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Table of Contents
Year : 2021  |  Volume : 11  |  Issue : 2  |  Page : 50-57

Current concepts in the management of acute st-elevation myocardial infarction with ventricular septal rupture – Early versus late approach: Part 2 – Surgical management of ventricular septal rupture

1 Department of Cardiology, Sunshine Hospital, Secunderabad, Telangana, India
2 Cardiothoracic Surgery, Sunshine Hospital, Secunderabad, Telangana, India

Date of Submission14-Nov-2019
Date of Acceptance30-Dec-2019
Date of Web Publication03-May-2021

Correspondence Address:
Dr. Sridhar Kasturi
Department of Cardiology, Sunshine Hospital, Secunderabad - 500 003, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JICC.JICC_49_19

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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 hrs and 100% within 30 days. Surgical closure of VSR a challenging procedure with mortality between 20% to 87% depending upon operator's experience and surgical facilities with backup system. In view of the poor prognosis of VSR patients and the ben¬efits from VSR closure, transcatheter closure or surgical repair of the VSR in the acute phase is usually the only option in order to stabilise haemodynamics and restore cardiac function for those with unstable hemodynamic status, despite high risk and mortal¬ity in both therapeutic operations.

Keywords: Acute myocardial infarction, surgical closure, 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 2 – Surgical management of ventricular septal rupture. J Indian coll cardiol 2021;11:50-7

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 2 – Surgical management of ventricular septal rupture. J Indian coll cardiol [serial online] 2021 [cited 2021 Sep 18];11:50-7. Available from:

  Introduction Top

Medical management of VSR is usually futile, with rare exceptions. Definitive surgery remains the treatment of choice but remains a challenging operation associated with high early mortality. Operative mortality was much lower for procedures considered elective (13.2% mortality) vs. emergent (56.0% mortality) vs. salvage (80.5% mortality). Mortality is reduced as the time between VSR and surgical intervention increases, likely due to a more stable and fibrotic myocardium, but also due to survival bias. A strategy of full mechanical support allowing for planned, delayed surgery at seven days may both improve survival while surgery is deferred, and allow for better surgical outcomes due to more stable myocardium.

  Case Reports Top

A case of Acute anterior wall STEMI with VSR – Surgical repair with IABP support and A case of Acute anterior wall STEMI with VSR – Surgical repair with VA-ECMO support

Case 1

A 49-year-old male, known hypertensive, presented with anterior wall ST-elevation myocardial infarction (STEMI) with a window period of 24 h. O/E Pulse rate-124; resp – 30/min; blood pressure (BP) – 106/70 mmHg; cardiovascular symptom (CVS) – S1+, S2+, S3+; pansystolic murmur (PSM) – 3/6 precordial area, lungs-bilateral basal rates; electrocardiogram (ECG) – acute STEMI of the anterior wall [Figure 1]a; investigations: random blood sugar – 124 mg/dl; echo-RWMA in left anterior descending artery (LAD) territory with moderate left ventricular (LV) dysfunction (ejection fraction [EF]: 38%); and apical muscular ventricular septal defect (VSD) with left-to-right shunt. Hemoglobin (Hb) – 14.4 g%, serum creatinine – 0.8 mg/dl, blood urea – 20 mg/dl, serum sodium – 139 mmol/L, serum potassium – 4.1 mmol/L, serum chloride – 106 mmol/L, and albumin – 3.4 g/dL. The patient was shifted to the intensive coronary care unit (ICCU) and treated with inotropic support and diuretics. Coronary angiogram revealed single vessel disease with proximal LAD total occlusion [Figure 2]a, [Figure 2]b. IABP was inserted after the angiogram [Figure 2]c, [Figure 2]d, and the patient shifted to ICCU, and ECG was taken [Figure 1]b.
Figure 1: (a) Preprocedure, (b) Postprocedure, (c) 1-year follow-up

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Figure 2: Emergency coronary angiogram with intra-aortic balloon pump support

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Emergency coronary artery bypass grafting (CABG) with left internal mammary artery to LAD, VSD repair with Gore-Tex cardiovascular patch, and LV repair with IABP and inotropic support were performed. The patient was extubated on the next day of surgery. Intraoperative transesophageal echocardiography revealed no residual VSD. The patient gradually improved and was weaned off the inotropic support. Postoperative transthoracic ECHO before discharge revealed small residual ventricular septal rupture (VSR) (2 mm) with left-to-right shunt. The patient was discharged on the 7th day of procedure with medical advice and he is under the 1-year follow-up [Figure 1]c without any CVS.

