriate in the setting of significant platelet inhibition from exposure to potent dual antiplatelet therapy. In recognition of the possible benefits of delayed repair, the 2017 European Society of Cardiology guidelines promote delayed elective repair in patients initially responding to aggressive conservative management.14

Figure 2: VSR Management Algorithm

Figure 2
(α) If deemed suitable for percutaneous repair, transcatheter septal closure (TSC) may be used as primary repair, bridge to surgery, in conjunction with surgery, or as salvage of residual defect following surgical repair. (β) Candidacy for total artificial heart and/or cardiac transplantation should be considered for any unstable patient whether as an alternative to, in addition to, or following failure of repair. (MCS = mechanical circulatory support; OHT = orthotopic heart transplant; TAH = total artificial heart.)

In stable but inoperable patients, percutaneous TSC may be considered.9,15,16 In a review of 13 case series encompassing a total of 273 patients treated with TSC, Schlotter et al. found an overall procedure success rate of 89% and a 30-day or in-hospital mortality of 32%. The mortality rate in individual studies correlated with the proportion of patients treated within 14 days of the MI, consistent with the higher mortality seen with early surgical closure.9 Reported procedure complications include arrhythmias, device embolization, ventricular rupture, device-related hemolysis, blood transfusion, and death. In the largest individual series of 53 patients, Calvert et al. found increased mortality with older age, female gender, larger defect size, lack of revascularization, and higher acuity disease (cardiogenic shock, inotropic support, and elevated creatinine); prior surgical closure and immediate shunt reduction were associated with survival.16 TSC involves obtaining both femoral arterial and femoral or internal jugular venous access, crossing the defect typically from the left to the right with a soft wire, landing the wire into the pulmonary artery, and snaring it from the venous circulation to form an arteriovenous rail.1 The latter is used to advance a device-delivery sheath from the venous side across the septal defect, through which a septal occluder is deployed with transesophageal or intracardiac echocardiographic guidance. The Amplatzer™ (St. Jude Medical; St. Paul, MN) devices are the most commonly used, designed with two discs that deploy on either side of the septum connected by a stem that traverses the VSR defect.9,10 Several factors are considered in patient selection and device sizing, primarily contingent on VSR morphology and relationship to nearby structures. Specifically designed for post-MI VSR repair, the Amplatzer™ PI Muscular VSD Occluder (St. Jude Medical; St. Paul, MN) is available with a maximum waist size of 24 mm and disc size of 34 mm.9,10 Using gated computed tomography and magnetic resonance imaging, Hamilton et al. showed that a 24 mm waist diameter would only occlude 50% of the left side of VSRs, and a 34 mm disc diameter would reach the margins of 75% of the defects in both systole and diastole.10 Defects <15 mm are considered optimal for TSC, but successful closure has been reported with larger defects.1,9,10 Oversizing the disc may improve procedure success by accounting for defect enlargement due to tissue necrosis. Challenges to TSC include inferior defects due to a lack of a circumferential septal rim, basal defects due to the proximity to the tricuspid valvular apparatus, serpiginous defects due to complicated morphology, and closure soon following infarction due to tissue instability. Diligent defect characterization, device selection, and patient selection are perquisites to successful TSC. On occasion, we have also utilized closure devices intra-operatively as an adjunct to surgical repair. Finally, TSC also has a role as salvage therapy for residual defects following initial surgical repair.

Surgical outcomes in the setting of cardiogenic shock are dismal. In the setting of the SHOCK trial, surgical VSR correction was associated with a mortality rate of 87%.7 Survival rates following TSC in this context are equally disappointing. In the series by Thiele et al., 30-day mortality following TSC was significantly greater in those with shock versus those without (88 vs. 38%).15 Extensive anatomical destruction of the ventricular septum, hepatic and renal dysfunction, and RV failure (from infarction, volume and pressure overload, and consequences of the index infarction) all contribute to prohibitive surgical risk even in the most experienced centers.

