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Table of Contents
Year : 2020  |  Volume : 10  |  Issue : 4  |  Page : 156-162

Current concepts in the management of acute ST-elevation myocardial infarction with ventricular septal rupture – Early versus late approach: Part 1 – Transcatheter device closure of ventricular septal rupture

1 Department of Cardiology, Sunshine Heart Institute, Secunderabad, Sunshine Hospitals, Secunderabad, Telangana, India
2 Department of Cardiothoracic Surgery, Sunshine Heart Institute, Secunderabad, Sunshine Hospitals, Secunderabad, Telangana, India

Date of Submission14-Nov-2019
Date of Decision01-Jan-2020
Date of Acceptance07-Jan-2020
Date of Web Publication21-Jan-2021

Correspondence Address:
Dr. Sridhar Kasturi
Department of Cardiology, Sunshine Hospital, Secunderabad - 03, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JICC.JICC_48_19

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Post-infarction ventricular septal rupture (VSR) is a rare but lethal mechanical complication of an acute myocardial infarction (AMI). Survival to 1 month without intervention is 6%. Given high surgical mortality, transcatheter closure has emerged as a potential strategy in selected cases. Indian data on percutaneous device closure of post AMI-VSR is scarce hence we report our single-centre experience with ASD occluder device (Amplatzer and lifetech) for closure of post-AMI VSR. Acquired ventricular septal defect (VSD) is uncommon, but serious mechanical complication of acute myocardial infarction with poor outcome and high mortality rate in surgically or medically treated patients. Percutaneous closure is a potential technique in a selected group of patients. The presence of cardiogenic shock, IWMI and serpigeneous form of VSR constitutes important risk factors for mortality. Device implantation is in general successful with few procedure-related complications and should be applied on a case-by-case basis.

Keywords: Device closure, postoperative myocardial infarction, ventricular septal rupture

How to cite this article:
Kasturi S, Pantula N. Current concepts in the management of acute ST-elevation myocardial infarction with ventricular septal rupture – Early versus late approach: Part 1 – Transcatheter device closure of ventricular septal rupture. J Indian coll cardiol 2020;10:156-62

How to cite this URL:
Kasturi S, Pantula N. Current concepts in the management of acute ST-elevation myocardial infarction with ventricular septal rupture – Early versus late approach: Part 1 – Transcatheter device closure of ventricular septal rupture. J Indian coll cardiol [serial online] 2020 [cited 2022 Sep 24];10:156-62. Available from: https://www.joicc.org/text.asp?2020/10/4/156/307616

  Introduction Top

Ventricular septal rupture (VSR) is an uncommon complication of acute ST-elevation myocardial infarction (STEMI) with poor prognosis. Mortality of patients with cardiogenic shock due to VSR is as high as 67% within 48 h and 100% within 30 days. Surgical closure of VSR is a challenging procedure with mortality between 20% and 87% depending on operators' experience and surgical facilities with backup system. Transcatheter closure is a promising alternative treatment modality for VSR, particularly when surgical treatment is not feasible, surgeon is reluctant to operate, and for postsurgical residual VSR. In view of the poor prognosis of VSR patients and the benefits from VSR closure, transcatheter closure or surgical repair of the VSR in the acute phase is usually the only option in order to stabilize hemodynamics and restore cardiac function for those with unstable hemodynamic status, despite high risk and mortality in both therapeutic operations.