Case 2

A 52-year-old female known hypertensive, acute STEMI of the anterior wall, VSR, and cardiogenic shock (CS) presented with the New York Heart Association Class IV (WP – 12 h). O/E – the patient was restless, PR –120 bpm, BP – 60 mmHg systolic with cold and clammy extremities, CVS – S1+, S2+, S3+, S40, PSM – 3/6 over the left sternal border and apex, ECG-sinus tachycardia (heart rate – 136), QS waves in V1–V2, with ST-elevation V1–V6 with small R-waves in V5 and V6 [Figure 3], two-dimensional echo-akinetic LAD territory, VSR with left-to-right shunt, severe LV dysfunction, and EF – 35%. Investigations: Hb – 12.9 g/dl, total leukocyte count – 22,230 cells/, platelet count – 4.52 lakhs/, international normalized ratio (INR) – 1.185, serum urea – 43 mg/dl, serum creatinine – 1.2 mg/dl, C-reactive protein – 75.41 mg/L, chest X-ray evidence of pulmonary edema, emergency coronary angiography (CAG) with IABP support through radiofrequency ablation-two-vessel disease, mid LAD 90% lesion after D1, distal small caliber thin vessel, right coronary artery (RCA) mid-long 80% lesion, and posterior descending artery (PDA) and posterior left ventricular branch were normal [Figure 4].
Figure 3: Electrocardiogram

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Figure 4: Coronary angiography: (a) Left anterior descending artery – mid 90% lesion, (b) right coronary artery mid long 80% lesion

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Emergency CABG (on the pump) saphenous vein grafts to LAD and distal RCA with the repair of VSR [Figure 5]a were done. Modified Dor's repair with VSD exclusion was done with polytetrafluoroethylene (PTFE) patch sutured to septum with multiple 3-0 pledgeted, patch included in suture line of ventriculotomy, thereby excluding VSD and infarct from the LV cavity. Postoperatively, the patient developed oliguria followed by anuria, although hemodynamically stable with IABP support. Hemodialysis was started for acute renal failure. On the 2nd postoperative day, hemodynamic status worsened despite IABP and high ionotropic support, venoarterial extracorporeal membrane oxygenation (VA-ECMO) with femoral vein to femoral artery circulatory support was started. Continuous renal replacement therapy was started in view of renal failure with serum creatinine 2.5 mg/dl and persistent hyperkalemia. The patient developed thrombocytopenia – 50,000 cells/mm3 and elevated INR – 4.56; on the 3rd postoperative day, arterial blood gas showed persistent metabolic acidosis and developed lower gastrointestinal bleed due to disseminated intravascular coagulation. Necessary supportive measures were extended, and the patient continued on VA-ECMO support [Figure 5]b. The patient developed asystole on the 3rd postoperative day and could not be revived despite immediate cardiopulmonary resuscitation with ionotrophic and ventilator support.
Figure 5: (a) Ventricular septal rupture repair, (b) venoarterial-extracorporeal membrane oxygenation support for acute anterior ST-elevation myocardial infarction with ventricular septal rupture

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  Surgical Management Top

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 to stabilize hemodynamics and restore cardiac function for those with unstable hemodynamic status despite high risk and mortality in both therapeutic operations.

The optimal timing of surgical repair is controversial and should be individualized. The 2013 American College of Cardiology and American Heart Association guidelines recommend emergent surgical repair regardless of hemodynamic data. In hemodynamically stable patients with preserved end-organ function and favorable anatomy, early surgery should be considered because sudden and unpredictable hemodynamic compromise is often noted. Delayed surgery may also be appropriate in stable patients with high comorbidities and with complex anatomy, particularly in the elderly and those with poor right ventricular (RV) function. 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 the deposition of new collagen begins by days 2–4 and necrotic myocytes are entirely replaced by collagen by 28 days.[1] Therefore, the 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 the chances of definitive repair. Taking this subgroup into consideration, the 2017 European Society of Cardiology Guidelines promotes delayed elective repair in patients responding to aggressive conservative management.[2] In stable but inoperable patients, percutaneous transcatheter septal closure (TSC) may be an option.