The availability of temporary MCS devices has revolutionized treatment strategies in patients with cardiogenic shock. It is our strategy to support such patients with venoarterial extracorporeal membrane oxygenation, which allows for 1) stabilization of hemodynamics, 2) recovery or prevention of end-organ injury, 3) washout of dual antiplatelet effect, and 4) strategy of bridge to decision. Experienced operators have successfully utilized TandemHeart (CardiacAssist, Inc.; Pittsburgh, PA) in this setting. In addition to optimizing hemodynamics and tissue oxygenation, this device decompresses the left atrium and therefore reduces the degree of left-to-right shunting. Kar et al. demonstrated the efficacy of TandemHeart in improving hemodynamic parameters and end-organ function in 117 patients with cardiogenic shock of various etiologies.17 Short-term MCS has received a Class IIa recommendation (level of evidence C) as a bridge in VSR patients.18

Patients with severe end-organ failure despite aggressive support may not be considered for further interventions, and transition to palliative care may be appropriate. Stabilized patients should be considered for eligibility for advanced options. Select patients can then be offered corrective surgery with TAH as back-up. In others with catastrophic cardiac destruction, listing for transplantation and/or TAH insertion may be the appropriate strategy.

Non-surgical management in this setting is only temporizing and involves afterload reduction with intravenous nitroprusside and/or intra-aortic balloon counterpulsation to mitigate shunting. Intravenous diuretics may reduce pulmonary congestion. Vasopressors may be necessary in the setting of circulatory collapse but may result in ischemia, arrhythmia, and worsened tissue perfusion and acidosis.


Post-infarction VSR is a rare complication with a grim prognosis. Once diagnosed, management includes any combination of aggressive medical management, MCS, surgical repair, transcatheter closure, novel surgical/percutaneous hybrid procedures, and palliative care. There remains equipoise regarding timing of repair. Use of early MCS in patients with hemodynamic instability appears to be a promising modality to bridge patients to a decision of delayed repair, transplantation, or palliative options. A multidisciplinary heart team must collaborate at an experienced center to devise a strategy that is tailored to each patient.


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Clinical Topics: Acute Coronary Syndromes, Anticoagulation Management, Arrhythmias and Clinical EP, Cardiac Surgery, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Valvular Heart Disease, ACS and Cardiac Biomarkers, Anticoagulation Management and ACS, Implantable Devices, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias, Aortic Surgery, Cardiac Surgery and Arrhythmias, Cardiac Surgery and Heart Failure, Cardiac Surgery and VHD, Acute Heart Failure, Heart Failure and Cardiac Biomarkers, Mechanical Circulatory Support, Interventions and ACS, Interventions and Imaging, Interventions and Structural Heart Disease, Angiography, Echocardiography/Ultrasound, Magnetic Resonance Imaging, Nuclear Imaging, Mitral Regurgitation

Keywords: Acute Coronary Syndrome, Thoracic Surgery, Angiography, Diagnostic Imaging, Shock, Cardiogenic, Systole, Ventricular Septum, Nitroprusside, Hospital Mortality, Diastole, Creatinine, American Heart Association, Infarction, Pulmonary Artery, Survival Rate, Septal Occluder Device, Hemolysis, Extracorporeal Membrane Oxygenation, Patient Selection, Salvage Therapy, Palliative Care, Diuretics, Watchful Waiting, Factor IX, Follow-Up Studies, Blood Platelets, Shock, Surgical, Shock, Intensive Care Units, Arrhythmias, Cardiac, Magnetic Resonance Imaging, Blood Transfusion, Hemodynamics, Heart Atria, Algorithms, Prognosis, Acidosis, Treatment Outcome, Echocardiography, Metalloproteases, Counterpulsation, Tomography, Anterior Wall Myocardial Infarction, Myocardial Infarction, Infarction, Blood Pressure, Cardiac Surgical Procedures, Catheterization, Swan-Ganz, Coronary Vessels, Diabetes Mellitus, Type 2, Echocardiography, Doppler, Echocardiography, Transesophageal, Heart Rate, Heart Sounds, Hematoma, Hypotension, Inferior Wall Myocardial Infarction, Intra-Aortic Balloon Pumping, Mitral Valve Insufficiency, Myocardium, Oliguria, Percutaneous Coronary Intervention, Pulmonary Edema, Registries, Renal Dialysis, Risk Factors, Shock, Cardiogenic, Systolic Murmurs, Tricuspid Valve Insufficiency, Vascular Resistance, Ventricular Septal Rupture

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