  Case Top

A 50-year-old male, known hypertensive and diabetic, presented with anterior wall STEMI with cardiogenic shock. On examination, the patient was breathless with hypoxemia, SPO2 was 85% with oxygen support, pulse rate was 110 bpm, blood pressure was 88/66 mmHg, was on high ionotropic support, respiratory rate was 28/min, cardiovascular system revealed S1+, S2+, S3+, and S40, and high-pitched systolic murmur over the precordial area. Lung examination revealed bilateral basal rales. [ECG showed ST elevation with T inversion in V1-V6, I and AVL lead [Figure 1], 2D - Echo - RWMA of LAD territory, VSR (6mm from the Apex) with the left to right shunt with severe LV dysfunction, EF-30%.] Transesophageal echocardiography (TEE) revealed apical VSR of 8–10 mm with good rims. Investigations demonstrated hemoglobin (Hb) of 12.0 g/dl, total leukocyte count of 14,140 cells/mm3, platelet count of 1.9 lakhs/mm3, international normalized ratio of 1.546, serum urea of 45 mg/dl, and serum creatinine of 1.3 mg/dl. Chest X-ray showed pulmonary venous hypertension with pulmonary edema, coronary angiogram with intra-aortic balloon pump (IABP) support-double-vessel disease, mid-LAD thrombotic total occlusion, and OM2 proximal 70% lesion [Figure 2].
Figure 1: Electrocardiogram

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Figure 2: (a) A-CAG Mid total occlusion of the left anterior descending artery due to thrombus containing lesion, LCX-Obtuse Marginal - Proximal 70% lesion, B-Left Ventricular Angio, C- Deployed Amplantzar duct occluder (18mm) across VSR

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[Judkins Right (JR – Metronic, Inc, 710 Medtronic Parkway, Minneapolis, MN USA 55432), AMPLATZER™ post-MI VSD occluder (St. Jude Medical (ABBOTT), St. Paul, MN, USA)]. [0.035” Exchange length Terumo guidewire with Judkins Right (JR – Metronic, Inc, 710 Medtronic Parkway, Minneapolis, MN USA 55432)) catheter was introduced from right femoral approach, to cross VSR retrogradely, and placed in pulmonary artery after crossing the VSR from left ventricular side, under TEE and Fluoroscopy guidance, after placing wire in LPA]. Snaring of Terumo was done through right internal jugular approach. The delivery sheath was made to cross across VSR, and the tip of the sheath was placed into the LV outflow tract. VSR closure was done with Amplatz 18-mm device. During the postprocedural period, the patient developed anuria and acute renal failure with serum creatinine 2.6 mg/dl. Continuous renal replacement therapy was started in view of renal failure. On the 5th postoperative day, hemodynamic status worsened despite IABP, high ionotropic, and venoarterial extracorporeal membrane oxygenation support. The patient developed cardiac arrest on the next day which was revived with cardiopulmonary resuscitation (CPR), for refractory hypotension and fall in Hb at 12.0–6.7 g/dl. Four units of blood transfusions were given. The patient developed asystole on the 7th day; immediate resuscitation measures were taken, but despite prolonged CPR, he could not be revived.

  ST-Elevation Myocardial Infarction with Ventricular Septal Rupture Top

VSR is an uncommon complication of acute STEMI with poor prognosis. Ventricular septal defect (VSD) was first described in vivo in 1923 by Brunn, and the first clinical criterion for its diagnosis was established in 1934 by Sager.[1] Cooley performed the 1st case of postmyocardial infarction (MI) VSR surgical repair in 1956.[2] VSR is commonly associated with low cardiac output, multiorgan failure requiring ionotropic and ventilatory support, and death. Risk factors for VSR include hypertension,[3],[4] advanced age,[3] female gender,[3],[5] diabetes mellitus, the absence of a history of angina or acute MI (AMI),[6],[7],[8],[9],[10] and severe coronary stenosis or chronic total occlusion without compensatory collateral circulation. It has a bimodal presentation with peak frequencies in the first 24 h and 3–5 days post-AMI. The incidence of VSR is 0.2% of all patients with STEMI; 80% of untreated patients die within the 1st month and >90% within the 1st year after VSR with STEMI. Survival without surgical treatment of patients with VSR after acute MI, based on analysis of all proven cases (n=139) reported in the literature until 1977. The solid line represents the proportion of surviving and dashed lines enclose 70 % confidence limits. A-Interval in months between rupture and death [Figure 3]A. B-Interval in days between rupture and death [Figure 3]B. Note that half the patients are dead within seven days of rupture.
Figure 3: Survival without surgical treatment of patients with ventricular septal rupture after acute myocardial infarction, based on analysis of all proven cases (n = 139) reported in the literature until 1977. Solid line represents the proportion surviving and dashed lines enclose 70% confidence limits. (a) Interval in months between rupture and death. (b) Interval in days between rupture and death. Note that half of the patients died within 7 days of rupture