The criteria for defaulting VSR surgery were as follows: (1) the absence of decreased cardiac output (exclude CS), (2) absence of significant symptoms and pulmonary venous hypertension, (3) absence of fluid retention, and (4) adequate renal function. If serum creatinine rises, develops CS/RV dysfunction needs early surgery.

Preoperative management is directed toward the stabilization of the hemodynamic condition and preservation of end-organ perfusion. This is best achieved by the IABP. IABP support decreases myocardial oxygen demand and improves myocardial and peripheral organ perfusion. However, the maximum benefit is achieved within 24 h, and no further benefit is observed with prolonged IABP usage.

  Operative Considerations Top

There are many different techniques to repair postinfarct VSRs. They include patch techniques, either single or double, or infarct exclusion techniques. The approach used for exposing the VSR by majority surgeons is through an incision made in the infarcted left ventricle. However, in selected cases, particularly in posterior or inferior VSRs, a RV or right atrial approach may provide equally good exposure and results.

The general principles of post-MI VSR repair were as follows:

  1. Transinfarct approach with the site of ventriculotomy by the location of infarction. For apical VSRs, 1-cm lateral and parallel to LAD, and for inferior defects, a cm lateral and parallel to PDA branch of the right coronary artery
  2. The infarcted and hemorrhagic septum makes the determination of the septal defect
  3. Excessive debridement is avoided
  4. Closure of the defect without tension, using a prosthetic material like Dacron or bovine pericardium
  5. Placing the sutures far from the defect through healthy myocardial tissue
  6. Closure of the ventriculotomy and buttressing the suture lines with strips of Teflon felt to prevent cutting off sutures through the friable tissue.

Closure of apical ventricular septal ruptures

Apical septal defects involve the apical portion of the right ventricle, septum, and the left ventricle. Daggett et al. described the technique of apical amputation and repair. An incision [Figure 6] is through the infarct is made, and all the necrotic materials are derided.[3] The remaining edges of the right ventricle, left ventricle, and septum are brought together and reapproximated using interrupted mattress sutures buttressed with strips of Teflon felt or the pericardium.
Figure 6: Apical ventricular septal rupture repair by apical amputation as described

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Closure of anterior septal rupture

Anterior VSRs involves the anterior septum as well as the anterior LV free wall as a result of an infarct in the LAD territory. David et al. described “infarct exclusion” technique to repair these defects. In this technique [Figure 7], instead of closing the septal defect, it is excluded from the high-pressure zone of the left ventricle.[4] In patients with anterior septal rupture, the septum is exposed through an incision in the infarcted anterior wall 1 cm lateral and parallel to the LAD artery. Using a Dacron, Gore-tex, or bovine pericardial patch, a “neoseptum” is created between the LV and the old septum where the septal defect lies. Using an interrupted or continuous technique of suturing, deep bites are taken through healthy tissue. Repair is completed by linear closure of the ventriculotomy reinforced with the strips of felt or pericardium.
Figure 7: Repair of anterior ventricular septal rupture by endocardial patch and infarct exclusion technique

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Closure of posterior ventricular septal ruptures

The posterior or inferior septal ruptures involve a transmural infarction of the myocardium in the PDA distribution. Closure of the posterior septal defects is challenging. The apex of the heart is elevated to expose the inferior wall, and the posterior VSD is exposed through a longitudinal incision made 1 cm lateral and parallel to PDA, directly through the infarcted, necrotic LV myocardium. Care is taken to avoid damage to the posterior papillary muscle. Debridement of the septum if required should be limited. An appropriately sized bovine pericardial or prosthetic patch like Dacron or PTFE material is sutured over the defect, along the mitral annulus at the base, the endocardium of the septum taking care to place the sutures through the healthy myocardial tissue. Another edge of the patch is brought out through the left ventricular incision and incorporated into the closure of the LV incision. The LV incision is closed in two layers, the first layer is interrupted horizontal mattress sutures buttressed with strips of felt on either side of the LV wall, incorporating full thickness of LV wall, septal patch, and felt strips. The second run of the suture is an over and over suture to provide additional hemostasis to the LV incision.

The lethal complications described of approaching through an incision in the infarcted LV and infarct exclusion technique are bleeding from left ventriculotomy, recurrence of the shunt (ranging from 13% to 40% in various reports), and low output syndrome.

  Alternative Approaches of Repair of Ventricular Septal Ruptures Top

The standard approach for VSR closure is through LV incision. Recently, alternative approaches through right ventriculotomy using an extended “sandwich” double-patch technique is described by Asai with good results.[5]

Right ventricular approach of repairing postmyocardial infarction ventricular septal ruptures

A RV incision [Figure 8] is made parallel to the LAD or PDA for repairing anterior or posterior VSR, respectively. A Dacron patch large enough to cover the defect with a margin of about 2 cm is introduced into the left ventricle through an RV incision and through the VSR. The patch is securely fixed by placing large mattress sutures transseptally and transmurally around the defect from the LV cavity to the RV side or the outside of the LV. The second patch is into the RV. After glue insertion, sutures are tied. The authors reported that this technique is safe and provides a lower incidence of residual leakage, and because of the large double patch, transmural full-thickness sutures are used. In addition, the RV gets blood supply independent of PDA or LAD. The better preservation of viable LV along with the low incidence of residual leaks is sited as the reason for the lower incidence of postoperative low cardiac output syndrome.
Figure 8: Cross-sectional view of posterior ventricular septal rupture repair by extended sandwich patch technique through right ventricular approach

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Right atrial approach of repairing postmyocardial infarction ventricular septal ruptures

The right atrial approach offers the theoretical advantages of avoiding left or RV incision and thereby the postoperative complications such as bleeding and ventricular dysfunction and arrhythmia.

Originally, the right atrial approach was proposed for repairing chronic posterior VSDs. However, the right atrial approach has not gained popularity; the identification and exposure of VSR are difficult because of the trabeculation of the right ventricle [Figure 9]a. Furthermore, the placement of the patch [Figure 9]b on the right side increases the chance of residual leaks because of the left-to-right pressure gradient. In addition, an optimal exposure of the VSR may require detachment of the septal leaflet. However, if these difficulties can be managed successfully, the right atrial approach offers a less complicated operation for the posterior VSR.
Figure 9: The repaired post-infarction ventricular septal rupture as seen through right atriotomy (a) and the Dacron patch sutured to the right side of the ventricular septum (b)

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  Essentials of Postoperative Care Top

Early postoperative diuresis and positive end-expiratory pressure ventilation are useful in reducing the alveolar-arteriolar gradient. If needed, continuous veno-venous hemofiltration is employed. Intravenous amiodarone is useful in controlling intractable postoperative ventricular arrhythmias secondary to reperfusion injury.

Post-VSR recur in 10%–20% of patients due to residual shunt, reopening of closed VSR, and rerupture, it may cause hemodynamic disturbance or hemolysis requiring reintervention. The size of the defect determines the degree of the shunting, the extent of hemodynamic compromise, and therefore, the likelihood of survival. Concomitant myocardial revascularization in patients with multivessel disease decreases operative mortality.

  Outcomes of Surgical Ventricular Septal Rupture Repair Top

The medical management of VSR is usually futile with rare exceptions. Definitive surgery remains the treatment of choice but remains a challenging operation associated with high early mortality. A recently published review of the Society of Thoracic Surgeons National Database identified 2876 individuals aged ≥18 years who underwent post-MI VSR repair between 1999 and 2010.[6] Overall operative mortality was 42.9%, which represented the highest mortality rate of any cardiac surgery. Patients who did not survive to 30 days are older, females, had higher serum creatinine levels, and higher acuity of disease (CS, reduced LVEF, triple-vessel coronary artery disease, or requirement for preoperative IABP). Operative mortality was much lower for procedures considered elective (13.2% mortality) versus emergent (56.0% mortality) versus salvage (80.5% mortality).[7] Mortality is reduced as the time between VSR and surgical intervention increases, likely due to a more stable and fibrosed myocardium but also due to survival bias. It is unknown what percentage of patients continues to survive as surgery is deferred. In the GUSTO-1 trial, there was 94% mortality at 30 days without surgery suggesting that conservative management is associated with very high mortality. A strategy of full mechanical support allowing for planned, delayed surgery at 7 days may both improve survival while surgery is deferred and allow for better surgical outcomes due to more stable myocardium, but data are currently limited to the case reports [Figure 10].[6]
Figure 10: Reported 30-day mortality for ventricular septal rupture with immediate surgical management or at various timepoints of delayed intervention

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The most common cause of death in post-MI VSR-operated patients was persistent low cardiac output. Predictors which increases surgical mortality were hemodynamic instability, ventricular dysfunction, inferior or posterior VSD location, early surgery, cardiogenic shock, raised systolic pulmonary artery pressure, post infarct VSR diameter, and emergency operation. Delaying VSR surgery by stabilizing the patients in critical care with IABP and medical therapy results in better surgical outcome; however, it should be performed immediately in patients with shock, unless there is a severe, life-shortening, underlying pathology. Surgical repair of VSR improves the survival, but acute and long-term results are determined by the magnitude of postsurgical residual shunt, which can be classified by measuring the width of shunt, trivial <1 mm, mild between 1 and 2 mm, moderate between 2 and 4 mm, and large >4 mm. Large residual VSR requires redo surgery or transcatheter closure.