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The mortality of patients with cardiogenic shock due to VSR is as high as 67% within 48 h and 100% within 30 days. Surgical closure of VSR is associated with large residual shunt, reopening of closed VSR, and re-rupture after surgery in 10%–20% of cases. Surgical closure of VSR is a challenging procedure with mortality between 20% and 87% depending on operators' experience and surgical facilities with backup system. Transcatheter closure is a promising alternative treatment modality for VSR, particularly when surgical treatment is not feasible, surgeon is reluctant to operate, and for postsurgical residual VSR.

STEMI management with early reperfusion strategies for AMI, including thrombolysis and percutaneous coronary intervention (PCI), has led to a decline in the incidence of VSR in recently published series. Restoration of flow in the infarct-related artery leading to myocardial salvage and reduced incidence of transmural infarct may account for this observation. In the prethrombolytic era, VSR was thought to complicate 1%–2% of AMI presentations. More contemporary series, however, show it to be increasingly rare, complicating between 0.17% and 0.31% of patients presenting with AMI.[11],[12],[13],[14] In view of better infarct-related artery patency with primary PCI compared to thrombolysis, PCI is associated with less incidence of VSR compared to thrombolytic therapy. Due to recent changes in STEMI strategies, the incidence of VSR has been significantly decreased with particular emphasis on early reperfusion by shortening door-to-balloon time, door-to-needle time, door-in and door-out time of peripheral referral centers, by-passing Emergency Medical Services (EMS) / Casualty in territory care and cell phone activation of EMS-Team and Cathlab team while shifting from periphery. There was also a significant linear relationship between shorter time to thrombolysis infusion and lower incidence of heart rupture (P = 0.02).

  Clinical Presentations of Ventricular Septal Rupture Top

Posterior MI may have associated mitral regurgitation due to papillary muscle dysfunction. Clinical features [Table 1] are usually due to increased left-to-right shunt QP/QS >2:1, increased LV diastolic pressure, and pulmonary capillary wedge pressure. High risk of death immediately after septal rupture then gradually decreases; <30% survive for the first 2 weeks after VSR and only 10%–20% survive >4 weeks. VSR with inferior wall MI at posterior location has worse prognosis than that at anterior location.
Table 1: Characteristics of ventricular septal rupture

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  Pathogenesis Top

VSR is due to coagulation necrosis of infarcted myocardium associated with the infiltration of numerous neutrophils. The neutrophils undergo apoptosis process and then release lytic enzymes, hastening the disintegration of necrotic myocardium. After several weeks if patients survive, the septum becomes fibrotic. VSR classification by Becker and van Mantgem of Type 1 ruptures are slit-like tears through normal thickness myocardium, occurring abruptly within 24 h 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 noninfarct LAD artery. Such VSRs can be present either at or shortly after clinical presentation. Type-II infarcted myocardium erodes before rupture occurs and is covered by a thrombus, and/or associated with neutrophilic infiltration and coagulation necrosis. Type-III marked thinning of the myocardium, secondary formation of an aneurysm, and perforation in the central portion of the aneurysmal myocardium in the late phase post-MI occur more frequently in the absence of reperfusion therapy. Post-MI VSR is anterior or apical in 60% of cases secondary to anterior wall MI (AWMI) and posterior position in 20%–40% of cases secondary to inferior wall MI. Usually, there is complication of first AWMI, with absent collaterals in the setting of complete occlusion with unprotected stenosis in the right coronary artery (RCA). VSR in these settings occurs subacutely or late after the index infarction. Simple septal rupture-discrete defect and a direct through-and-through communication across the septum. Septal ruptures in patients with anterior MI are generally apical and simple. Complex septal rupture – extensive hemorrhage with irregular, serpiginous tracts within necrotic tissue. Inferior MI and septal ruptures involve the basal inferoposterior septum and are often complex.[15] Occasionally, muscles of the ventricular free wall or papillary muscles may tear, especially in the case of complex septal ruptures. 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 [Should We emergently Revascularize Occluded Coronaries for Cardiogenic Shock] SHOCK registry).[16] Anterior and inferior infarctions contribute roughly equally to the VSR burden.[11],[16],[17],[18] On imaging with computed tomography and magnetic resonance imaging (MRI), LAD VSRs were smaller, had thinner margins, and were more likely surrounded entirely by septum. In contrast, RCA VSRs were more likely complex with associated intramyocardial dissection and involvement of the free wall.[19]