Post-MI VSR corrective procedures were (surgical or minimally invasive) performed in only 7.65% of the patients. More than one-third of patients (36.5%) required some form of assistive support device, with IABP being by far the most commonly used (35%). Of all these support devices, IABP was also related to lower mortality rates, but it was still high, almost half of the patients (47.09%, P < 0.0001). It is reasonable to consider IABP as a feasible support device to reduce afterload and possibly minimize the amount of left-to-right shunt while also decreasing the oxygen demand and possibly ischemia.

UNM Malhotra A et al. reported Post-MI VSR Scoring Systems [Figure 11] to guide management and indicate the prognosis of patients. A “heart team” evaluates the patient. Patients with UNM Post-MI VSR Management Scoring System (UPMS) of <25 undergo emergency surgery with ECMO support if required. Patients with UPMS of 25–75 are optimally stabilized before being taken up for the surgery. This group benefits the most from “Optimal Delay” in surgery. Patients with a score of over 75 are most likely to survive and undergo planned device or surgical closure. As described earlier, UNM Post-MI VSR Prognosis Scoring System (UPPS) helps to prognosticate patients with post-MI VSR. All patients with UPPS of <25 died, whereas none of the patients with UPPS >75 died. Therefore, patients with higher UPPS have higher chances of survival.[8]
Figure 11: University of New Mexico post-myocardial infarction ventricular septal rupture Management Scoring System

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Low mean blood pressure after IABP insertion, higher EuroSCORE II, higher Killip class, shorter intervals between MI and VSR surgery (odds ratio 5.76, P = 0.016) were independent predictors of mortality.

Hemodynamic patterns after IABP institution and suggested timing of intervention: (1) patients who were not improving hemodynamically, even after IABP, high inotropic supports and ventilatory support, represented a true surgical emergency and needed immediate surgery, (2) few patients who were stable, with no clinical deterioration, underwent elective repair/percutaneous closure after 4–6 weeks, and (3) patients usually improved hemodynamically with institution of IABP, inotropic support, and with/without ventilatory support. The improvement brought them to the lower Killip class. After this phase, deterioration started by the virtue of infection and vascular complications. This period, in which the patient's condition was optimum, was the window of opportunity for the surgeon.

Surgical outcomes in the setting of CS are dismal. In the setting of the SHOCK trial, surgical VSR correction was associated with a mortality rate of 87%. Survival rates following TSC in this context are equally disappointing.

The availability of temporary mechanical circulatory support (MCS) devices has revolutionized the treatment strategies in patients with CS. Current evidence suggests to support such patients with VA-ECMO and ventricular assist devices (VADs) which allow for (1) stabilization of hemodynamics, (2) recovery or prevention of end-organ injury, (3) washout of dual antiplatelet effect, and (4) strategy of the bridge to decision. Experienced operators have successfully utilized the 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 CS of various etiologies.[9] Short-term MCS has received a Class IIa recommendation (level of evidence C) as a bridge in VSR patients.[10]

ECMO is economically efficient, prevents sternotomy, provides oxygenation support, and is easily reversible. Recently published meta-analysis showed that in acute MI (AMI) patients with CS and undergoing percutaneous coronary intervention (PCI), the in-hospital mortality was significantly higher with IABP support versus medical therapy, percutaneous left ventricular assist devices (PLVADs) increased, although nonsignificantly, the mortality as compared with IABP; and ECMO plus IABP had a significant protective effect compared to IABP or ECMO alone. CS due to VSR complicating AMI, routinely use of IABP and PLVADs is not recommended; and the beneficial effect of the reduction in hospital mortality provided by ECMO plus IABP could be attributed to the synergistic action of the two devices in supporting the failing heart.[11] IABP decreasing afterload and myocardial oxygen consumption can avoid the negative effects on myocardial protection that can occur when using ECMO alone. Impella mechanical support device use can be complicated by pump failure due to the aspiration of necrotic debris into the impeller pumps and can induce right-to-left shunt, leading onto hypoxic brain damage, although limited case reports are available with Impella-supported VSR, which did not showed any survival benefit.

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. 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 total artificial heart (TAH) as back up. In others with catastrophic cardiac destruction, listing for transplantation and/or TAH insertion may be the appropriate strategy.[12]

  Timing of Procedures and Antiplatelet Therapy in ST-Elevation Myocardial Infarction with Ventricular Septal Rupture Top

VSD closure was before PCI; however, the PCI procedure would be performed first if the patient presented with unstable angina and if coronary angiography showed a culprit lesion in proximal vessels with heavy thrombosis which might cause recurrent MI. In patients who underwent VSD closure first, no antiplatelet drugs were used before the procedure, and aspirin was prescribed after VSR closure if there was no residual shunt. For patients with a residual shunt after VSR closure, no antiplatelet drugs were used until 1–3 days before the PCI procedure and dual-antiplatelet therapy administration (DAPT, including aspirin and thienopyridines). In patients who underwent PCI first, DAPT was initiated before PCI and ceased 2 days before VSR closure. DAPT was then resumed if there was no residual shunt after VSR closure, otherwise, only aspirin was administered [Figure 12].
Figure 12: A simplified version of multidisciplinary strategy for managing patients with ST-elevation myocardial infarction with ventricular septal rupture (ventricular septal rupture Management Algorithm) (a) if deemed suitable for percutaneous repair, transcatheter septal closure 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 the failure of repair. (MCS: Mechanical circulatory support; OHT: Orthotopic heart transplant, TAH: Total artificial heart)

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

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction: Pathophysiology and therapy. Circulation 2000;101:2981-8.  Back to cited text no. 1
Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2018;39:119-77.  Back to cited text no. 2
Daggett WM, Guyton RA, Mundth ED, Buckley MJ, McEnany MT, Gold HK, et al. Surgery for post-myocardial infarct ventricular septal defect. Ann Surg 1977;186:260-71.  Back to cited text no. 3
David TE, Dale L, Sun Z. Postinfarction ventricular septal rupture: Repair by endocardial patch with infarct exclusion. J Thorac Cardiovasc Surg 1995;110:1315-22.  Back to cited text no. 4
Asai T. Postinfarction ventricular septal rupture: Can we improve clinical outcome of surgical repair? Gen Thorac Cardiovasc Surg 2016;64:121-30.  Back to cited text no. 5
Arnaoutakis GJ, Zhao Y, George TJ, Sciortino CM, McCarthy PM, Conte JV. Surgical repair of ventricular septal defect after myocardial infarction: Outcomes from the Society of Thoracic Surgeons National Database. Ann Thorac Surg 2012;94:436-43.  Back to cited text no. 6
Fukushima S, Tesar PJ, Jalali H, Clarke AJ, Sharma H, Choudhary J, et al. Determinants of in-hospital and long-term surgical outcomes after repair of postinfarction ventricular septal rupture. J Thorac Cardiovasc Surg 2010;140:59-65.  Back to cited text no. 7
Malhotra A, Patel K, Sharma P, Wadhawa V, Madan T, Khandeparkar J, et al. Techniques, timing and prognosis of post infarct ventricular septal repair: A re-look at old dogmas. Braz J Cardiovasc Surg 2017;32:147-55.  Back to cited text no. 8
Kar B, Gregoric ID, Basra SS, Idelchik GM, Loyalka P. The percutaneous ventricular assist device in severe refractory cardiogenic shock. J Am Coll Cardiol 2011;57:688-96.  Back to cited text no. 9
McMurray JJ, Adamopoulos S, Anker SD, Auricchio A, Böhm M, Dickstein K, et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The task force for the diagnosis and treatment of acute and chronic heart failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail 2012;14:803-69.  Back to cited text no. 10
Romeo F, Acconcia MC, Sergi D, Romeo A, Francioni S, Chiarotti F, et al. Percutaneous assist devices in acute myocardial infarction with cardiogenic shock: Review, meta-analysis. World J Cardiol 2016;8:98-111.  Back to cited text no. 11
O'Gara PT, Kushner FG, Ascheim DD, Casey DE Jr, Chung MK, de Lemos JA, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2013;61:e78-140.  Back to cited text no. 12


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12]


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