  ST-Elevation Myocardial Infarction with Ventricular Septal Rupture: -Does Percutaneous Coronary Intervention Worsen Clinical Outcome? Top

Cardiac MRI – late reperfusion – appeared to increase the infarction area compared with conservative therapy for patients with STEMI; among these patients, the supply of late coronary flow into the infarction area might influence the microvascular blood flow and induce reperfusion injury, thus resulting in the enlargement of the infarction area. Early reperfusion decreases the incidence of VSR and increases the overall mortality; if VSR occurred, higher mortality was observed in both the SHOCK: Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock and Apex-AMI: Assessment of Pexelizumab in Acute Myocardial Infarction (APEX-AMI) trials.

  Transcatheter Closure of Postinfarct Ventricular Septal Rupture Top

The percutaneous closure of post-MI VSR has become a promising option in a variety of situations: to close a residual leak after VSR surgical repair, to stabilize high-risk patients for future surgery, and to serve as a primary intervention. The considerable advantage of a percutaneous approach to repeat VSR repair is that the patient does not undergo a 2nd surgery.[20],[21],[22] Transjugular approach is preferred to transfemoral approach. Favorable VSR amenable to device closure, simple defects <15 mm with adequate rims subacute or chronic VSR with onset duration >3.5 weeks. Large VSR measuring 35 mm; apical VSR without a suitable rim; basal VSR that was situated too close to the mitral, tricuspid, and/or aortic valvular apparatus; and complex VSR with serpiginous borders are unsuitable for device closure of VSR.

VSR device closure usually performed through the femoral artery and femoral vein using the antegrade and retrograde approach. In some cases, Apical VSR device closure can be performed using the Right Internal jugular venous and femoral artery approach for arteriovenous guide wire loop creation. The VSR was crossed by using a retrograde approach with a 6 Fr JR coronary catheter which introduced a 0.032” ×260 cm exchange wire (Terumo/Amplatz) across the defect into the pulmonary artery or through the right atrium into the superior vena cava. The tip of the exchange wire was snared in the pulmonary artery or superior vena cava by using a 10-mm Amplatz GooseNeck snare catheter (COOK/EV3) and exteriorized via the right femoral vein or internal jugular vein. Subsequent delivery proceeded similarly to congenital muscular VSR closure. After transthoracic echocardiography and left ventriculography, ideal placement without or with only a mild (<2 mm)-to-moderate (<4 mm) residual shunt, the device was released. Post device implantation, patients will be checked with chest X-ray, transthoracic echocardiography, and ECG within 24 h following the procedure.[23]

Thrombolytic treatment increases early and complex VSR, therefore it is more difficult to repair major complications which can occur in up to 41% of patients, major residual shunting, LV rupture, device displacement and embolization, malignant arrhythmias, and contrast-induced nephropathy. Sometimes, the rigid delivery sheath might tear the borders of the VSR, increase VSR size, and cause LV rupture. Balloon dilatation is usually discouraged in acute or subacute settings to assess the size of VSR, which may lead to worsening of VSR. There are no guidelines available for device closure.

The first report by Landzberg and Lock[24] in 1998 described the use of Clamshell devices (C. R. Bard, Inc., Murray Hill, NJ, USA) or the CardioSEAL® device (NMT Medical, Boston, MA, USA) in 18 patients. Seven patients underwent primary device closure with survival to discharge in three patients, all of whom had presented months after VSR. Better outcomes were seen in 11 patients who had prior surgical repair with patch leaks (median survival of 54 months). A more recent series reported the use of a dedicated Amplatzer post-MI VSD occluder (St. Jude Medical, St. Paul, MN, USA) or similarly designed devices.[25],[26] Specifically designed for post-MI VSR repair, the Amplatzer Post-Infarct (PI) muscular VSD occluder (St. Jude Medical; St. Paul, MN, USA) is available with a maximum waist size of 24 mm and a disc size of 34 mm.[9],[10] Using gated computed tomography and MRI, 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 tuberous sclerosis complex, but successful closure has been reported with larger defects.[1],[9],[10] The procedure itself is demanding but less complicated than noninfarct VSD closure. Issues that plague early surgical repair, in particular fragile myocardial tissue at the defect margins, are also relevant to percutaneous closure. A device may be successfully implanted, only to place tension on poor-quality adjacent tissue that had yet to liquefy and cause VSR expansion. Abnormal geometry is common and can complicate device closure (one autopsy series identified only 53% of VSR being “through-and-through,” whereas the remainder were complex and serpiginous,[27] such that the LV entry and RV exit are distant from each other). Furthermore, it is common for these infarcts to be in locations that abut the free wall or apex that may prevent devices from sitting in a manner whereby they are most effective. Important aspects to consider when reviewing device series for postinfarct VSR (PIVSR) closure are the timing of the closure (acute vs. subacute >2–3 weeks) and whether it is performed as a primary VSR closure versus postsurgical repair (for patch leaks). In a study by Calvert et al.,[26] postinfarction VSD closure was attempted in 53 patients from 11 centers (1997–2012, aged 72 ± 11 years, 42% female). In their study, 19% of the patients had previous surgical closure. Time from MI to closure procedure was 13 (1st and 3rd quartiles, 5–54) days. Devices were successfully implanted in 89% of patients. In-hospital mortality was 42%. Major immediate complications included procedural death (3.8%) and emergency cardiac surgery (7.6%) device embolization (3.8%). [Some other articles describing in detail about device closure of post infarct VSR [Table 2] Series describing device closure of post-infarct VSR].
Table 2: Series describing device closure of postinfarct ventricular septal rupture

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Recently, in one case of PIVSR with LV aneurysm, LV EF of 49% was repaired with an 85-mm Parachute device (CardioKinetix, Inc., Menlo Park, California, USA) to restore the left ventricle and close the apical VSR simultaneously[Figure 4].[31]
Figure 4: The Parachute device partitions the apical cavity, as well as the apical ventricular septal rupture

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  Conclusion Top

Early surgical closure is recommended for all STEMI patients with VSR, particularly who are unstable due to large defect with significant left-to-right shunt. Delaying surgery may increase mortality rate though high operative mortality can be observed in early surgical group versus late surgical group. Possible better outcome observed in late surgical group is due to operating on low-risk group. Transcatheter closure is an alternative modality of treatment for patients who are unsuitable or those at high risk to surgery and for postsurgical residual VSR. In high-risk post VSR patients, postponing the procedure is sometimes associated with sudden clinical deterioration and multiorgan failure, leading to sudden death, hence surgery should be done as early as possible to improve survival rate compared to conservative medical management.


The authors are thankful to Mr. Chandrashekar Challa and Mr. Manikandhar Pendyala, for their research assistance.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

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Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: A quantitative review of 23 randomised trials. Lancet 2003;361:13-20.  Back to cited text no. 15
Menon V, Webb JG, Hillis LD, Sleeper LA, Abboud R, Dzavik V, et al. Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarction: A report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK? J Am Coll Cardiol 2000;36:1110-6.  Back to cited text no. 16
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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1], [Table 2]


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